Featured Publications
Ubiquitination of ATF6 by disease-associated RNF186 promotes the innate receptor-induced unfolded protein response
Ranjan K, Hedl M, Sinha S, Zhang X, Abraham C. Ubiquitination of ATF6 by disease-associated RNF186 promotes the innate receptor-induced unfolded protein response. Journal Of Clinical Investigation 2021, 131: e145472. PMID: 34623328, PMCID: PMC8409591, DOI: 10.1172/jci145472.Peer-Reviewed Original ResearchMeSH KeywordsActivating Transcription Factor 6AnimalsEndoplasmic Reticulum StressGenetic VariationHost Microbial InteractionsHumansImmunity, InnateInflammatory Bowel DiseasesMacrophagesMiceMice, Inbred C57BLMice, KnockoutNod2 Signaling Adaptor ProteinReceptors, Pattern RecognitionRisk FactorsSignal TransductionUbiquitinationUbiquitin-Protein LigasesUnfolded Protein ResponseConceptsPattern recognition receptorsUnfolded protein responseInflammatory bowel diseaseER stress sensorsHuman macrophagesIntestinal immune homeostasisProtein responseInnate immune systemRisk variantsKey macrophage functionsBowel diseaseOral challengeTranscription factor 6Immune homeostasisCytokine secretionColonic tissueMacrophage functionStress sensorImmune systemRecognition receptorsEffective clearanceMicrobial responsesWeight lossMacrophagesUbiquitinationThe E3 ubiquitin ligase RNF186 and RNF186 risk variants regulate innate receptor-induced outcomes
Ranjan K, Hedl M, Abraham C. The E3 ubiquitin ligase RNF186 and RNF186 risk variants regulate innate receptor-induced outcomes. Proceedings Of The National Academy Of Sciences Of The United States Of America 2021, 118: e2013500118. PMID: 34353900, PMCID: PMC8364215, DOI: 10.1073/pnas.2013500118.Peer-Reviewed Original ResearchMeSH KeywordsCytokinesHumansImmunity, InnateInflammatory Bowel DiseasesIntestinesMacrophagesMyeloid CellsNF-kappa BNod2 Signaling Adaptor ProteinPolymorphism, Single NucleotideReceptor-Interacting Protein Serine-Threonine Kinase 2Receptors, Pattern RecognitionToll-Like Receptor 2Toll-Like Receptor 4UbiquitinationUbiquitin-Protein LigasesConceptsPattern recognition receptorsE3 ubiquitin ligase activityStimulation of PRRsAntimicrobial reactive oxygen speciesMultiple pattern recognition receptorsLoss of functionLigase activityReactive nitrogen speciesComplex assemblyIntestinal myeloid cellsReactive oxygen speciesAutophagy pathwayDownstream signalingRNF186Bacterial clearanceRisk variantsRecognition receptorsHuman macrophagesOxygen speciesInnate immunityInflammatory bowel diseaseNitrogen speciesMicrobial clearanceSpeciesMyeloid cellsCOVID-19: Unmasking Emerging SARS-CoV-2 Variants, Vaccines and Therapeutic Strategies
Raman R, Patel KJ, Ranjan K. COVID-19: Unmasking Emerging SARS-CoV-2 Variants, Vaccines and Therapeutic Strategies. Biomolecules 2021, 11: 993. PMID: 34356617, PMCID: PMC8301790, DOI: 10.3390/biom11070993.Peer-Reviewed Original ResearchConceptsSARS-CoV-2 infectionSARS-CoV-2 variantsSevere acute respiratory syndrome coronavirus 2Acute respiratory syndrome coronavirus 2Different SARS-CoV-2 variantsRespiratory syndrome coronavirus 2Emerging SARS-CoV-2 VariantsCoronavirus disease 2019 (COVID-19) pandemicSyndrome coronavirus 2Disease 2019 pandemicCOVID-19 pandemicOngoing vaccinesMedical comorbiditiesCoronavirus 2Prophylactic interventionsImmune responseTherapeutic modalitiesTherapeutic strategiesGlobal human healthIncreased transmissibilityEtiological agentVaccineComorbiditiesInfectionPandemicMyeloid Cell Expression of LACC1 Is Required for Bacterial Clearance and Control of Intestinal Inflammation
Kang JW, Yan J, Ranjan K, Zhang X, Turner JR, Abraham C. Myeloid Cell Expression of LACC1 Is Required for Bacterial Clearance and Control of Intestinal Inflammation. Gastroenterology 2020, 159: 1051-1067. PMID: 32693188, PMCID: PMC8139320, DOI: 10.1053/j.gastro.2020.07.024.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCD4-Positive T-LymphocytesCells, CulturedCoculture TechniquesColitis, UlcerativeCytokinesDextran SulfateDisease Models, AnimalDNA-Binding ProteinsFemaleHost Microbial InteractionsHumansImmunity, MucosalIntestinal MucosaIntracellular Signaling Peptides and ProteinsMaleMiceMice, KnockoutMyeloid CellsPrimary Cell CultureSalmonella InfectionsSalmonella typhimuriumConceptsIntestinal lymphoid organsBurden of bacteriaDextran sodium sulfateWild-type miceLymphoid organsTh17 cytokinesIntestinal inflammationDendritic cellsMyeloid cellsT cellsTh2 cytokinesMesenteric lymph node dendritic cellsLymph node dendritic cellsMyeloid cell-derived cytokinesAdaptive T cell responsesT cell transfer colitisMyeloid-specific disruptionInflammatory bowel diseaseReactive oxygen speciesImmune-mediated diseasesT cell responsesT helper 1Cell-derived cytokinesT cell cytokinesBone marrow-derived macrophagesInsights of Endocytosis Signaling in Health and Disease
