2025
MIF as an oncogenic driver of low‐heterogeneity melanomas
Tran T, Sánchez‐Zuno G, Kulkarni R, Kluger H, Bucala R. MIF as an oncogenic driver of low‐heterogeneity melanomas. Molecular Oncology 2025, 19: 1295-1298. PMID: 40131169, PMCID: PMC12077282, DOI: 10.1002/1878-0261.70031.Peer-Reviewed Original ResearchConceptsMacrophage migration inhibitory factorImproving therapeutic outcomesMigration inhibitory factorPotential therapeutic utilityImmune landscapeMelanoma clonesImmune escapeT cellsImmunoregulatory cytokinesTumor heterogeneityTumor progressionOncogenic driversPathway inhibitorTherapeutic outcomesTumor evolutionInhibitory factorCell proliferationMelanomaTumorCellsAntagonistCytokinesTranscriptomic Alterations Induced by Tetrahydrocannabinol in SIV/HIV Infection: A Systematic Review
Valizadeh A, Veenhuis R, Bradley B, Xu K. Transcriptomic Alterations Induced by Tetrahydrocannabinol in SIV/HIV Infection: A Systematic Review. International Journal Of Molecular Sciences 2025, 26: 2598. PMID: 40141240, PMCID: PMC11942185, DOI: 10.3390/ijms26062598.Peer-Reviewed Original ResearchConceptsSimian immunodeficiency virus (SIV)-infected macaquesPrevalence of cannabis useSIV-infected macaquesChronic immune activationHIV-infected human cellsEpithelial cell proliferationModulate immune responsesSystematic reviewSIV/HIV infectionHIV infectionPreclinical evidencePathways related to inflammationImmune activationCannabis useMicro-RNA expressionImmunomodulatory roleImmunomodulatory effectsReduce inflammationImmune responseTetrahydrocannabinolComprehensive searchCell proliferationTranscriptomic alterationsMethodological qualityPWHTumorigenesis Driven by BRAFV600E Requires Secondary Mutations that Overcome it's Feedback Inhibition of RAC1 and Migration.
Gadal S, Boyer J, Roy S, Outmezguine N, Sharma M, Li H, Fan N, Chan E, Romin Y, Barlas A, Chang Q, Pancholi P, Timaul N, Overholtzer M, Yaeger R, Manova-Todorova K, de Stanchina E, Bosenberg M, Rosen N. Tumorigenesis Driven by BRAFV600E Requires Secondary Mutations that Overcome it's Feedback Inhibition of RAC1 and Migration. Cancer Research 2025 PMID: 39992718, DOI: 10.1158/0008-5472.can-24-2220.Peer-Reviewed Original ResearchInhibition of Rac1Rac1 activationLevels of ERK activationSecondary mutationsBRAFV600E mutationInhibition of Rac1 activityMutant Rac1Cell motilityRac1ERK activationMesenchymal migrationFeedback inhibitionRestored migrationMutationsGenetically engineered mouse modelsCell proliferationSelection of lesionsTumor evolutionPTEN inactivationTumorigenesisOncogenic driversBRAFV600EMalignant transformationBenign neviMouse model
2024
Future directions in myelodysplastic syndromes/neoplasms and acute myeloid leukaemia classification: from blast counts to biology
Della Porta M, Bewersdorf J, Wang Y, Hasserjian R. Future directions in myelodysplastic syndromes/neoplasms and acute myeloid leukaemia classification: from blast counts to biology. Histopathology 2024, 86: 158-170. PMID: 39450427, DOI: 10.1111/his.15353.Peer-Reviewed Original ResearchAcute myeloid leukemiaIntegration of genomic dataGenomic informationGenomic dataPresence of SF3B1 mutationsDisease entityMethylation profilesAML classificationRecurrent genetic abnormalitiesHaematopoietic cell proliferationPercentage of myeloblastsGene expressionGenetic featuresMultiple diagnostic modalitiesPatient risk stratificationSF3B1 mutationsBlast countDisease pathogenesisGenetic abnormalitiesCell proliferationTP53 abnormalitiesDiagnostic modalitiesMyeloid leukemiaBone marrowPatient cohortLimiting 20S proteasome assembly leads to unbalanced nucleo-cytoplasmic distribution of 26S/30S proteasomes and chronic proteotoxicity
