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CK2 constitutively associates with and phosphorylates chicken erythroid ankyrin and regulates its ability to bind to spectrin. 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While inflammation is a cardinal feature for immune defense, the magnitude and period of the inflammatory response has to follow the ‘Goldilocks Principle’ wherein inflammation would be detrimental if its amplitude is too little or too much, or its period too short or too long. Drs. Rothlin and Ghosh investigates the principles and molecular mechanisms that negatively regulate inflammation and ensure that the amplitude and period of inflammation is ‘just right’. 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Mitotic regulation of ribosomal S6 kinase 1 involves Ser/Thr, Pro phosphorylation of consensus and non-consensus sites by Cdc2. 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While inflammation is a cardinal feature for immune defense, the magnitude and period of the inflammatory response has to follow the ‘Goldilocks Principle’ wherein inflammation would be detrimental if its amplitude is too little or too much, or its period too short or too long. Drs. Rothlin and Ghosh investigates the principles and molecular mechanisms that negatively regulate inflammation and ensure that the amplitude and period of inflammation is ‘just right’. 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Downregulation of caveolin-1 function by EGF leads to the loss of E-cadherin, increased transcriptional activity of beta-catenin, and enhanced tumor cell invasion. 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Essential role of tuberous sclerosis genes TSC1 and TSC2 in NF-kappaB activation and cell survival. Cancer Cell 2006, 10:215-26.\\\",\\\"@context\\\":\\\"http://schema.org\\\"}\"},{\"schemaName\":\"MedicalScholarlyArticle\",\"jsonData\":\"{\\\"@type\\\":\\\"MedicalScholarlyArticle\\\",\\\"publicationType\\\":\\\"Journal Article\\\",\\\"inLanguage\\\":\\\"en-US\\\",\\\"headline\\\":\\\"TAM receptors are pleiotropic inhibitors of the innate immune response.\\\",\\\"url\\\":\\\"https://www.ncbi.nlm.nih.gov/pubmed/18083102/\\\",\\\"author\\\":[{\\\"@type\\\":\\\"Person\\\",\\\"mainEntityOfPage\\\":{\\\"@type\\\":\\\"WebPage\\\",\\\"@id\\\":\\\"https://medicine.yale.edu/ysm/profile/sourav_ghosh/\\\",\\\"@context\\\":\\\"http://schema.org\\\"},\\\"name\\\":\\\"Sourav Ghosh\\\",\\\"description\\\":\\\"Sourav Ghosh, Ph.D., is an Associate Professor of Neurology and Pharmacology at the Yale University School of Medicine. Dr. Ghosh obtained a M.Sc. in Zoology at the University of Calcutta, where he studied Drosophila and mosquito genetics. Next, he completed his graduate studies on cell cytoskeleton and protein trafficking under the direction of John V. Cox at the University of Tennessee, Memphis. Subsequently, Dr. Ghosh did his postdoctoral research on cell signaling at the Salk Institute for Biological Studies under the guidance of Tony Hunter. In 2007, Dr. Ghosh joined University of Arizona as an Assistant Professor, and in 2014 he moved to Yale University School of Medicine and is currently an Associate Professor in the Departments of Neurology and Pharmacology. Dr. Ghosh and Dr. Carla Rothlin co-direct a lab studying the regulation of inflammation (Rothin, Ghosh et al. Cell, 2007, Carrera Silva et al. Immunity, 2013, Bosurgi et al. Science, 2017). While inflammation is a cardinal feature for immune defense, the magnitude and period of the inflammatory response has to follow the ‘Goldilocks Principle’ wherein inflammation would be detrimental if its amplitude is too little or too much, or its period too short or too long. Drs. Rothlin and Ghosh investigates the principles and molecular mechanisms that negatively regulate inflammation and ensure that the amplitude and period of inflammation is ‘just right’. 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Instructive role of aPKCzeta subcellular localization in the assembly of adherens junctions in neural progenitors. 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Telomere-independent Rap1 is an IKK adaptor and regulates NF-kappaB-dependent gene expression. Nature Cell Biology 2010, 12:758-67.\\\",\\\"@context\\\":\\\"http://schema.org\\\"}\"},{\"schemaName\":\"MedicalScholarlyArticle\",\"jsonData\":\"{\\\"@type\\\":\\\"MedicalScholarlyArticle\\\",\\\"publicationType\\\":\\\"Journal Article\\\",\\\"inLanguage\\\":\\\"en-US\\\",\\\"headline\\\":\\\"Spinal protein kinase M ζ underlies the maintenance mechanism of persistent nociceptive sensitization.\\\",\\\"url\\\":\\\"https://www.ncbi.nlm.nih.gov/pubmed/21543593/\\\",\\\"author\\\":[{\\\"@type\\\":\\\"Person\\\",\\\"mainEntityOfPage\\\":{\\\"@type\\\":\\\"WebPage\\\",\\\"@id\\\":\\\"https://medicine.yale.edu/ysm/profile/sourav_ghosh/\\\",\\\"@context\\\":\\\"http://schema.org\\\"},\\\"name\\\":\\\"Sourav Ghosh\\\",\\\"description\\\":\\\"Sourav Ghosh, Ph.D., is an Associate Professor of Neurology and Pharmacology at the Yale University School of Medicine. 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While inflammation is a cardinal feature for immune defense, the magnitude and period of the inflammatory response has to follow the ‘Goldilocks Principle’ wherein inflammation would be detrimental if its amplitude is too little or too much, or its period too short or too long. Drs. Rothlin and Ghosh investigates the principles and molecular mechanisms that negatively regulate inflammation and ensure that the amplitude and period of inflammation is ‘just right’. 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The TAM family receptor tyrosine kinase TYRO3 is a negative regulator of type 2 immunity. Science (New York, N.Y.) 2016, 352:99-103.\\\",\\\"@context\\\":\\\"http://schema.org\\\"}\"},{\"schemaName\":\"MedicalScholarlyArticle\",\"jsonData\":\"{\\\"@type\\\":\\\"MedicalScholarlyArticle\\\",\\\"publicationType\\\":\\\"Journal Article\\\",\\\"inLanguage\\\":\\\"en-US\\\",\\\"headline\\\":\\\"Macrophage function in tissue repair and remodeling requires IL-4 or IL-13 with apoptotic cells.\\\",\\\"url\\\":\\\"https://www.ncbi.nlm.nih.gov/pubmed/28495875/\\\",\\\"author\\\":[{\\\"@type\\\":\\\"Person\\\",\\\"mainEntityOfPage\\\":{\\\"@type\\\":\\\"WebPage\\\",\\\"@id\\\":\\\"https://medicine.yale.edu/ysm/profile/sourav_ghosh/\\\",\\\"@context\\\":\\\"http://schema.org\\\"},\\\"name\\\":\\\"Sourav Ghosh\\\",\\\"description\\\":\\\"Sourav Ghosh, Ph.D., is an Associate Professor of Neurology and Pharmacology at the Yale University School of Medicine. 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While inflammation is a cardinal feature for immune defense, the magnitude and period of the inflammatory response has to follow the ‘Goldilocks Principle’ wherein inflammation would be detrimental if its amplitude is too little or too much, or its period too short or too long. Drs. Rothlin and Ghosh investigates the principles and molecular mechanisms that negatively regulate inflammation and ensure that the amplitude and period of inflammation is ‘just right’. 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Macrophage function in tissue repair and remodeling requires IL-4 or IL-13 with apoptotic cells. Science (New York, N.Y.) 2017, 356:1072-1076.\\\",\\\"@context\\\":\\\"http://schema.org\\\"}\"},{\"schemaName\":\"MedicalScholarlyArticle\",\"jsonData\":\"{\\\"@type\\\":\\\"MedicalScholarlyArticle\\\",\\\"publicationType\\\":\\\"Journal Article\\\",\\\"inLanguage\\\":\\\"en-US\\\",\\\"headline\\\":\\\"Negative Regulation of Type 2 Immunity.\\\",\\\"url\\\":\\\"https://www.ncbi.nlm.nih.gov/pubmed/28082101/\\\",\\\"author\\\":[{\\\"@type\\\":\\\"Person\\\",\\\"mainEntityOfPage\\\":{\\\"@type\\\":\\\"WebPage\\\",\\\"@id\\\":\\\"https://medicine.yale.edu/ysm/profile/sourav_ghosh/\\\",\\\"@context\\\":\\\"http://schema.org\\\"},\\\"name\\\":\\\"Sourav Ghosh\\\",\\\"description\\\":\\\"Sourav Ghosh, Ph.D., is an Associate Professor of Neurology and Pharmacology at the Yale University School of Medicine. 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While inflammation is a cardinal feature for immune defense, the magnitude and period of the inflammatory response has to follow the ‘Goldilocks Principle’ wherein inflammation would be detrimental if its amplitude is too little or too much, or its period too short or too long. Drs. Rothlin and Ghosh investigates the principles and molecular mechanisms that negatively regulate inflammation and ensure that the amplitude and period of inflammation is ‘just right’. 