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 B, Deen I, Costantini A, de Rodas M, Desai S, Scallo F, Gianino N, Ferrone S, Schalper K. IL-4 mediated TAP2 downregulation is a dominant and reversible mechanism of immune evasion and immunotherapy resistance in non-small cell lung cancer. Molecular Cancer 2025, 24: 80. PMID: 40091029, PMCID: PMC11912681, DOI: 10.1186/s12943-025-02276-z.Peer-Reviewed Original ResearchThis study investigates IL-4's role in TAP2 downregulation as a reversible mechanism of immune evasion and resistance to immunotherapy in non-small cell lung cancer, highlighting potential therapeutic strategies to restore TAP2 expression and enhance treatment efficacy.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 ResearchActivating Transcription Factor 6AnimalsEndoplasmic Reticulum StressGenetic VariationHost Microbial InteractionsHumansImmunity, InnateInflammatory Bowel DiseasesMacrophagesMiceMice, Inbred C57BLMice, KnockoutNod2 Signaling Adaptor ProteinReceptors, Pattern RecognitionRisk FactorsSignal TransductionUbiquitin-Protein LigasesUbiquitinationUnfolded Protein ResponseThe 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 ResearchCytokinesHumansImmunity, InnateInflammatory Bowel DiseasesIntestinesMacrophagesMyeloid CellsNF-kappa BNod2 Signaling Adaptor ProteinPolymorphism, Single NucleotideReceptor-Interacting Protein Serine-Threonine Kinase 2Receptors, Pattern RecognitionToll-Like Receptor 2Toll-Like Receptor 4Ubiquitin-Protein LigasesUbiquitinationMyeloid 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 ResearchAnimalsCD4-Positive T-LymphocytesCells, CulturedCoculture TechniquesColitis, UlcerativeCytokinesDextran SulfateDisease Models, AnimalDNA-Binding ProteinsFemaleHost Microbial InteractionsHumansImmunity, MucosalIntestinal MucosaIntracellular Signaling Peptides and ProteinsMaleMiceMice, KnockoutMyeloid CellsPrimary Cell CultureSalmonella InfectionsSalmonella typhimuriumLACC1 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 ResearchActivating 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 TransductionFADD 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 ResearchA549 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-alphaUbiquitin-Protein LigasesUbiquitination
2026
NSCLC brain metastases exhibit reduced HLA-I antigen presentation machinery and immune evasion independent of IFNγ signaling defects
Vilariño N, de Rodas M, Villalba-Esparza M, Rajendran B, Huang B, Hijazo-Pechero S, Costantini A, Ranjan K, Ramos-Paradas J, Lu B, Nadal E, Goldberg S, Nguyen D, Schalper K. NSCLC brain metastases exhibit reduced HLA-I antigen presentation machinery and immune evasion independent of IFNγ signaling defects. Molecular Cancer 2026 PMID: 42210261, DOI: 10.1186/s12943-026-02687-6.Peer-Reviewed Original Research
2025
Molecular Perspective on Proteases: Regulation of Programmed Cell Death Signaling, Inflammation and Pathological Outcomes
Ansari A, Ranjan K, Kumar A, Pathak C. Molecular Perspective on Proteases: Regulation of Programmed Cell Death Signaling, Inflammation and Pathological Outcomes. Journal Of Molecular Pathology 2025, 6: 32. DOI: 10.3390/jmp6040032.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsTumor microenvironment of non-small cell lung cancer impairs immune cell function among people with HIV
Desai S, Salahuddin S, Yusuf R, Ranjan K, Gu J, Osmani L, Lin Y, Mehta S, Talmon R, Kang I, Kluger Y, Zhao H, Schalper K, Emu B. Tumor microenvironment of non-small cell lung cancer impairs immune cell function among people with HIV. Journal Of Clinical Investigation 2025, 135: e177310. PMID: 40459946, PMCID: PMC12259253, DOI: 10.1172/jci177310.Peer-Reviewed Original ResearchEmerging Concept of Receptor Endocytosis and Signaling
Kumar A, Panda A, Kumar S, Ranjan K. Emerging Concept of Receptor Endocytosis and Signaling. The Receptors 2025, 2: 61-84. DOI: 10.1007/978-3-031-81991-9_3.Chapters
Academic Achievements & Community Involvement
News & Links
News
- June 24, 2026
Award to Support Ranjan’s Research on Non-Small Cell Lung Cancer
- 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
Get In Touch
Contacts
Mailing Address
Department Faculty
BML113, 310 Cedar st
NEW HAVEN, CT 06519
United States
Locations
Brady Memorial Laboratory
Lab
310 Cedar St
New Haven, CT 06510
Business Office
203.785.7792