Ruiz-Romero G, Berdún M, Hochstrasser M, Salas-Pino S, Daga R. Limiting 20S proteasome assembly leads to unbalanced nucleo-cytoplasmic distribution of 26S/30S proteasomes and chronic proteotoxicity. IScience 2024, 27: 111095. PMID: 39473973, PMCID: PMC11513537, DOI: 10.1016/j.isci.2024.111095.Peer-Reviewed Original ResearchProteasome assemblyDegradation of cell cycle proteinsNucleo-cytoplasmic distributionCell cycle proteinsHeat shock responseCytoplasmic proteostasisFission yeastMitotic substratesProteasome regulationCytoplasmic aggregatesUnfolded proteinsProteasome activityProteasomeConstitutive activationFunctional relevanceShock responseUmp1Cell proliferationProteinCellsCompartmentalizationAssemblyProteostasisYeastChaperoneO-083 A METABOLOME-WIDE ASSOCIATION STUDY OF OCCUPATIONAL EXPOSURE TO FORMALDEHYDE
Rothman N, Lin X, Vermeulen R, Zhang L, Pinto-Pacheco B, Tang X, Hu W, Jones D, Guo W, Wen C, Huang Y, Reiss B, Guangdong L, Rappaport S, Smith M, Lan Q, Walker D. O-083 A METABOLOME-WIDE ASSOCIATION STUDY OF OCCUPATIONAL EXPOSURE TO FORMALDEHYDE. Occupational Medicine 2024, 74: 0-0. DOI: 10.1093/occmed/kqae023.0604.Peer-Reviewed Original ResearchEffects of exposure to FAFA exposureImmune system disordersSystemic metabolic processesAssociated with alterationsUntargeted liquid chromatographyPlasma metabolomeMetabolic pathway enrichment analysisNasopharyngeal cancerProstaglandin metabolismOccupational exposure to formaldehydeSystem disordersHuman studiesFatty acid uptakeOccupational exposureArachidonic acidCell proliferationExposure to FAOxidative stressCarnitine shuttleAcid uptakeMitochondrial dysfunctionBiological effectsExposure to formaldehydeAssociation studiesNeutrophils insert elastase into hepatocytes to regulate calcium signaling in alcohol-associated hepatitis
Ogino N, Leite M, Guerra M, Kruglov E, Asashima H, Hafler D, Ito T, Pereira J, Peiffer B, Sun Z, Ehrlich B, Nathanson M. Neutrophils insert elastase into hepatocytes to regulate calcium signaling in alcohol-associated hepatitis. Journal Of Clinical Investigation 2024, 134: e171691. PMID: 38916955, PMCID: PMC11324315, DOI: 10.1172/jci171691.Peer-Reviewed Original ResearchAlcohol-associated hepatitisReduced cell proliferationCalcium channel expressionCalcium signaling mechanismsIntracellular calcium channelsCell proliferationRegulate calcium signalingNeutrophil extracellular trapsChannel expressionNeutrophil granule proteinsCalcium channelsNeutrophil infiltrationPatient specimensGranule proteasesMouse modelHealthy subjectsLiver diseaseExtracellular trapsCalcium signalingSerpin E2NeutrophilsElastase activityHepatitisTissue remodelingSignaling mechanismsA Prostatic Intraepithelial Neoplasia-Dependent p27Kip1 Checkpoint Induces Senescence and Inhibits Cell Proliferation and Cancer Progression