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TAM receptor tyrosine kinases as emerging targets of innate immune checkpoint blockade for cancer therapy. Immunological Reviews 2017, 276:165-177.\\\",\\\"@context\\\":\\\"http://schema.org\\\"}\"},{\"schemaName\":\"MedicalScholarlyArticle\",\"jsonData\":\"{\\\"@type\\\":\\\"MedicalScholarlyArticle\\\",\\\"publicationType\\\":\\\"Journal Article\\\",\\\"inLanguage\\\":\\\"en-US\\\",\\\"headline\\\":\\\"The receptor tyrosine kinase AXL promotes migration and invasion in colorectal cancer.\\\",\\\"url\\\":\\\"https://www.ncbi.nlm.nih.gov/pubmed/28727830/\\\",\\\"author\\\":[{\\\"@type\\\":\\\"Person\\\",\\\"mainEntityOfPage\\\":{\\\"@type\\\":\\\"WebPage\\\",\\\"@id\\\":\\\"https://medicine.yale.edu/ysm/profile/sourav_ghosh/\\\",\\\"@context\\\":\\\"http://schema.org\\\"},\\\"name\\\":\\\"Sourav Ghosh\\\",\\\"description\\\":\\\"Sourav Ghosh, Ph.D., is an Associate Professor of Neurology and Pharmacology at the Yale University School of Medicine. 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The receptor tyrosine kinase AXL promotes migration and invasion in colorectal cancer. PloS One 2017, 12:e0179979.\\\",\\\"@context\\\":\\\"http://schema.org\\\"}\"},{\"schemaName\":\"MedicalScholarlyArticle\",\"jsonData\":\"{\\\"@type\\\":\\\"MedicalScholarlyArticle\\\",\\\"publicationType\\\":\\\"Journal Article\\\",\\\"inLanguage\\\":\\\"en-US\\\",\\\"headline\\\":\\\"Death begets a new beginning.\\\",\\\"url\\\":\\\"https://www.ncbi.nlm.nih.gov/pubmed/29027219/\\\",\\\"author\\\":[{\\\"@type\\\":\\\"Person\\\",\\\"mainEntityOfPage\\\":{\\\"@type\\\":\\\"WebPage\\\",\\\"@id\\\":\\\"https://medicine.yale.edu/ysm/profile/sourav_ghosh/\\\",\\\"@context\\\":\\\"http://schema.org\\\"},\\\"name\\\":\\\"Sourav Ghosh\\\",\\\"description\\\":\\\"Sourav Ghosh, Ph.D., is an Associate Professor of Neurology and Pharmacology at the Yale University School of Medicine. Dr. Ghosh obtained a M.Sc. in Zoology at the University of Calcutta, where he studied Drosophila and mosquito genetics. 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While inflammation is a cardinal feature for immune defense, the magnitude and period of the inflammatory response has to follow the ‘Goldilocks Principle’ wherein inflammation would be detrimental if its amplitude is too little or too much, or its period too short or too long. Drs. Rothlin and Ghosh investigates the principles and molecular mechanisms that negatively regulate inflammation and ensure that the amplitude and period of inflammation is ‘just right’. 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Sourav Ghosh, Ph.D., is an Associate Professor of Neurology and Pharmacology at the Yale University School of Medicine. Dr. Ghosh obtained a M.Sc. in Zoology at the University of Calcutta, where he studied Drosophila and mosquito genetics. Next, he completed his graduate studies on cell cytoskeleton and protein trafficking under the direction of John V. Cox at the University of Tennessee, Memphis. Subsequently, Dr. Ghosh did his postdoctoral research on cell signaling at the Salk Institute for Biological Studies under the guidance of Tony Hunter. In 2007, Dr. Ghosh joined University of Arizona as an Assistant Professor, and in 2014 he moved to Yale University School of Medicine and is currently an Associate Professor in the Departments of Neurology and Pharmacology. Dr. Ghosh and Dr. Carla Rothlin co-direct a lab studying the regulation of inflammation (Rothin, Ghosh et al. Cell, 2007, Carrera Silva et al. Immunity, 2013, Bosurgi et al. Science, 2017). While inflammation is a cardinal feature for immune defense, the magnitude and period of the inflammatory response has to follow the ‘Goldilocks Principle’ wherein inflammation would be detrimental if its amplitude is too little or too much, or its period too short or too long. Drs. Rothlin and Ghosh investigates the principles and molecular mechanisms that negatively regulate inflammation and ensure that the amplitude and period of inflammation is ‘just right’. Defects in these molecular circuits can manifest as wide ranging clinical problems including chronic or pathological inflammation, autoimmunity and pathological wound healing, while harnessing these checkpoints can improve anti-cancer immunity.

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I co-lead our group with Carla Rothlin, Professor of Immunobiology and Pharmacology. We are interested in tissue morphogenesis, maintenance and repair with specific emphasis on the functional role of the immune system in development, tissue maintenance and repair/regeneration, as well as the role of cell polarity in these processes. One of the current interests in the lab is cell death and its clearance, and how this can function as a signal for specific effector responses during morphogenesis, homeostatic tissue renewal, or resolution and wound repair after damage. We hypothesize that the integration of cell death recognition, environmental signals (including tissue-specific signals) and the identity of the efferocyte (the cell that recognizes dead cells) determines the specificity for removal of dead/damaged cells, renewal of lost cells, or repair and regeneration. We use a variety of approaches including molecular, cell biology, immunology, imaging and genetics and mouse models of development/tissue homeostasis/injury or diseases to address fundamental biological mechanisms. \\n

Current projects:

1. Astrocytes, oligodendrocytes and microglia during the formation, function and after injury in the nervous systems

2. Macrophage-stromal interactions during tissue homeostasis and wound repair

3. Tumorigenesis and tumor progression, including innate immune checkpoints and anti-tumor immunity

\",\"researchInterests\":[\"Glioblastoma\",\"Immune System\",\"Inflammation\",\"Cell Death\",\"Neurodegenerative Diseases\",\"Neurodevelopmental Disorders\"],\"healthInterests\":[],\"researchImagesGallery\":null},\"publications\":[{\"title\":\"Chicken erythroid AE1 anion exchangers associate with the cytoskeleton during recycling to the Golgi.\",\"citation\":\"Ghosh S, Cox KH, Cox JV. Chicken erythroid AE1 anion exchangers associate with the cytoskeleton during recycling to the Golgi. Molecular Biology Of The Cell 1999, 10:455-69.\",\"year\":1999,\"link\":{\"url\":\"https://www.ncbi.nlm.nih.gov/pubmed/9950688/\",\"text\":\"Chicken erythroid AE1 anion exchangers associate with the cytoskeleton during recycling to the Golgi.\"}},{\"title\":\"Dynamics of ankyrin-containing complexes in chicken embryonic erythroid cells: role of phosphorylation.\",\"citation\":\"Ghosh S, Cox JV. Dynamics of ankyrin-containing complexes in chicken embryonic erythroid cells: role of phosphorylation. Molecular Biology Of The Cell 2001, 12:3864-74.\",\"year\":2001,\"link\":{\"url\":\"https://www.ncbi.nlm.nih.gov/pubmed/11739786/\",\"text\":\"Dynamics of ankyrin-containing complexes in chicken embryonic erythroid cells: role of phosphorylation.\"}},{\"title\":\"CK2 constitutively associates with and phosphorylates chicken erythroid ankyrin and regulates its ability to bind to spectrin.\",\"citation\":\"Ghosh S, Dorsey FC, Cox JV. CK2 constitutively associates with and phosphorylates chicken erythroid ankyrin and regulates its ability to bind to spectrin. Journal Of Cell Science 2002, 115:4107-15.\",\"year\":2002,\"link\":{\"url\":\"https://www.ncbi.nlm.nih.gov/pubmed/12356915/\",\"text\":\"CK2 constitutively associates with and phosphorylates chicken erythroid ankyrin and regulates its ability to bind to spectrin.\"}},{\"title\":\"Mitotic regulation of ribosomal S6 kinase 1 involves Ser/Thr, Pro phosphorylation of consensus and non-consensus sites by Cdc2.\",\"citation\":\"Shah OJ, Ghosh S, Hunter T. Mitotic regulation of ribosomal S6 kinase 1 involves Ser/Thr, Pro phosphorylation of consensus and non-consensus sites by Cdc2. The Journal Of Biological Chemistry 2003, 278:16433-42.\",\"year\":2003,\"link\":{\"url\":\"https://www.ncbi.nlm.nih.gov/pubmed/12586835/\",\"text\":\"Mitotic regulation of ribosomal S6 kinase 1 involves Ser/Thr, Pro phosphorylation of consensus and non-consensus sites by Cdc2.\"}},{\"title\":\"Downregulation of caveolin-1 function by EGF leads to the loss of E-cadherin, increased transcriptional activity of beta-catenin, and enhanced tumor cell invasion.\",\"citation\":\"Lu Z, Ghosh S, Wang Z, Hunter T. Downregulation of caveolin-1 function by EGF leads to the loss of E-cadherin, increased transcriptional activity of beta-catenin, and enhanced tumor cell invasion. Cancer Cell 2003, 4:499-515.\",\"year\":2003,\"link\":{\"url\":\"https://www.ncbi.nlm.nih.gov/pubmed/14706341/\",\"text\":\"Downregulation of caveolin-1 function by EGF leads to the loss of E-cadherin, increased transcriptional activity of beta-catenin, and enhanced tumor cell invasion.