Pathak C, Vaidya F, Waghela B, Jaiswara P, Gupta V, Kumar A, Rajendran B, Ranjan K. Insights of Endocytosis Signaling in Health and Disease. International Journal Of Molecular Sciences 2023, 24: 2971. PMID: 36769293, PMCID: PMC9918140, DOI: 10.3390/ijms24032971.Peer-Reviewed Original ResearchConceptsEndocytic machineryPlasma membraneCellular defenseFundamental cellular machinerySignal transduction modulesDifferent cellular compartmentsVital physiological processesProcess of endocytosisEndocytic proteinsIndependent endocytosisEndocytosis machineryTransduction modulesEukaryotic cellsCaveolar pathwayCellular machineryMammalian cellsEndocytic pathwayCell divisionCellular compartmentsComplex proteinsFunctional characterizationPhysiological processesMachinery resultsHuman diseasesEndocytosisLACC1 Required for NOD2-Induced, ER Stress-Mediated Innate Immune Outcomes in Human Macrophages and LACC1 Risk Variants Modulate These Outcomes
Huang C, Hedl M, Ranjan K, Abraham C. LACC1 Required for NOD2-Induced, ER Stress-Mediated Innate Immune Outcomes in Human Macrophages and LACC1 Risk Variants Modulate These Outcomes. Cell Reports 2019, 29: 4525-4539.e4. PMID: 31875558, PMCID: PMC7372507, DOI: 10.1016/j.celrep.2019.11.105.Peer-Reviewed Original ResearchMeSH KeywordsActivating Transcription Factor 6EIF-2 KinaseEndoplasmic ReticulumEndoplasmic Reticulum StressEndoribonucleasesEnterococcus faecalisEscherichia coliGene Expression RegulationHeLa CellsHost-Pathogen InteractionsHumansImmunity, InnateIntracellular Signaling Peptides and ProteinsMacrophagesNod2 Signaling Adaptor ProteinPhagocytosisPrimary Cell CultureProtein Serine-Threonine KinasesRiskSignal TransductionConceptsEndoplasmic reticulumER stressER stress sensorsHuman macrophagesInnate immune outcomesDisease risk variantsMultiple immune-mediated diseasesLaccase domainPattern recognition receptor NOD2HeLa cellsAntimicrobial pathwaysRisk variantsGenetic variantsLACC1Critical roleVariantsMacrophagesATF6IRE1αArg284SignalingReticulumStressTransfectionPERKFADD regulates NF-κB activation and promotes ubiquitination of cFLIPL to induce apoptosis
Ranjan K, Pathak C. FADD regulates NF-κB activation and promotes ubiquitination of cFLIPL to induce apoptosis. Scientific Reports 2016, 6: 22787. PMID: 26972597, PMCID: PMC4789601, DOI: 10.1038/srep22787.Peer-Reviewed Original ResearchMeSH KeywordsA549 CellsAnimalsApoptosisBaculoviral IAP Repeat-Containing 3 ProteinBlotting, WesternCASP8 and FADD-Like Apoptosis Regulating ProteinCaspase 8Cell LineCell SurvivalFas-Associated Death Domain ProteinHCT116 CellsHEK293 CellsHeLa CellsHT29 CellsHumansInhibitor of Apoptosis ProteinsMCF-7 CellsMiceNF-kappa BNIH 3T3 CellsProtein BindingRepressor ProteinsRNA InterferenceTumor Necrosis Factor-alphaUbiquitinationUbiquitin-Protein LigasesConceptsCell deathProcaspase-8Molecular mechanismsCellular FLICE-like inhibitory proteinFLICE-like inhibitory proteinExpression of cFLIPLCell death signalingApoptosis protein 2Apoptotic cell death signalingHEK 293T cellsNovel molecular mechanismApoptotic cell deathNF-κB activationFasL stimulationCellular inhibitorE3 ubiquitinTNF-α stimulationDeath domainDeath inducingDeath signalingEctopic expressionFADDCaspase-8NF-κBCell survival
2024
Cellular 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 signaling
2020
AGE-RAGE synergy influences programmed cell death signaling to promote cancer