Majumder P, Grisanzio C, O'Connell F, Barry M, Brito J, Xu Q, Guney I, Berger R, Herman P, Bikoff R, Fedele G, Baek W, Wang S, Ellwood-Yen K, Wu H, Sawyers C, Signoretti S, Hahn W, Loda M, Sellers W. A Prostatic Intraepithelial Neoplasia-Dependent p27Kip1 Checkpoint Induces Senescence and Inhibits Cell Proliferation and Cancer Progression. Cancer Cell 2024, 42: 1126. PMID: 38866454, DOI: 10.1016/j.ccell.2024.05.008.Peer-Reviewed Original ResearchCOX2-dependent suppression of anticancer immunity
Lira M, Galluzzi L, Vanpouille-Box C. COX2-dependent suppression of anticancer immunity. Trends In Cancer 2024, 10: 573-575. PMID: 38821853, PMCID: PMC11236508, DOI: 10.1016/j.trecan.2024.05.006.Peer-Reviewed Original ResearchInterleukin-2Tumor-targeting immune responsesPromote tumor progressionProstaglandin E<sub>2</sub>Inhibition of mitochondrial metabolismDownregulation of interleukin 2Cancer cell proliferationAnticancer immunityT cellsTumor progressionImmune responseCell proliferationMitochondrial metabolismProstaglandinCancerLoss of function of FAM177A1, a Golgi complex localized protein, causes a novel neurodevelopmental disorder
Kohler J, Legro N, Baldridge D, Shin J, Bowman A, Ugur B, Jackstadt M, Shriver L, Patti G, Zhang B, Feng W, McAdow A, Goddard P, Ungar R, Jensen T, Smith K, Fresard L, Alvarez R, Bonner D, Reuter C, McCormack C, Kravets E, Marwaha S, Holt J, Network U, Acosta M, Adam M, Adams D, Alvarez R, Alvey J, Amendola L, Andrews A, Ashley E, Bacino C, Bademci G, Balasubramanyam A, Baldridge D, Bale J, Bamshad M, Barbouth D, Bayrak-Toydemir P, Beck A, Beggs A, Behrens E, Bejerano G, Bellen H, Bennett J, Berg-Rood B, Bernstein J, Berry G, Bican A, Bivona S, Blue E, Bohnsack J, Bonner D, Botto L, Boyd B, Briere L, Burke E, Burrage L, Butte M, Byers P, Byrd W, Carey J, Carrasquillo O, Cassini T, Chang T, Chanprasert S, Chao H, Chinn I, Clark G, Coakley T, Cobban L, Cogan J, Coggins M, Cole F, Colley H, Cope H, Corner B, Corona R, Craigen W, Crouse A, Cunningham M, D’Souza P, Dai H, Dasari S, Davis J, Dayal J, Dell’Angelica E, Dickson P, Dipple K, Doherty D, Dorrani N, Doss A, Douine E, Earl D, Eckstein D, Emrick L, Eng C, Ezell K, Falk M, Fieg E, Fisher P, Fogel B, Forghani I, Gahl W, Glass I, Gochuico B, Goddard P, Godfrey R, Golden-Grant K, Grajewski A, Hadley D, Hahn S, Halley M, Hamid R, Hassey K, Hayes N, High F, Hing A, Hisama F, Holm I, Hom J, Horike-Pyne M, Huang A, Hutchison S, Introne W, Isasi R, Izumi K, Jamal F, Jarvik G, Jarvik J, Jayadev S, Jean-Marie O, Jobanputra V, Karaviti L, Ketkar S, Kiley D, Kilich G, Kobren S, Kohane I, Kohler J, Korrick S, Kozuira M, Krakow D, Krasnewich D, Kravets E, Lalani S, Lam B, Lam C, Lanpher B, Lanza I, LeBlanc K, Lee B, Levitt R, Lewis R, Liu P, Liu X, Longo N, Loo S, Loscalzo J, Maas R, Macnamara E, MacRae C, Maduro V, Maghiro A, Mahoney R, Malicdan M, Mamounas L, Manolio T, Mao R, Maravilla K, Marom R, Marth G, Martin B, Martin M, Martínez-Agosto J, Marwaha S, McCauley J, McConkie-Rosell A, McCray A, McGee E, Mefford H, Merritt J, Might M, Mirzaa G, Morava E, Moretti P, Mulvihill J, Nakano-Okuno M, Nelson S, Neumann S, Newman J, Nicholas S, Nickerson D, Nieves-Rodriguez S, Novacic D, Oglesbee D, Orengo J, Pace L, Pak S, Pallais J, Palmer C, Papp J, Parker N, Phillips J, Posey J, Potocki L, Swerdzewski B, Quinlan A, Rao D, Raper A, Raskind W, Renteria G, Reuter C, Rives L, Robertson A, Rodan L, Rosenfeld J, Rosenwasser N, Rossignol F, Ruzhnikov M, Sacco R, Sampson J, Saporta M, Schaechter J, Schedl T, Schoch K, Scott D, Scott C, Seto E, Shashi V, Shin J, Silverman E, Sinsheimer J, Sisco