\"}},{\"title\":\"Coexpressed EphA receptors and ephrin-A ligands mediate opposing actions on growth cone navigation from distinct membrane domains.\",\"citation\":\"Marquardt T, Shirasaki R, Ghosh S, Andrews SE, Carter N, Hunter T, Pfaff SL. Coexpressed EphA receptors and ephrin-A ligands mediate opposing actions on growth cone navigation from distinct membrane domains. Cell 2005, 121:127-39.\",\"year\":2005,\"link\":{\"url\":\"https://www.ncbi.nlm.nih.gov/pubmed/15820684/\",\"text\":\"Coexpressed EphA receptors and ephrin-A ligands mediate opposing actions on growth cone navigation from distinct membrane domains.\"}},{\"title\":\"Essential role of tuberous sclerosis genes TSC1 and TSC2 in NF-kappaB activation and cell survival.\",\"citation\":\"Ghosh S, Tergaonkar V, Rothlin CV, Correa RG, Bottero V, Bist P, Verma IM, Hunter T. Essential role of tuberous sclerosis genes TSC1 and TSC2 in NF-kappaB activation and cell survival. Cancer Cell 2006, 10:215-26.\",\"year\":2006,\"link\":{\"url\":\"https://www.ncbi.nlm.nih.gov/pubmed/16959613/\",\"text\":\"Essential role of tuberous sclerosis genes TSC1 and TSC2 in NF-kappaB activation and cell survival.\"}},{\"title\":\"TAM receptors are pleiotropic inhibitors of the innate immune response.\",\"citation\":\"Rothlin CV, Ghosh S, Zuniga EI, Oldstone MB, Lemke G. TAM receptors are pleiotropic inhibitors of the innate immune response. Cell 2007, 131:1124-36.\",\"year\":2007,\"link\":{\"url\":\"https://www.ncbi.nlm.nih.gov/pubmed/18083102/\",\"text\":\"TAM receptors are pleiotropic inhibitors of the innate immune response.\"}},{\"title\":\"Instructive role of aPKCzeta subcellular localization in the assembly of adherens junctions in neural progenitors.\",\"citation\":\"Ghosh S, Marquardt T, Thaler JP, Carter N, Andrews SE, Pfaff SL, Hunter T. Instructive role of aPKCzeta subcellular localization in the assembly of adherens junctions in neural progenitors. Proceedings Of The National Academy Of Sciences Of The United States Of America 2008, 105:335-40.\",\"year\":2008,\"link\":{\"url\":\"https://www.ncbi.nlm.nih.gov/pubmed/18162555/\",\"text\":\"Instructive role of aPKCzeta subcellular localization in the assembly of adherens junctions in neural progenitors.\"}},{\"title\":\"Telomere-independent Rap1 is an IKK adaptor and regulates NF-kappaB-dependent gene expression.\",\"citation\":\"Teo H, Ghosh S, Luesch H, Ghosh A, Wong ET, Malik N, Orth A, de Jesus P, Perry AS, Oliver JD, Tran NL, Speiser LJ, Wong M, Saez E, Schultz P, Chanda SK, Verma IM, Tergaonkar V. Telomere-independent Rap1 is an IKK adaptor and regulates NF-kappaB-dependent gene expression. Nature Cell Biology 2010, 12:758-67.\",\"year\":2010,\"link\":{\"url\":\"https://www.ncbi.nlm.nih.gov/pubmed/20622870/\",\"text\":\"Telomere-independent Rap1 is an IKK adaptor and regulates NF-kappaB-dependent gene expression.\"}},{\"title\":\"Spinal protein kinase M ζ underlies the maintenance mechanism of persistent nociceptive sensitization.\",\"citation\":\"Asiedu MN, Tillu DV, Melemedjian OK, Shy A, Sanoja R, Bodell B, Ghosh S, Porreca F, Price TJ. Spinal protein kinase M ζ underlies the maintenance mechanism of persistent nociceptive sensitization. The Journal Of Neuroscience : The Official Journal Of The Society For Neuroscience 2011, 31:6646-53.\",\"year\":2011,\"link\":{\"url\":\"https://www.ncbi.nlm.nih.gov/pubmed/21543593/\",\"text\":\"Spinal protein kinase M ζ underlies the maintenance mechanism of persistent nociceptive sensitization.\"}},{\"title\":\"Contribution of PKMζ-dependent and independent amplification to components of experimental neuropathic pain.\",\"citation\":\"King T, Qu C, Okun A, Melemedjian OK, Mandell EK, Maskaykina IY, Navratilova E, Dussor GO, Ghosh S, Price TJ, Porreca F. Contribution of PKMζ-dependent and independent amplification to components of experimental neuropathic pain. Pain 2012, 153:1263-73.\",\"year\":2012,\"link\":{\"url\":\"https://www.ncbi.nlm.nih.gov/pubmed/22482911/\",\"text\":\"Contribution of PKMζ-dependent and independent amplification to components of experimental neuropathic pain.\"}},{\"title\":\"BDNF regulates atypical PKC at spinal synapses to initiate and maintain a centralized chronic pain state.\",\"citation\":\"Melemedjian OK, Tillu DV, Asiedu MN, Mandell EK, Moy JK, Blute VM, Taylor CJ, Ghosh S, Price TJ. BDNF regulates atypical PKC at spinal synapses to initiate and maintain a centralized chronic pain state. Molecular Pain 2013, 9:12.\",\"year\":2013,\"link\":{\"url\":\"https://www.ncbi.nlm.nih.gov/pubmed/23510079/\",\"text\":\"BDNF regulates atypical PKC at spinal synapses to initiate and maintain a centralized chronic pain state.\"}},{\"title\":\"mTORC1 inhibition induces pain via IRS-1-dependent feedback activation of ERK.\",\"citation\":\"Melemedjian OK, Khoutorsky A, Sorge RE, Yan J, Asiedu MN, Valdez A, Ghosh S, Dussor G, Mogil JS, Sonenberg N, Price TJ. mTORC1 inhibition induces pain via IRS-1-dependent feedback activation of ERK. Pain 2013, 154:1080-91.\",\"year\":2013,\"link\":{\"url\":\"https://www.ncbi.nlm.nih.gov/pubmed/23607966/\",\"text\":\"mTORC1 inhibition induces pain via IRS-1-dependent feedback activation of ERK.\"}},{\"title\":\"ZIPping to pain relief: the role (or not) of PKMζ in chronic pain.\",\"citation\":\"Price TJ, Ghosh S. ZIPping to pain relief: the role (or not) of PKMζ in chronic pain. Molecular Pain 2013, 9:6.\",\"year\":2013,\"link\":{\"url\":\"https://www.ncbi.nlm.nih.gov/pubmed/23433248/\",\"text\":\"ZIPping to pain relief: the role (or not) of PKMζ in chronic pain.\"}},{\"title\":\"Paradoxical role of the proto-oncogene Axl and Mer receptor tyrosine kinases in colon cancer.\",\"citation\":\"Bosurgi L, Bernink JH, Delgado Cuevas V, Gagliani N, Joannas L, Schmid ET, Booth CJ, Ghosh S, Rothlin CV. Paradoxical role of the proto-oncogene Axl and Mer receptor tyrosine kinases in colon cancer. Proceedings Of The National Academy Of Sciences Of The United States Of America 2013, 110:13091-6.\",\"year\":2013,\"link\":{\"url\":\"https://www.ncbi.nlm.nih.gov/pubmed/23878224/\",\"text\":\"Paradoxical role of the proto-oncogene Axl and Mer receptor tyrosine kinases in colon cancer.\"}},{\"title\":\"T cell-derived protein S engages TAM receptor signaling in dendritic cells to control the magnitude of the immune response.\",\"citation\":\"Carrera Silva EA, Chan PY, Joannas L, Errasti AE, Gagliani N, Bosurgi L, Jabbour M, Perry A, Smith-Chakmakova F, Mucida D, Cheroutre H, Burstyn-Cohen T, Leighton JA, Lemke G, Ghosh S, Rothlin CV. T cell-derived protein S engages TAM receptor signaling in dendritic cells to control the magnitude of the immune response. Immunity 2013, 39:160-70.\",\"year\":2013,\"link\":{\"url\":\"https://www.ncbi.nlm.nih.gov/pubmed/23850380/\",\"text\":\"T cell-derived protein S engages TAM receptor signaling in dendritic cells to control the magnitude of the immune response.\"}},{\"title\":\"Competing molecular interactions of aPKC isoforms regulate neuronal polarity.\",\"citation\":\"Parker SS, Mandell EK, Hapak SM, Maskaykina IY, Kusne Y, Kim JY, Moy JK, St John PA, Wilson JM, Gothard KM, Price TJ, Ghosh S. Competing molecular interactions of aPKC isoforms regulate neuronal polarity. Proceedings Of The National Academy Of Sciences Of The United States Of America 2013, 110:14450-5.\",\"year\":2013,\"link\":{\"url\":\"https://www.ncbi.nlm.nih.gov/pubmed/23940317/\",\"text\":\"Competing molecular interactions of aPKC isoforms regulate neuronal polarity.\"}},{\"title\":\"Local translation and retrograde axonal transport of CREB regulates IL-6-induced nociceptive plasticity.\",\"citation\":\"Melemedjian OK, Tillu DV, Moy JK, Asiedu MN, Mandell EK, Ghosh S, Dussor G, Price TJ. Local translation and retrograde axonal transport of CREB regulates IL-6-induced nociceptive plasticity. Molecular Pain 2014, 10:45.\",\"year\":2014,\"link\":{\"url\":\"https://www.ncbi.nlm.nih.gov/pubmed/24993495/\",\"text\":\"Local translation and retrograde axonal transport of CREB regulates IL-6-induced nociceptive plasticity.\"}},{\"title\":\"Increased aPKC Expression Correlates with Prostatic Adenocarcinoma Gleason Score and Tumor Stage in the Japanese Population.\",\"citation\":\"Perry AS, Furusato B, Nagle RB, Ghosh S. Increased aPKC Expression Correlates with Prostatic Adenocarcinoma Gleason Score and Tumor Stage in the Japanese Population. Prostate Cancer 2014, 2014:481697.\",\"year\":2014,\"link\":{\"url\":\"https://www.ncbi.nlm.nih.gov/pubmed/24868468/\",\"text\":\"Increased aPKC Expression Correlates with Prostatic Adenocarcinoma Gleason Score and Tumor Stage in the Japanese Population.