Featured Publications
FADD 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
2022
Advanced Glycation End Products-Mediated Oxidative Stress and Regulated Cell Death Signaling in Cancer
Pathak C, Vaidya F, Waghela B, Chhipa A, Tiwari B, Ranjan K. Advanced Glycation End Products-Mediated Oxidative Stress and Regulated Cell Death Signaling in Cancer. 2022, 535-550. DOI: 10.1007/978-981-15-9411-3_44.ChaptersRegulated cell deathCell deathDanger-associated molecular patternsOxidative stressTranscription factorsMolecular mechanismsCancer progressionCellular dysfunctionMolecular patternsRedox imbalanceCancer cellsPathological consequencesTypes of cancerROS generationCurrent understandingAGEs/RAGENucleic acidsAdvanced glycation end productsEnd productsGlycation of proteinsRAGE interactionAccumulationPathophysiological effectsGenesGlycation end products
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