K, Smith E, Smith K, Solnica-Krezel L, Solomon B, Spillmann R, Stoler J, Sullivan K, Sullivan J, Sun A, Sutton S, Sweetser D, Sybert V, Tabor H, Tan Q, Tan A, Tarakad A, Tekin M, Telischi F, Thorson W, Tifft C, Toro C, Tran A, Ungar R, Urv T, Vanderver A, Velinder M, Viskochil D, Vogel T, Wahl C, Walker M, Wallace S, Walley N, Wambach J, Wan J, Wangler M, Ward P, Wegner D, Hubshman M, Wener M, Wenger T, Westerfield M, Wheeler M, Whitlock J, Wolfe L, Worley K, Xiao C, Yamamoto S, Yang J, Zhang Z, Zuchner S, Worthey E, Ashley E, Montgomery S, Fisher P, Postlethwait J, De Camilli P, Solnica-Krezel L, Bernstein J, Wheeler M. Loss of function of FAM177A1, a Golgi complex localized protein, causes a novel neurodevelopmental disorder. Genetics In Medicine 2024, 26: 101166. PMID: 38767059, PMCID: PMC11451386, DOI: 10.1016/j.gim.2024.101166.Peer-Reviewed Original ResearchNegative regulation of cell proliferationLoss-of-function variantsPathways associated with apoptosisRegulation of cell proliferationRelationship to human diseaseHuman cell linesNeurodevelopmental disordersRNA-seqLocalized proteinsImmune-associated genesZebrafish cellsGolgi complexModel organismsGlobal developmental delayBiallelic variantsFAM177A1Negative regulatorHuman diseasesZebrafish model organismPhysiological functionsCell linesGolgiHuman fibroblastsZebrafishCell proliferationPerivascular NOTCH3+ Stem Cells Drive Meningioma Tumorigenesis and Resistance to Radiotherapy.
Choudhury A, Cady M, Lucas C, Najem H, Phillips J, Palikuqi B, Zakimi N, Joseph T, Birrueta J, Chen W, Oberheim Bush N, Hervey-Jumper S, Klein O, Toedebusch C, Horbinski C, Magill S, Bhaduri A, Perry A, Dickinson P, Heimberger A, Ashworth A, Crouch E, Raleigh D. Perivascular NOTCH3+ Stem Cells Drive Meningioma Tumorigenesis and Resistance to Radiotherapy. Cancer Discovery 2024, 14: 1823-1837. PMID: 38742767, PMCID: PMC11452293, DOI: 10.1158/2159-8290.cd-23-1459.Peer-Reviewed Original ResearchConceptsResistance to radiotherapyMeningioma tumorigenesisSystemic therapyTreating meningiomasStem cellsGenetically engineered mouse modelsTumor-initiating capacityHigh-grade meningiomasReduced tumor growthPrimary intracranial tumorsMeningioma growthImproved survivalIntracranial tumorsRadiotherapyTherapeutic vulnerabilitiesTumor growthMeningiomasMouse modelSingle-cell transcriptomicsLineage tracingNotch3TumorigenesisCell proliferationReduced survivalCell typesMLL1 regulates cytokine-driven cell migration and metastasis
Nair P, Danilova L, Gómez-de-Mariscal E, Kim D, Fan R, Muñoz-Barrutia A, Fertig E, Wirtz D. MLL1 regulates cytokine-driven cell migration and metastasis. Science Advances 2024, 10: eadk0785. PMID: 38478601, PMCID: PMC10936879, DOI: 10.1126/sciadv.adk0785.Peer-Reviewed Original ResearchConceptsMethyltransferase mixed-lineage leukemia 1Cell migrationControls actin filament assemblyRegulation of cell migrationHistone methyltransferase mixed-lineage leukemia 1Actin filament assemblyCell cycle-related pathwaysCancer cell migrationMixed-lineage leukemia 1Regulating cell proliferationMyosin contractilityFilament assemblyProtein meninAssociated with immune cellsMetastatic burdenCancer cellsCell proliferationPrimary tumor growth rateLung metastatic burdenTumor growth rateGrowth rateCellsPreexisting metastasesMetastatic diseaseTumor growthDe novo-designed transmembrane proteins bind and regulate a cytokine receptor