\"}},{\"title\":\"Targeting aPKC disables oncogenic signaling by both the EGFR and the proinflammatory cytokine TNFα in glioblastoma.\",\"citation\":\"Kusne Y, Carrera-Silva EA, Perry AS, Rushing EJ, Mandell EK, Dietrich JD, Errasti AE, Gibbs D, Berens ME, Loftus JC, Hulme C, Yang W, Lu Z, Aldape K, Sanai N, Rothlin CV, Ghosh S. Targeting aPKC disables oncogenic signaling by both the EGFR and the proinflammatory cytokine TNFα in glioblastoma. Science Signaling 2014, 7:ra75.\",\"year\":2014,\"link\":{\"url\":\"https://www.ncbi.nlm.nih.gov/pubmed/25118327/\",\"text\":\"Targeting aPKC disables oncogenic signaling by both the EGFR and the proinflammatory cytokine TNFα in glioblastoma.\"}},{\"title\":\"Contrasting effects of chronic, systemic treatment with mTOR inhibitors rapamycin and metformin on adult neural progenitors in mice.\",\"citation\":\"Kusne Y, Goldberg EL, Parker SS, Hapak SM, Maskaykina IY, Chew WM, Limesand KH, Brooks HL, Price TJ, Sanai N, Nikolich-Zugich J, Ghosh S. Contrasting effects of chronic, systemic treatment with mTOR inhibitors rapamycin and metformin on adult neural progenitors in mice. Age (Dordrecht, Netherlands) 2014, 36:199-212.\",\"year\":2014,\"link\":{\"url\":\"https://www.ncbi.nlm.nih.gov/pubmed/23949159/\",\"text\":\"Contrasting effects of chronic, systemic treatment with mTOR inhibitors rapamycin and metformin on adult neural progenitors in mice.\"}},{\"title\":\"Tyro3, Axl, and Mertk receptor signaling in inflammatory bowel disease and colitis-associated cancer.\",\"citation\":\"Rothlin CV, Leighton JA, Ghosh S. Tyro3, Axl, and Mertk receptor signaling in inflammatory bowel disease and colitis-associated cancer. Inflammatory Bowel Diseases 2014, 20:1472-80.\",\"year\":2014,\"link\":{\"url\":\"https://www.ncbi.nlm.nih.gov/pubmed/24846720/\",\"text\":\"Tyro3, Axl, and Mertk receptor signaling in inflammatory bowel disease and colitis-associated cancer.\"}},{\"title\":\"PKCι interacts with Rab14 and modulates epithelial barrier function through regulation of claudin-2 levels.\",\"citation\":\"Lu R, Dalgalan D, Mandell EK, Parker SS, Ghosh S, Wilson JM. PKCι interacts with Rab14 and modulates epithelial barrier function through regulation of claudin-2 levels. Molecular Biology Of The Cell 2015, 26:1523-31.\",\"year\":2015,\"link\":{\"url\":\"https://www.ncbi.nlm.nih.gov/pubmed/25694446/\",\"text\":\"PKCι interacts with Rab14 and modulates epithelial barrier function through regulation of claudin-2 levels.\"}},{\"title\":\"TAM receptor signaling in immune homeostasis.\",\"citation\":\"Rothlin CV, Carrera-Silva EA, Bosurgi L, Ghosh S. TAM receptor signaling in immune homeostasis. Annual Review Of Immunology 2015, 33:355-91.\",\"year\":2015,\"link\":{\"url\":\"https://www.ncbi.nlm.nih.gov/pubmed/25594431/\",\"text\":\"TAM receptor signaling in immune homeostasis.\"}},{\"title\":\"Endosomal regulation of contact inhibition through the AMOT:YAP pathway.\",\"citation\":\"Cox CM, Mandell EK, Stewart L, Lu R, Johnson DL, McCarter SD, Tavares A, Runyan R, Ghosh S, Wilson JM. Endosomal regulation of contact inhibition through the AMOT:YAP pathway. Molecular Biology Of The Cell 2015, 26:2673-84.\",\"year\":2015,\"link\":{\"url\":\"https://www.ncbi.nlm.nih.gov/pubmed/25995376/\",\"text\":\"Endosomal regulation of contact inhibition through the AMOT:YAP pathway.\"}},{\"title\":\"The TAM family receptor tyrosine kinase TYRO3 is a negative regulator of type 2 immunity.\",\"citation\":\"Chan PY, Carrera Silva EA, De Kouchkovsky D, Joannas LD, Hao L, Hu D, Huntsman S, Eng C, Licona-Limón P, Weinstein JS, Herbert DR, Craft JE, Flavell RA, Repetto S, Correale J, Burchard EG, Torgerson DG, Ghosh S, Rothlin CV. The TAM family receptor tyrosine kinase TYRO3 is a negative regulator of type 2 immunity. Science (New York, N.Y.) 2016, 352:99-103.\",\"year\":2016,\"link\":{\"url\":\"https://www.ncbi.nlm.nih.gov/pubmed/27034374/\",\"text\":\"The TAM family receptor tyrosine kinase TYRO3 is a negative regulator of type 2 immunity.\"}},{\"title\":\"Macrophage function in tissue repair and remodeling requires IL-4 or IL-13 with apoptotic cells.\",\"citation\":\"Bosurgi L, Cao YG, Cabeza-Cabrerizo M, Tucci A, Hughes LD, Kong Y, Weinstein JS, Licona-Limon P, Schmid ET, Pelorosso F, Gagliani N, Craft JE, Flavell RA, Ghosh S, Rothlin CV. Macrophage function in tissue repair and remodeling requires IL-4 or IL-13 with apoptotic cells. Science (New York, N.Y.) 2017, 356:1072-1076.\",\"year\":2017,\"link\":{\"url\":\"https://www.ncbi.nlm.nih.gov/pubmed/28495875/\",\"text\":\"Macrophage function in tissue repair and remodeling requires IL-4 or IL-13 with apoptotic cells.\"}},{\"title\":\"Negative Regulation of Type 2 Immunity.\",\"citation\":\"de Kouchkovsky DA, Ghosh S, Rothlin CV. Negative Regulation of Type 2 Immunity. Trends In Immunology 2017, 38:154-167.\",\"year\":2017,\"link\":{\"url\":\"https://www.ncbi.nlm.nih.gov/pubmed/28082101/\",\"text\":\"Negative Regulation of Type 2 Immunity.\"}},{\"title\":\"TAM receptor tyrosine kinases as emerging targets of innate immune checkpoint blockade for cancer therapy.\",\"citation\":\"Akalu YT, Rothlin CV, Ghosh S. TAM receptor tyrosine kinases as emerging targets of innate immune checkpoint blockade for cancer therapy. Immunological Reviews 2017, 276:165-177.\",\"year\":2017,\"link\":{\"url\":\"https://www.ncbi.nlm.nih.gov/pubmed/28258690/\",\"text\":\"TAM receptor tyrosine kinases as emerging targets of innate immune checkpoint blockade for cancer therapy.\"}},{\"title\":\"The receptor tyrosine kinase AXL promotes migration and invasion in colorectal cancer.\",\"citation\":\"Uribe DJ, Mandell EK, Watson A, Martinez JD, Leighton JA, Ghosh S, Rothlin CV. The receptor tyrosine kinase AXL promotes migration and invasion in colorectal cancer. PloS One 2017, 12:e0179979.\",\"year\":2017,\"link\":{\"url\":\"https://www.ncbi.nlm.nih.gov/pubmed/28727830/\",\"text\":\"The receptor tyrosine kinase AXL promotes migration and invasion in colorectal cancer.\"}},{\"title\":\"Death begets a new beginning.\",\"citation\":\"Bosurgi L, Hughes LD, Rothlin CV, Ghosh S. Death begets a new beginning. Immunological Reviews 2017, 280:8-25.\",\"year\":2017,\"link\":{\"url\":\"https://www.ncbi.nlm.nih.gov/pubmed/29027219/\",\"text\":\"Death begets a new beginning.\"}},{\"title\":\"Chronicles of Cell Death Foretold: Specificities in the Mechanism of Disposal.\",\"citation\":\"Hughes LD, Bosurgi L, Ghosh S, Rothlin CV. Chronicles of Cell Death Foretold: Specificities in the Mechanism of Disposal. 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The Journal Of Clinical Investigation 2018, 128:607-624.\",\"year\":2018,\"link\":{\"url\":\"https://www.ncbi.nlm.nih.gov/pubmed/29251628/\",\"text\":\"Erythrocyte efferocytosis modulates macrophages towards recovery after intracerebral hemorrhage.\"}},{\"title\":\"PAR3-PAR6-atypical PKC polarity complex proteins in neuronal polarization.\",\"citation\":\"Hapak SM, Rothlin CV, Ghosh S. PAR3-PAR6-atypical PKC polarity complex proteins in neuronal polarization. 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Dr. Ghosh obtained a M.Sc. in Zoology at the University of Calcutta, where he studied Drosophila and mosquito genetics. Next, he completed his graduate studies on cell cytoskeleton and protein trafficking under the direction of John V. Cox at the University of Tennessee, Memphis. Subsequently, Dr. Ghosh did his postdoctoral research on cell signaling at the Salk Institute for Biological Studies under the guidance of Tony Hunter. In 2007, Dr. Ghosh joined University of Arizona as an Assistant Professor, and in 2014 he moved to Yale University School of Medicine and is currently an Associate Professor in the Departments of Neurology and Pharmacology. Dr. Ghosh and Dr. Carla Rothlin co-direct a lab studying the regulation of inflammation (Rothin, Ghosh et al. Cell, 2007, Carrera Silva et al. Immunity, 2013, Bosurgi et al. Science, 2017). While inflammation is a cardinal feature for immune defense, the magnitude and period of the inflammatory response has to follow the ‘Goldilocks Principle’ wherein inflammation would be detrimental if its amplitude is too little or too much, or its period too short or too long. Drs. Rothlin and Ghosh investigates the principles and molecular mechanisms that negatively regulate inflammation and ensure that the amplitude and period of inflammation is ‘just right’. Defects in these molecular circuits can manifest as wide ranging clinical problems including chronic or pathological inflammation, autoimmunity and pathological wound healing, while harnessing these checkpoints can improve anti-cancer immunity.