Waghela BN, Vaidya FU, Ranjan K, Chhipa AS, Tiwari BS, Pathak C. AGE-RAGE synergy influences programmed cell death signaling to promote cancer. Molecular And Cellular Biochemistry 2020, 476: 585-598. PMID: 33025314, DOI: 10.1007/s11010-020-03928-y.Peer-Reviewed Original ResearchConceptsCell deathCancer cellsCell death machinerySet of genesCellular redox balanceSignal transduction pathwaysCell death pathwaysComplex signaling mechanismsCell survival mechanismAGE-RAGEDeath machineryCellular reprogrammingTransduction pathwaysDeath pathwaysMolecular paradigmRedox balanceSurvival mechanismSignaling mechanismCancer progressionAGE-RAGE signalingPresent review focusProgression of malignancyTypes of cancerUpregulated expressionChronic hyperglycemic conditionsCell-Penetrable Peptide-Conjugated FADD Induces Apoptosis and Regulates Inflammatory Signaling in Cancer Cells
Ranjan K, Waghela BN, Vaidya FU, Pathak C. Cell-Penetrable Peptide-Conjugated FADD Induces Apoptosis and Regulates Inflammatory Signaling in Cancer Cells. International Journal Of Molecular Sciences 2020, 21: 6890. PMID: 32961826, PMCID: PMC7555701, DOI: 10.3390/ijms21186890.Peer-Reviewed Original ResearchConceptsFADD proteinCancer cellsAnti-apoptotic genesCaveolar pathwayDeath domainCellular pathwaysCancer cell proliferationCytosolic expressionFADD expressionCell deathApoptosis inducersInduces ApoptosisExpression of FasProteinCell proliferationApoptosisNF-κB activationSimultaneous regulationInflammatory signalingExpressionCellsNLRP3 inflammasome primingRegulationPathwayInflammasome priming
2016
Expression of FADD and cFLIPL balances mitochondrial integrity and redox signaling to substantiate apoptotic cell death
Ranjan K, Pathak C. Expression of FADD and cFLIPL balances mitochondrial integrity and redox signaling to substantiate apoptotic cell death. Molecular And Cellular Biochemistry 2016, 422: 135-150. PMID: 27619661, DOI: 10.1007/s11010-016-2813-z.Peer-Reviewed Original ResearchConceptsExpression of FADDMitochondrial integrityCell deathDeath receptorsMutant of FADDInduced expressionNon-apoptotic functionsDeath receptor signalingFate of cellsMitochondrial-associated apoptosisApoptotic cell deathCancer cellsCellular signalingEctopic expressionJNK1 activationFADDCellular respirationHA14-1Independent pathwaysReceptor signalingCFLIPCFLIPLBcl-2ApoptosisIntracellular ROSExpression of cFLIPL Determines the Basal Interaction of Bcl‐2 With Beclin‐1 and Regulates p53 Dependent Ubiquitination of Beclin‐1 During Autophagic Stress
Ranjan K, Pathak C. Expression of cFLIPL Determines the Basal Interaction of Bcl‐2 With Beclin‐1 and Regulates p53 Dependent Ubiquitination of Beclin‐1 During Autophagic Stress. Journal Of Cellular Biochemistry 2016, 117: 1757-1768. PMID: 26682748, DOI: 10.1002/jcb.25474.Peer-Reviewed Original ResearchConceptsAutophagic stressDependent ubiquitinationBeclin-1Bcl-2Cell deathExpression of cFLIPLCo-immunoprecipitation analysisRegulation of autophagyHEK 293T cellsDifferent physiological processesAnti-apoptotic proteinsCellular homeostasisCellular stressEctopic expressionKnockdown cellsJNK1 activationCanonical interactionsProtein HMGB1Physiological processesBasal interactionCFLIPLSelective knockdownUbiquitinationAutophagyH2 O2
2013
Regulation of HA14‐1 mediated oxidative stress, toxic response, and autophagy by curcumin to enhance apoptotic activity in human embryonic kidney cells
Ranjan K, Sharma A, Surolia A, Pathak C. Regulation of HA14‐1 mediated oxidative stress, toxic response, and autophagy by curcumin to enhance apoptotic activity in human embryonic kidney cells. BioFactors 2013, 40: 157-169. PMID: 23559532, DOI: 10.1002/biof.1098.Peer-Reviewed Original ResearchMeSH KeywordsAntineoplastic AgentsApoptosisAutophagyBenzopyransCaspase 3CatalaseCell ProliferationCell SurvivalCurcuminDrug Resistance, NeoplasmDrug SynergismHEK293 CellsHumansMembrane Potential, MitochondrialNitrilesOxidative StressProto-Oncogene Proteins c-bcl-2Reactive Oxygen SpeciesSuperoxide DismutaseTranscription Factor RelAConceptsHuman embryonic kidney cellsHA14-1Embryonic kidney cellsProcess of autophagyHEK 293T cellsOxidative stressAntiapoptotic protein Bcl-2Kidney cellsProtein Bcl-2Toxic responsePromotion of malignancyAugmentation of apoptosisGeneration of ROSSignaling mechanismAntiapoptotic proteinsCell deathCancerous cell linesApoptotic activityCell proliferationBcl-2Cell linesPathological consequencesROS generationApoptosisROS