Mravic M, He L, Kratochvil H, Hu H, Nick S, Bai W, Edwards A, Jo H, Wu Y, DiMaio D, DeGrado W. De novo-designed transmembrane proteins bind and regulate a cytokine receptor. Nature Chemical Biology 2024, 20: 751-760. PMID: 38480980, PMCID: PMC11142920, DOI: 10.1038/s41589-024-01562-z.Peer-Reviewed Original ResearchTM proteinsTM regionTarget membrane proteinsComplex biological functionsTM domainTM helicesInteraction partnersTransmembrane proteinsMembrane proteinsReceptor homodimerizationBiological functionsCytokine receptorsBinding topologyAmino acidsProteinErythropoietin receptorHomodimerizationCell proliferationTransmembraneEpoRIn vitroMolecular modelingBinding modeReceptorsMotifCellular Dynamics of Fas-Associated Death Domain in the Regulation of Cancer and Inflammation
Ranjan K, Pathak C. Cellular Dynamics of Fas-Associated Death Domain in the Regulation of Cancer and Inflammation. International Journal Of Molecular Sciences 2024, 25: 3228. PMID: 38542202, PMCID: PMC10970579, DOI: 10.3390/ijms25063228.Peer-Reviewed Original ResearchConceptsFas-associated death domainDeath domainDeath receptorsInitiation of apoptotic signalingRegulate programmed cell deathExpression of Fas-associated death domainSignaling pathwayCellular dynamicsRegulator of inflammatory signalingRegulation of cancerAdaptor proteinActivated caspasesApoptotic functionApoptosis signalingSubcellular localizationApoptotic signalingCellular homeostasisCell deathCell survivalCoordinated removalCellular senescenceIntracellular expressionCell proliferationSpatiotemporal mechanismsInflammatory signalingDimeric Tubulin Modifies Mechanical Properties of Lipid Bilayer, as Probed Using Gramicidin A Channel
Rostovtseva T, Weinrich M, Jacobs D, Rosencrans W, Bezrukov S. Dimeric Tubulin Modifies Mechanical Properties of Lipid Bilayer, as Probed Using Gramicidin A Channel. International Journal Of Molecular Sciences 2024, 25: 2204. PMID: 38396879, PMCID: PMC10889239, DOI: 10.3390/ijms25042204.Peer-Reviewed Original ResearchConceptsRegulation of protein-protein interactionsProtein-protein interactionsNon-lamellar lipidsMembrane hydrophobic coreMembrane remodelingMechanical properties of lipid bilayersMembrane bindingProperties of lipid bilayersRegulatory functionsTubulin bindingTubulinHydrophobic regionLipid headgroupsHydrophobic coreCell proliferationLipid bilayerPlanar lipid membranesMembrane mechanical propertiesMembraneMolecular probesLipid packingLipidLipid membranesGramicidin A channelBindingWnt Signaling in Atherosclerosis: Mechanisms to Therapeutic Implications
Afroz R, Goodwin J. Wnt Signaling in Atherosclerosis: Mechanisms to Therapeutic Implications. Biomedicines 2024, 12: 276. PMID: 38397878, PMCID: PMC10886882, DOI: 10.3390/biomedicines12020276.Peer-Reviewed Original ResearchWnt pathwayWnt signalingAtherosclerosis progressionSmooth muscle cell proliferationMuscle cell proliferationPathophysiology of atherosclerosisBlock Wnt signalingDownstream signaling moleculesStages of atherosclerosis progressionPreclinical modelsMonocyte infiltrationEndothelial dysfunctionSmall molecule inhibitorsTreatment of atherosclerosisVascular inflammationTherapeutic approachesTherapeutic implicationsCo-receptorVascular diseaseAtherosclerosis developmentAtherosclerosisCell proliferationWnt ligandsMolecule inhibitorsWntSH2 domain protein E and ABL signaling regulate blood vessel size