\\\",\\\"url\\\":\\\"https://medicine.yale.edu/ysm/profile/sourav_ghosh/\\\",\\\"email\\\":\\\"sourav.ghosh@yale.edu\\\",\\\"telephone\\\":\\\"\\\",\\\"honorificSuffix\\\":[null,\\\"PhD\\\"],\\\"award\\\":[],\\\"jobTitle\\\":[\\\"Associate Professor of Neurology and Pharmacology\\\"],\\\"affiliation\\\":[{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Cancer Signaling Networks\\\",\\\"url\\\":\\\"https://medicine.yale.edu/cancer/research/programs/transduction/index.aspx\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Interdepartmental Neuroscience Program\\\",\\\"url\\\":\\\"https://medicine.yale.edu/INP/index.aspx\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Molecular Medicine, Pharmacology, and Physiology\\\",\\\"url\\\":\\\"http://bbs.yale.edu/molmed/index.aspx\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Neural Disorders\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Neurology\\\",\\\"url\\\":\\\"https://medicine.yale.edu/neurology\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Neuroscience\\\",\\\"url\\\":\\\"http://bbs.yale.edu/neuroscience\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Secondary Faculty\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Yale Cancer Center\\\",\\\"url\\\":\\\"https://www.yalecancercenter.org\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Yale Combined Program in the Biological and Biomedical Sciences (BBS)\\\",\\\"url\\\":\\\"http://bbs.yale.edu\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Yale University\\\",\\\"url\\\":\\\"https://www.yale.edu/\\\",\\\"@context\\\":\\\"http://schema.org\\\"}],\\\"alumniOf\\\":[{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"University of Tennessee, Molecular Sciences (2000)\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"University of Calcutta, Zoology (1992)\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Salk Institute for Biological Studies\\\",\\\"@context\\\":\\\"http://schema.org\\\"}],\\\"image\\\":{\\\"@type\\\":\\\"ImageObject\\\",\\\"url\\\":\\\"https://ysm-res.cloudinary.com/image/upload/c_limit,f_auto,h_630,q_auto,w_1200/v1/yms/prod/353f686f-9b80-47a1-96b0-391d14f042ab\\\",\\\"description\\\":\\\"\\\",\\\"height\\\":1200,\\\"width\\\":630,\\\"@context\\\":\\\"http://schema.org\\\"},\\\"@context\\\":\\\"http://schema.org\\\"}],\\\"description\\\":\\\"Teo H, Ghosh S, Luesch H, Ghosh A, Wong ET, Malik N, Orth A, de Jesus P, Perry AS, Oliver JD, Tran NL, Speiser LJ, Wong M, Saez E, Schultz P, Chanda SK, Verma IM, Tergaonkar V. Telomere-independent Rap1 is an IKK adaptor and regulates NF-kappaB-dependent gene expression. Nature Cell Biology 2010, 12:758-67.\\\",\\\"@context\\\":\\\"http://schema.org\\\"}\"},{\"schemaName\":\"MedicalScholarlyArticle\",\"jsonData\":\"{\\\"@type\\\":\\\"MedicalScholarlyArticle\\\",\\\"publicationType\\\":\\\"Journal Article\\\",\\\"inLanguage\\\":\\\"en-US\\\",\\\"headline\\\":\\\"Spinal protein kinase M ζ underlies the maintenance mechanism of persistent nociceptive sensitization.\\\",\\\"url\\\":\\\"https://www.ncbi.nlm.nih.gov/pubmed/21543593/\\\",\\\"author\\\":[{\\\"@type\\\":\\\"Person\\\",\\\"mainEntityOfPage\\\":{\\\"@type\\\":\\\"WebPage\\\",\\\"@id\\\":\\\"https://medicine.yale.edu/ysm/profile/sourav_ghosh/\\\",\\\"@context\\\":\\\"http://schema.org\\\"},\\\"name\\\":\\\"Sourav Ghosh\\\",\\\"description\\\":\\\"Sourav Ghosh, Ph.D., is an Associate Professor of Neurology and Pharmacology at the Yale University School of Medicine. Dr. Ghosh obtained a M.Sc. in Zoology at the University of Calcutta, where he studied Drosophila and mosquito genetics. Next, he completed his graduate studies on cell cytoskeleton and protein trafficking under the direction of John V. Cox at the University of Tennessee, Memphis. Subsequently, Dr. Ghosh did his postdoctoral research on cell signaling at the Salk Institute for Biological Studies under the guidance of Tony Hunter. In 2007, Dr. Ghosh joined University of Arizona as an Assistant Professor, and in 2014 he moved to Yale University School of Medicine and is currently an Associate Professor in the Departments of Neurology and Pharmacology. Dr. Ghosh and Dr. Carla Rothlin co-direct a lab studying the regulation of inflammation (Rothin, Ghosh et al. Cell, 2007, Carrera Silva et al. Immunity, 2013, Bosurgi et al. Science, 2017). While inflammation is a cardinal feature for immune defense, the magnitude and period of the inflammatory response has to follow the ‘Goldilocks Principle’ wherein inflammation would be detrimental if its amplitude is too little or too much, or its period too short or too long. Drs. Rothlin and Ghosh investigates the principles and molecular mechanisms that negatively regulate inflammation and ensure that the amplitude and period of inflammation is ‘just right’. Defects in these molecular circuits can manifest as wide ranging clinical problems including chronic or pathological inflammation, autoimmunity and pathological wound healing, while harnessing these checkpoints can improve anti-cancer immunity.\\\",\\\"url\\\":\\\"https://medicine.yale.edu/ysm/profile/sourav_ghosh/\\\",\\\"email\\\":\\\"sourav.ghosh@yale.edu\\\",\\\"telephone\\\":\\\"\\\",\\\"honorificSuffix\\\":[null,\\\"PhD\\\"],\\\"award\\\":[],\\\"jobTitle\\\":[\\\"Associate Professor of Neurology and Pharmacology\\\"],\\\"affiliation\\\":[{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Cancer Signaling Networks\\\",\\\"url\\\":\\\"https://medicine.yale.edu/cancer/research/programs/transduction/index.aspx\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Interdepartmental Neuroscience Program\\\",\\\"url\\\":\\\"https://medicine.yale.edu/INP/index.aspx\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Molecular Medicine, Pharmacology, and Physiology\\\",\\\"url\\\":\\\"http://bbs.yale.edu/molmed/index.aspx\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Neural Disorders\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Neurology\\\",\\\"url\\\":\\\"https://medicine.yale.edu/neurology\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Neuroscience\\\",\\\"url\\\":\\\"http://bbs.yale.edu/neuroscience\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Secondary Faculty\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Yale Cancer Center\\\",\\\"url\\\":\\\"https://www.yalecancercenter.org\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Yale Combined Program in the Biological and Biomedical Sciences (BBS)\\\",\\\"url\\\":\\\"http://bbs.yale.edu\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Yale University\\\",\\\"url\\\":\\\"https://www.yale.edu/\\\",\\\"@context\\\":\\\"http://schema.org\\\"}],\\\"alumniOf\\\":[{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"University of Tennessee, Molecular Sciences (2000)\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"University of Calcutta, Zoology (1992)\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Salk Institute for Biological Studies\\\",\\\"@context\\\":\\\"http://schema.org\\\"}],\\\"image\\\":{\\\"@type\\\":\\\"ImageObject\\\",\\\"url\\\":\\\"https://ysm-res.cloudinary.com/image/upload/c_limit,f_auto,h_630,q_auto,w_1200/v1/yms/prod/353f686f-9b80-47a1-96b0-391d14f042ab\\\",\\\"description\\\":\\\"\\\",\\\"height\\\":1200,\\\"width\\\":630,\\\"@context\\\":\\\"http://schema.org\\\"},\\\"@context\\\":\\\"http://schema.org\\\"}],\\\"description\\\":\\\"Asiedu MN, Tillu DV, Melemedjian OK, Shy A, Sanoja R, Bodell B, Ghosh S, Porreca F, Price TJ. Spinal protein kinase M ζ underlies the maintenance mechanism of persistent nociceptive sensitization. The Journal Of Neuroscience : The Official Journal Of The Society For Neuroscience 2011, 31:6646-53.\\\",\\\"@context\\\":\\\"http://schema.org\\\"}\"},{\"schemaName\":\"MedicalScholarlyArticle\",\"jsonData\":\"{\\\"@type\\\":\\\"MedicalScholarlyArticle\\\",\\\"publicationType\\\":\\\"Journal Article\\\",\\\"inLanguage\\\":\\\"en-US\\\",\\\"headline\\\":\\\"Contribution of PKMζ-dependent and independent amplification to components of experimental neuropathic pain.\\\",\\\"url\\\":\\\"https://www.ncbi.nlm.nih.gov/pubmed/22482911/\\\",\\\"author\\\":[{\\\"@type\\\":\\\"Person\\\",\\\"mainEntityOfPage\\\":{\\\"@type\\\":\\\"WebPage\\\",\\\"@id\\\":\\\"https://medicine.yale.edu/ysm/profile/sourav_ghosh/\\\",\\\"@context\\\":\\\"http://schema.org\\\"},\\\"name\\\":\\\"Sourav Ghosh\\\",\\\"description\\\":\\\"Sourav Ghosh, Ph.D., is an Associate Professor of Neurology and Pharmacology at the Yale University School of Medicine. 