Kishu Ranjan, PhD
Associate Research Scientist in PathologyCards
About
Research
Publications
Featured Publications
IL-4 mediated TAP2 downregulation is a dominant and reversible mechanism of immune evasion and immunotherapy resistance in non-small cell lung cancer.
Ranjan K, Rajendran BK, Deen IU, Costantini A, de Rodas ML, Desai SS, Scallo F, Gianino N, Ferrone S, Schalper KA. IL-4 mediated TAP2 downregulation is a dominant and reversible mechanism of immune evasion and immunotherapy resistance in non-small cell lung cancer. Mol Cancer 2025, 24: 80. PMID: 40091029, DOI: 10.1186/s12943-025-02276-z.Peer-Reviewed Original ResearchUbiquitination 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 macrophagesLACC1 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
Editorial: Engineered medicines to mitigate resistance to cancer immunotherapy
Ranjan K, Dube P, Mishra S. Editorial: Engineered medicines to mitigate resistance to cancer immunotherapy. Frontiers In Medicine 2024, 11: 1452812. PMID: 39165370, PMCID: PMC11333442, DOI: 10.3389/fmed.2024.1452812.Peer-Reviewed Original ResearchHLA class-I antigen presentation machinery (APM) alterations mediate immune evasion in lung cancer brain metastases.
Vilariño N, Lopez De Rodas M, Ranjan K, Costantini A, Villalba M, Lu B, Kravitz C, Nadal E, Goldberg S, Nguyen D, Schalper K. HLA class-I antigen presentation machinery (APM) alterations mediate immune evasion in lung cancer brain metastases. Journal Of Clinical Oncology 2024, 42: e14014-e14014. DOI: 10.1200/jco.2024.42.16_suppl.e14014.Peer-Reviewed Original ResearchLung cancer brain metastasisPrimary lung tumorsTumor-infiltrating lymphocytesImmune checkpoint inhibitorsCancer brain metastasesAntigen presentation machineryB2M expressionIFN-gBrain metastasesB2MImmune evasionAssociated with shorter overall survivalMultiplexed quantitative immunofluorescenceM expressionExpression of B2MB2M levelsExpression of pSTAT1Shorter overall survivalUnfavorable clinical featuresNo significant associationAssociated with unfavorable clinical featuresCheckpoint inhibitorsImmunotherapy resistanceProperties of tumorsPresentation machineryCellular 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
Academic Achievements & Community Involvement
News & Links
News
- January 18, 2023
Resistance to immune checkpoint inhibitors in NSCLC
- December 01, 2022Source: Bioanalysis Zone
COVID-19 variants and cell and gene therapies – panel discussion
- November 28, 2022Source: VuMedi
SITC 2022: TAP2 Deficiency Mediates Adaptive Immune Evasion and Immunotherapy Resistance in Human NSCLC
- November 10, 2022
Non–Small Cell Lung Cancer: New Findings on a Biomarker and Immunotherapy Resistance
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