Schumacher J, Wright Z, Florat D, Anand S, Dasyani M, Batta S, Laverde V, Ferrari K, Klimkaite L, Bredemeier N, Gurung S, Koller G, Aguera K, Chadwick G, Johnson R, Davis G, Sumanas S. SH2 domain protein E and ABL signaling regulate blood vessel size. PLOS Genetics 2024, 20: e1010851. PMID: 38190417, PMCID: PMC10798624, DOI: 10.1371/journal.pgen.1010851.Peer-Reviewed Original ResearchZebrafish embryosDorsal aortaSrc homology 2 domainMutant phenotypeVascular tubulogenesisCell numberNegative regulatorBiological roleMolecular mechanismsProtein EChemical inhibitionUmbilical vein cellsE proteinEndothelial cell proliferationHuman endothelial cell culturesCell proliferationVein cellsProteinMutantsVascular tubesSpecific overexpressionTubulogenesisEndothelial cell culturesTight junctionsABLMacrophage migration inhibitory factor as a therapeutic target in neuro-oncology: A review
Jarmula J, Lee J, Lauko A, Rajappa P, Grabowski M, Dhawan A, Chen P, Bucala R, Vogelbaum M, Lathia J. Macrophage migration inhibitory factor as a therapeutic target in neuro-oncology: A review. Neuro-Oncology Advances 2024, 6: vdae142. PMID: 39233830, PMCID: PMC11372298, DOI: 10.1093/noajnl/vdae142.Peer-Reviewed Original ResearchMacrophage migration inhibitory factorPrimary CNS tumorsCentral nervous systemMigration inhibitory factorCNS tumorsPrimary central nervous systemInhibitory factorTherapeutic targetPre-clinical studiesFunctions of macrophage migration inhibitory factorPreclinical modelsImmune evasionSmall molecule inhibitorsNeuro-oncologyClinical trialsTumor initiationClinical translationMonoclonal antibodiesTumorigenic processNervous systemTherapeutic requirementsCell proliferationTherapeutic developmentTumorEffective target
2023
Transcriptome Analysis of Escherichia coli Dormant Cystlike Cells
Nikolaev Y, Loiko N, Galuza O, Mardanov A, Beletskii A, Deryabin D, Demkina E, El’-Registan G. Transcriptome Analysis of Escherichia coli Dormant Cystlike Cells. Microbiology 2023, 92: 775-791. DOI: 10.1134/s0026261723602233.Peer-Reviewed Original ResearchDormant cellsHeterogeneity of bacterial populationsE. coli populationsActive genesGene readsCell envelopeGenome activationBiofilm formationBacterial populationsGrowing cellsStress adaptationSixty genesGenesDifferential expressionCell heterogeneityRNA contentMRNA amountsCell proliferationPresence of mRNACell populationsCellsGenomeTranscriptomeTranscriptionRNACalponin 2 regulates ketogenesis to mitigate acute kidney injury
Gui Y, Palanza Z, Gupta P, Li H, Pan Y, Wang Y, Hargis G, Kreutzer D, Wang Y, Bastacky S, Liu Y, Liu S, Zhou D. Calponin 2 regulates ketogenesis to mitigate acute kidney injury. JCI Insight 2023, 8: e170521. PMID: 37751293, PMCID: PMC10721266, DOI: 10.1172/jci.insight.170521.Peer-Reviewed Original ResearchConceptsAcute kidney injuryEstrogen receptor 2Fatty acid oxidationKidney injuryKidney fibrosisCalponin 2Ketone body β-hydroxybutyrateTubular cell deathBody β-hydroxybutyrateSirtuin 5Endogenous ketogenesisKidney functionReceptor 2Protein posttranslational modificationsRate-limiting enzymeFAO pathwayMitochondrial sirtuin 5Animal kidneysΒ-hydroxybutyrateOrgan performanceCell proliferationSynthase 2FibrosisPosttranslational modificationsInjury
This site is protected by hCaptcha and its Privacy Policy and Terms of Service apply