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While inflammation is a cardinal feature for immune defense, the magnitude and period of the inflammatory response has to follow the ‘Goldilocks Principle’ wherein inflammation would be detrimental if its amplitude is too little or too much, or its period too short or too long. Drs. Rothlin and Ghosh investigates the principles and molecular mechanisms that negatively regulate inflammation and ensure that the amplitude and period of inflammation is ‘just right’. Defects in these molecular circuits can manifest as wide ranging clinical problems including chronic or pathological inflammation, autoimmunity and pathological wound healing, while harnessing these checkpoints can improve anti-cancer immunity.\\\",\\\"url\\\":\\\"https://medicine.yale.edu/ysm/profile/sourav_ghosh/\\\",\\\"email\\\":\\\"sourav.ghosh@yale.edu\\\",\\\"telephone\\\":\\\"\\\",\\\"honorificSuffix\\\":[null,\\\"PhD\\\"],\\\"award\\\":[],\\\"jobTitle\\\":[\\\"Associate Professor of Neurology and Pharmacology\\\"],\\\"affiliation\\\":[{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Cancer Signaling Networks\\\",\\\"url\\\":\\\"https://medicine.yale.edu/cancer/research/programs/transduction/index.aspx\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Interdepartmental Neuroscience Program\\\",\\\"url\\\":\\\"https://medicine.yale.edu/INP/index.aspx\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Molecular Medicine, Pharmacology, and Physiology\\\",\\\"url\\\":\\\"http://bbs.yale.edu/molmed/index.aspx\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Neural Disorders\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Neurology\\\",\\\"url\\\":\\\"https://medicine.yale.edu/neurology\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Neuroscience\\\",\\\"url\\\":\\\"http://bbs.yale.edu/neuroscience\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Secondary Faculty\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Yale Cancer Center\\\",\\\"url\\\":\\\"https://www.yalecancercenter.org\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Yale Combined Program in the Biological and Biomedical Sciences (BBS)\\\",\\\"url\\\":\\\"http://bbs.yale.edu\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Yale University\\\",\\\"url\\\":\\\"https://www.yale.edu/\\\",\\\"@context\\\":\\\"http://schema.org\\\"}],\\\"alumniOf\\\":[{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"University of Tennessee, Molecular Sciences (2000)\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"University of Calcutta, Zoology (1992)\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Salk Institute for Biological Studies\\\",\\\"@context\\\":\\\"http://schema.org\\\"}],\\\"image\\\":{\\\"@type\\\":\\\"ImageObject\\\",\\\"url\\\":\\\"https://ysm-res.cloudinary.com/image/upload/c_limit,f_auto,h_630,q_auto,w_1200/v1/yms/prod/353f686f-9b80-47a1-96b0-391d14f042ab\\\",\\\"description\\\":\\\"\\\",\\\"height\\\":1200,\\\"width\\\":630,\\\"@context\\\":\\\"http://schema.org\\\"},\\\"@context\\\":\\\"http://schema.org\\\"}],\\\"description\\\":\\\"King T, Qu C, Okun A, Melemedjian OK, Mandell EK, Maskaykina IY, Navratilova E, Dussor GO, Ghosh S, Price TJ, Porreca F. Contribution of PKMζ-dependent and independent amplification to components of experimental neuropathic pain. Pain 2012, 153:1263-73.\\\",\\\"@context\\\":\\\"http://schema.org\\\"}\"},{\"schemaName\":\"MedicalScholarlyArticle\",\"jsonData\":\"{\\\"@type\\\":\\\"MedicalScholarlyArticle\\\",\\\"publicationType\\\":\\\"Journal Article\\\",\\\"inLanguage\\\":\\\"en-US\\\",\\\"headline\\\":\\\"BDNF regulates atypical PKC at spinal synapses to initiate and maintain a centralized chronic pain state.\\\",\\\"url\\\":\\\"https://www.ncbi.nlm.nih.gov/pubmed/23510079/\\\",\\\"author\\\":[{\\\"@type\\\":\\\"Person\\\",\\\"mainEntityOfPage\\\":{\\\"@type\\\":\\\"WebPage\\\",\\\"@id\\\":\\\"https://medicine.yale.edu/ysm/profile/sourav_ghosh/\\\",\\\"@context\\\":\\\"http://schema.org\\\"},\\\"name\\\":\\\"Sourav Ghosh\\\",\\\"description\\\":\\\"Sourav Ghosh, Ph.D., is an Associate Professor of Neurology and Pharmacology at the Yale University School of Medicine. 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While inflammation is a cardinal feature for immune defense, the magnitude and period of the inflammatory response has to follow the ‘Goldilocks Principle’ wherein inflammation would be detrimental if its amplitude is too little or too much, or its period too short or too long. Drs. Rothlin and Ghosh investigates the principles and molecular mechanisms that negatively regulate inflammation and ensure that the amplitude and period of inflammation is ‘just right’. 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BDNF regulates atypical PKC at spinal synapses to initiate and maintain a centralized chronic pain state. Molecular Pain 2013, 9:12.\\\",\\\"@context\\\":\\\"http://schema.org\\\"}\"},{\"schemaName\":\"MedicalScholarlyArticle\",\"jsonData\":\"{\\\"@type\\\":\\\"MedicalScholarlyArticle\\\",\\\"publicationType\\\":\\\"Journal Article\\\",\\\"inLanguage\\\":\\\"en-US\\\",\\\"headline\\\":\\\"mTORC1 inhibition induces pain via IRS-1-dependent feedback activation of ERK.\\\",\\\"url\\\":\\\"https://www.ncbi.nlm.nih.gov/pubmed/23607966/\\\",\\\"author\\\":[{\\\"@type\\\":\\\"Person\\\",\\\"mainEntityOfPage\\\":{\\\"@type\\\":\\\"WebPage\\\",\\\"@id\\\":\\\"https://medicine.yale.edu/ysm/profile/sourav_ghosh/\\\",\\\"@context\\\":\\\"http://schema.org\\\"},\\\"name\\\":\\\"Sourav Ghosh\\\",\\\"description\\\":\\\"Sourav Ghosh, Ph.D., is an Associate Professor of Neurology and Pharmacology at the Yale University School of Medicine. Dr. Ghosh obtained a M.Sc. in Zoology at the University of Calcutta, where he studied Drosophila and mosquito genetics. Next, he completed his graduate studies on cell cytoskeleton and protein trafficking under the direction of John V. Cox at the University of Tennessee, Memphis. Subsequently, Dr. Ghosh did his postdoctoral research on cell signaling at the Salk Institute for Biological Studies under the guidance of Tony Hunter. In 2007, Dr. Ghosh joined University of Arizona as an Assistant Professor, and in 2014 he moved to Yale University School of Medicine and is currently an Associate Professor in the Departments of Neurology and Pharmacology. Dr. Ghosh and Dr. Carla Rothlin co-direct a lab studying the regulation of inflammation (Rothin, Ghosh et al. Cell, 2007, Carrera Silva et al. Immunity, 2013, Bosurgi et al. Science, 2017). While inflammation is a cardinal feature for immune defense, the magnitude and period of the inflammatory response has to follow the ‘Goldilocks Principle’ wherein inflammation would be detrimental if its amplitude is too little or too much, or its period too short or too long. Drs. Rothlin and Ghosh investigates the principles and molecular mechanisms that negatively regulate inflammation and ensure that the amplitude and period of inflammation is ‘just right’. 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Pain 2013, 154:1080-91.\\\",\\\"@context\\\":\\\"http://schema.org\\\"}\"},{\"schemaName\":\"MedicalScholarlyArticle\",\"jsonData\":\"{\\\"@type\\\":\\\"MedicalScholarlyArticle\\\",\\\"publicationType\\\":\\\"Journal Article\\\",\\\"inLanguage\\\":\\\"en-US\\\",\\\"headline\\\":\\\"ZIPping to pain relief: the role (or not) of PKMζ in chronic pain.\\\",\\\"url\\\":\\\"https://www.ncbi.nlm.nih.gov/pubmed/23433248/\\\",\\\"author\\\":[{\\\"@type\\\":\\\"Person\\\",\\\"mainEntityOfPage\\\":{\\\"@type\\\":\\\"WebPage\\\",\\\"@id\\\":\\\"https://medicine.yale.edu/ysm/profile/sourav_ghosh/\\\",\\\"@context\\\":\\\"http://schema.org\\\"},\\\"name\\\":\\\"Sourav Ghosh\\\",\\\"description\\\":\\\"Sourav Ghosh, Ph.D., is an Associate Professor of Neurology and Pharmacology at the Yale University School of Medicine. Dr. Ghosh obtained a M.Sc. in Zoology at the University of Calcutta, where he studied Drosophila and mosquito genetics. 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While inflammation is a cardinal feature for immune defense, the magnitude and period of the inflammatory response has to follow the ‘Goldilocks Principle’ wherein inflammation would be detrimental if its amplitude is too little or too much, or its period too short or too long. Drs. Rothlin and Ghosh investigates the principles and molecular mechanisms that negatively regulate inflammation and ensure that the amplitude and period of inflammation is ‘just right’. 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ZIPping to pain relief: the role (or not) of PKMζ in chronic pain. Molecular Pain 2013, 9:6.\\\",\\\"@context\\\":\\\"http://schema.org\\\"}\"},{\"schemaName\":\"MedicalScholarlyArticle\",\"jsonData\":\"{\\\"@type\\\":\\\"MedicalScholarlyArticle\\\",\\\"publicationType\\\":\\\"Journal Article\\\",\\\"inLanguage\\\":\\\"en-US\\\",\\\"headline\\\":\\\"Paradoxical role of the proto-oncogene Axl and Mer receptor tyrosine kinases in colon cancer.\\\",\\\"url\\\":\\\"https://www.ncbi.nlm.nih.gov/pubmed/23878224/\\\",\\\"author\\\":[{\\\"@type\\\":\\\"Person\\\",\\\"mainEntityOfPage\\\":{\\\"@type\\\":\\\"WebPage\\\",\\\"@id\\\":\\\"https://medicine.yale.edu/ysm/profile/sourav_ghosh/\\\",\\\"@context\\\":\\\"http://schema.org\\\"},\\\"name\\\":\\\"Sourav Ghosh\\\",\\\"description\\\":\\\"Sourav Ghosh, Ph.D., is an Associate Professor of Neurology and Pharmacology at the Yale University School of Medicine. 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While inflammation is a cardinal feature for immune defense, the magnitude and period of the inflammatory response has to follow the ‘Goldilocks Principle’ wherein inflammation would be detrimental if its amplitude is too little or too much, or its period too short or too long. Drs. Rothlin and Ghosh investigates the principles and molecular mechanisms that negatively regulate inflammation and ensure that the amplitude and period of inflammation is ‘just right’. 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While inflammation is a cardinal feature for immune defense, the magnitude and period of the inflammatory response has to follow the ‘Goldilocks Principle’ wherein inflammation would be detrimental if its amplitude is too little or too much, or its period too short or too long. Drs. Rothlin and Ghosh investigates the principles and molecular mechanisms that negatively regulate inflammation and ensure that the amplitude and period of inflammation is ‘just right’. 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Dr. Ghosh obtained a M.Sc. in Zoology at the University of Calcutta, where he studied Drosophila and mosquito genetics. Next, he completed his graduate studies on cell cytoskeleton and protein trafficking under the direction of John V. Cox at the University of Tennessee, Memphis. Subsequently, Dr. Ghosh did his postdoctoral research on cell signaling at the Salk Institute for Biological Studies under the guidance of Tony Hunter. In 2007, Dr. Ghosh joined University of Arizona as an Assistant Professor, and in 2014 he moved to Yale University School of Medicine and is currently an Associate Professor in the Departments of Neurology and Pharmacology. Dr. Ghosh and Dr. Carla Rothlin co-direct a lab studying the regulation of inflammation (Rothin, Ghosh et al. Cell, 2007, Carrera Silva et al. Immunity, 2013, Bosurgi et al. Science, 2017). While inflammation is a cardinal feature for immune defense, the magnitude and period of the inflammatory response has to follow the ‘Goldilocks Principle’ wherein inflammation would be detrimental if its amplitude is too little or too much, or its period too short or too long. Drs. Rothlin and Ghosh investigates the principles and molecular mechanisms that negatively regulate inflammation and ensure that the amplitude and period of inflammation is ‘just right’. 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Competing molecular interactions of aPKC isoforms regulate neuronal polarity. 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While inflammation is a cardinal feature for immune defense, the magnitude and period of the inflammatory response has to follow the ‘Goldilocks Principle’ wherein inflammation would be detrimental if its amplitude is too little or too much, or its period too short or too long. Drs. Rothlin and Ghosh investigates the principles and molecular mechanisms that negatively regulate inflammation and ensure that the amplitude and period of inflammation is ‘just right’. 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Local translation and retrograde axonal transport of CREB regulates IL-6-induced nociceptive plasticity. Molecular Pain 2014, 10:45.\\\",\\\"@context\\\":\\\"http://schema.org\\\"}\"},{\"schemaName\":\"MedicalScholarlyArticle\",\"jsonData\":\"{\\\"@type\\\":\\\"MedicalScholarlyArticle\\\",\\\"publicationType\\\":\\\"Journal Article\\\",\\\"inLanguage\\\":\\\"en-US\\\",\\\"headline\\\":\\\"Increased aPKC Expression Correlates with Prostatic Adenocarcinoma Gleason Score and Tumor Stage in the Japane\\\",\\\"url\\\":\\\"https://www.ncbi.nlm.nih.gov/pubmed/24868468/\\\",\\\"author\\\":[{\\\"@type\\\":\\\"Person\\\",\\\"mainEntityOfPage\\\":{\\\"@type\\\":\\\"WebPage\\\",\\\"@id\\\":\\\"https://medicine.yale.edu/ysm/profile/sourav_ghosh/\\\",\\\"@context\\\":\\\"http://schema.org\\\"},\\\"name\\\":\\\"Sourav Ghosh\\\",\\\"description\\\":\\\"Sourav Ghosh, Ph.D., is an Associate Professor of Neurology and Pharmacology at the Yale University School of Medicine. 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While inflammation is a cardinal feature for immune defense, the magnitude and period of the inflammatory response has to follow the ‘Goldilocks Principle’ wherein inflammation would be detrimental if its amplitude is too little or too much, or its period too short or too long. Drs. Rothlin and Ghosh investigates the principles and molecular mechanisms that negatively regulate inflammation and ensure that the amplitude and period of inflammation is ‘just right’. Defects in these molecular circuits can manifest as wide ranging clinical problems including chronic or pathological inflammation, autoimmunity and pathological wound healing, while harnessing these checkpoints can improve anti-cancer immunity.\\\",\\\"url\\\":\\\"https://medicine.yale.edu/ysm/profile/sourav_ghosh/\\\",\\\"email\\\":\\\"sourav.ghosh@yale.edu\\\",\\\"telephone\\\":\\\"\\\",\\\"honorificSuffix\\\":[null,\\\"PhD\\\"],\\\"award\\\":[],\\\"jobTitle\\\":[\\\"Associate Professor of Neurology and Pharmacology\\\"],\\\"affiliation\\\":[{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Cancer Signaling Networks\\\",\\\"url\\\":\\\"https://medicine.yale.edu/cancer/research/programs/transduction/index.aspx\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Interdepartmental Neuroscience Program\\\",\\\"url\\\":\\\"https://medicine.yale.edu/INP/index.aspx\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Molecular Medicine, Pharmacology, and Physiology\\\",\\\"url\\\":\\\"http://bbs.yale.edu/molmed/index.aspx\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Neural Disorders\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Neurology\\\",\\\"url\\\":\\\"https://medicine.yale.edu/neurology\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Neuroscience\\\",\\\"url\\\":\\\"http://bbs.yale.edu/neuroscience\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Secondary Faculty\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Yale Cancer Center\\\",\\\"url\\\":\\\"https://www.yalecancercenter.org\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Yale Combined Program in the Biological and Biomedical Sciences (BBS)\\\",\\\"url\\\":\\\"http://bbs.yale.edu\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Yale University\\\",\\\"url\\\":\\\"https://www.yale.edu/\\\",\\\"@context\\\":\\\"http://schema.org\\\"}],\\\"alumniOf\\\":[{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"University of Tennessee, Molecular Sciences (2000)\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"University of Calcutta, Zoology (1992)\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Salk Institute for Biological Studies\\\",\\\"@context\\\":\\\"http://schema.org\\\"}],\\\"image\\\":{\\\"@type\\\":\\\"ImageObject\\\",\\\"url\\\":\\\"https://ysm-res.cloudinary.com/image/upload/c_limit,f_auto,h_630,q_auto,w_1200/v1/yms/prod/353f686f-9b80-47a1-96b0-391d14f042ab\\\",\\\"description\\\":\\\"\\\",\\\"height\\\":1200,\\\"width\\\":630,\\\"@context\\\":\\\"http://schema.org\\\"},\\\"@context\\\":\\\"http://schema.org\\\"}],\\\"description\\\":\\\"Kusne Y, Goldberg EL, Parker SS, Hapak SM, Maskaykina IY, Chew WM, Limesand KH, Brooks HL, Price TJ, Sanai N, Nikolich-Zugich J, Ghosh S. Contrasting effects of chronic, systemic treatment with mTOR inhibitors rapamycin and metformin on adult neural progenitors in mice. Age (Dordrecht, Netherlands) 2014, 36:199-212.\\\",\\\"@context\\\":\\\"http://schema.org\\\"}\"},{\"schemaName\":\"MedicalScholarlyArticle\",\"jsonData\":\"{\\\"@type\\\":\\\"MedicalScholarlyArticle\\\",\\\"publicationType\\\":\\\"Journal Article\\\",\\\"inLanguage\\\":\\\"en-US\\\",\\\"headline\\\":\\\"Tyro3, Axl, and Mertk receptor signaling in inflammatory bowel disease and colitis-associated cancer.\\\",\\\"url\\\":\\\"https://www.ncbi.nlm.nih.gov/pubmed/24846720/\\\",\\\"author\\\":[{\\\"@type\\\":\\\"Person\\\",\\\"mainEntityOfPage\\\":{\\\"@type\\\":\\\"WebPage\\\",\\\"@id\\\":\\\"https://medicine.yale.edu/ysm/profile/sourav_ghosh/\\\",\\\"@context\\\":\\\"http://schema.org\\\"},\\\"name\\\":\\\"Sourav Ghosh\\\",\\\"description\\\":\\\"Sourav Ghosh, Ph.D., is an Associate Professor of Neurology and Pharmacology at the Yale University School of Medicine. Dr. Ghosh obtained a M.Sc. in Zoology at the University of Calcutta, where he studied Drosophila and mosquito genetics. 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While inflammation is a cardinal feature for immune defense, the magnitude and period of the inflammatory response has to follow the ‘Goldilocks Principle’ wherein inflammation would be detrimental if its amplitude is too little or too much, or its period too short or too long. Drs. Rothlin and Ghosh investigates the principles and molecular mechanisms that negatively regulate inflammation and ensure that the amplitude and period of inflammation is ‘just right’. 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Tyro3, Axl, and Mertk receptor signaling in inflammatory bowel disease and colitis-associated cancer. Inflammatory Bowel Diseases 2014, 20:1472-80.\\\",\\\"@context\\\":\\\"http://schema.org\\\"}\"},{\"schemaName\":\"MedicalScholarlyArticle\",\"jsonData\":\"{\\\"@type\\\":\\\"MedicalScholarlyArticle\\\",\\\"publicationType\\\":\\\"Journal Article\\\",\\\"inLanguage\\\":\\\"en-US\\\",\\\"headline\\\":\\\"PKCι interacts with Rab14 and modulates epithelial barrier function through regulation of claudin-2 levels.\\\",\\\"url\\\":\\\"https://www.ncbi.nlm.nih.gov/pubmed/25694446/\\\",\\\"author\\\":[{\\\"@type\\\":\\\"Person\\\",\\\"mainEntityOfPage\\\":{\\\"@type\\\":\\\"WebPage\\\",\\\"@id\\\":\\\"https://medicine.yale.edu/ysm/profile/sourav_ghosh/\\\",\\\"@context\\\":\\\"http://schema.org\\\"},\\\"name\\\":\\\"Sourav Ghosh\\\",\\\"description\\\":\\\"Sourav Ghosh, Ph.D., is an Associate Professor of Neurology and Pharmacology at the Yale University School of Medicine. 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While inflammation is a cardinal feature for immune defense, the magnitude and period of the inflammatory response has to follow the ‘Goldilocks Principle’ wherein inflammation would be detrimental if its amplitude is too little or too much, or its period too short or too long. Drs. Rothlin and Ghosh investigates the principles and molecular mechanisms that negatively regulate inflammation and ensure that the amplitude and period of inflammation is ‘just right’. 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Macrophage function in tissue repair and remodeling requires IL-4 or IL-13 with apoptotic cells. Science (New York, N.Y.) 2017, 356:1072-1076.\\\",\\\"@context\\\":\\\"http://schema.org\\\"}\"},{\"schemaName\":\"MedicalScholarlyArticle\",\"jsonData\":\"{\\\"@type\\\":\\\"MedicalScholarlyArticle\\\",\\\"publicationType\\\":\\\"Journal Article\\\",\\\"inLanguage\\\":\\\"en-US\\\",\\\"headline\\\":\\\"Negative Regulation of Type 2 Immunity.\\\",\\\"url\\\":\\\"https://www.ncbi.nlm.nih.gov/pubmed/28082101/\\\",\\\"author\\\":[{\\\"@type\\\":\\\"Person\\\",\\\"mainEntityOfPage\\\":{\\\"@type\\\":\\\"WebPage\\\",\\\"@id\\\":\\\"https://medicine.yale.edu/ysm/profile/sourav_ghosh/\\\",\\\"@context\\\":\\\"http://schema.org\\\"},\\\"name\\\":\\\"Sourav Ghosh\\\",\\\"description\\\":\\\"Sourav Ghosh, Ph.D., is an Associate Professor of Neurology and Pharmacology at the Yale University School of Medicine. 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Apical-Basal Polarity Signaling Components, Lgl1 and aPKCs, Control Glutamatergic Synapse Number and Function. IScience 2019, 20:25-41.\\\",\\\"@context\\\":\\\"http://schema.org\\\"}\"},{\"schemaName\":\"MedicalScholarlyArticle\",\"jsonData\":\"{\\\"@type\\\":\\\"MedicalScholarlyArticle\\\",\\\"publicationType\\\":\\\"Journal Article\\\",\\\"inLanguage\\\":\\\"en-US\\\",\\\"headline\\\":\\\"Cracking the Cell Death Code.\\\",\\\"url\\\":\\\"https://www.ncbi.nlm.nih.gov/pubmed/31548182/\\\",\\\"author\\\":[{\\\"@type\\\":\\\"Person\\\",\\\"mainEntityOfPage\\\":{\\\"@type\\\":\\\"WebPage\\\",\\\"@id\\\":\\\"https://medicine.yale.edu/ysm/profile/sourav_ghosh/\\\",\\\"@context\\\":\\\"http://schema.org\\\"},\\\"name\\\":\\\"Sourav Ghosh\\\",\\\"description\\\":\\\"Sourav Ghosh, Ph.D., is an Associate Professor of Neurology and Pharmacology at the Yale University School of Medicine. Dr. Ghosh obtained a M.Sc. in Zoology at the University of Calcutta, where he studied Drosophila and mosquito genetics. Next, he completed his graduate studies on cell cytoskeleton and protein trafficking under the direction of John V. Cox at the University of Tennessee, Memphis. Subsequently, Dr. Ghosh did his postdoctoral research on cell signaling at the Salk Institute for Biological Studies under the guidance of Tony Hunter. In 2007, Dr. Ghosh joined University of Arizona as an Assistant Professor, and in 2014 he moved to Yale University School of Medicine and is currently an Associate Professor in the Departments of Neurology and Pharmacology. Dr. Ghosh and Dr. Carla Rothlin co-direct a lab studying the regulation of inflammation (Rothin, Ghosh et al. Cell, 2007, Carrera Silva et al. Immunity, 2013, Bosurgi et al. Science, 2017). While inflammation is a cardinal feature for immune defense, the magnitude and period of the inflammatory response has to follow the ‘Goldilocks Principle’ wherein inflammation would be detrimental if its amplitude is too little or too much, or its period too short or too long. Drs. Rothlin and Ghosh investigates the principles and molecular mechanisms that negatively regulate inflammation and ensure that the amplitude and period of inflammation is ‘just right’. Defects in these molecular circuits can manifest as wide ranging clinical problems including chronic or pathological inflammation, autoimmunity and pathological wound healing, while harnessing these checkpoints can improve anti-cancer immunity.\\\",\\\"url\\\":\\\"https://medicine.yale.edu/ysm/profile/sourav_ghosh/\\\",\\\"email\\\":\\\"sourav.ghosh@yale.edu\\\",\\\"telephone\\\":\\\"\\\",\\\"honorificSuffix\\\":[null,\\\"PhD\\\"],\\\"award\\\":[],\\\"jobTitle\\\":[\\\"Associate Professor of Neurology and Pharmacology\\\"],\\\"affiliation\\\":[{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Cancer Signaling Networks\\\",\\\"url\\\":\\\"https://medicine.yale.edu/cancer/research/programs/transduction/index.aspx\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Interdepartmental Neuroscience Program\\\",\\\"url\\\":\\\"https://medicine.yale.edu/INP/index.aspx\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Molecular Medicine, Pharmacology, and Physiology\\\",\\\"url\\\":\\\"http://bbs.yale.edu/molmed/index.aspx\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Neural Disorders\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Neurology\\\",\\\"url\\\":\\\"https://medicine.yale.edu/neurology\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Neuroscience\\\",\\\"url\\\":\\\"http://bbs.yale.edu/neuroscience\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Secondary Faculty\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Yale Cancer Center\\\",\\\"url\\\":\\\"https://www.yalecancercenter.org\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Yale Combined Program in the Biological and Biomedical Sciences (BBS)\\\",\\\"url\\\":\\\"http://bbs.yale.edu\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Yale University\\\",\\\"url\\\":\\\"https://www.yale.edu/\\\",\\\"@context\\\":\\\"http://schema.org\\\"}],\\\"alumniOf\\\":[{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"University of Tennessee, Molecular Sciences (2000)\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"University of Calcutta, Zoology (1992)\\\",\\\"@context\\\":\\\"http://schema.org\\\"},{\\\"@type\\\":\\\"Organization\\\",\\\"name\\\":\\\"Salk Institute for Biological Studies\\\",\\\"@context\\\":\\\"http://schema.org\\\"}],\\\"image\\\":{\\\"@type\\\":\\\"ImageObject\\\",\\\"url\\\":\\\"https://ysm-res.cloudinary.com/image/upload/c_limit,f_auto,h_630,q_auto,w_1200/v1/yms/prod/353f686f-9b80-47a1-96b0-391d14f042ab\\\",\\\"description\\\":\\\"\\\",\\\"height\\\":1200,\\\"width\\\":630,\\\"@context\\\":\\\"http://schema.org\\\"},\\\"@context\\\":\\\"http://schema.org\\\"}],\\\"description\\\":\\\"Rothlin CV, Ghosh S. Cracking the Cell Death Code. Cold Spring Harbor Perspectives In Biology 2019.\\\",\\\"@context\\\":\\\"http://schema.org\\\"}\"}],\"isResearchProfile\":false}}],\"sidebarComponents\":[]}"

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