2024
The CUL5 E3 ligase complex negatively regulates central signaling pathways in CD8+ T cells
Liao X, Li W, Zhou H, Rajendran B, Li A, Ren J, Luan Y, Calderwood D, Turk B, Tang W, Liu Y, Wu D. The CUL5 E3 ligase complex negatively regulates central signaling pathways in CD8+ T cells. Nature Communications 2024, 15: 603. PMID: 38242867, PMCID: PMC10798966, DOI: 10.1038/s41467-024-44885-0.Peer-Reviewed Original ResearchConceptsCD8+ T cellsT cellsCancer immunotherapyMouse CD8+ T cellsAnti-tumor immunityTumor growth inhibition abilityAnti-tumor effectsInhibition of neddylationCD8Effector functionsTCR stimulationIL2 signalingCentral signaling pathwaysCore signaling pathwaysEffector activityNegative regulatory mechanismsTranslational implicationsImmunotherapyGrowth inhibition abilityCytokine signalingTCRProteomic alterationsSignaling pathwayCancerCRISPR-based screens
2023
Role of homeobox d10 gene targeted signaling pathways in cancers
Surendran H, Palaniyandi T, Natarajan S, Hari R, Viwanathan S, Baskar G, Abdul Wahab M, Ravi M, Rajendran B. Role of homeobox d10 gene targeted signaling pathways in cancers. Pathology - Research And Practice 2023, 248: 154643. PMID: 37406379, DOI: 10.1016/j.prp.2023.154643.Peer-Reviewed Original ResearchMeSH KeywordsGenes, HomeoboxHomeodomain ProteinsHumansMaleSignal TransductionStomach NeoplasmsTranscription FactorsConceptsTranscription factorsHomeobox gene familyHomeotic transcription factorsGene expression changesTumor suppressor geneD10 geneGene familyHomeobox genesCancer signalingOrgan developmentTissue homeostasisGene expressionExpression changesSignaling pathwaysCell differentiationSuppressor geneFunctional interactionGenesHOXD10 geneCancer treatment targetHOXD10Pathway dysregulationTherapeutic resistancePathwayMolecule actionInsights 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 ResearchMeSH KeywordsAnimalsBiological TransportCaveolaeCell MembraneEndocytosisHumansMammalsSignal TransductionConceptsEndocytic 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 diseasesEndocytosis
2020
NOTCH1 activation compensates BRCA1 deficiency and promotes triple-negative breast cancer formation
Miao K, Lei J, Valecha M, Zhang A, Xu J, Wang L, Lyu X, Chen S, Miao Z, Zhang X, Su S, Shao F, Rajendran B, Bao J, Zeng J, Sun H, Chen P, Tan K, Chen Q, Wong K, Xu X, Deng C. NOTCH1 activation compensates BRCA1 deficiency and promotes triple-negative breast cancer formation. Nature Communications 2020, 11: 3256. PMID: 32591500, PMCID: PMC7320176, DOI: 10.1038/s41467-020-16936-9.Peer-Reviewed Original ResearchMeSH KeywordsAllelesAnimalsAtaxia Telangiectasia Mutated ProteinsBRCA1 ProteinCarcinogenesisCell DeathCell Line, TumorCheckpoint Kinase 1Disease ProgressionDNA Transposable ElementsEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansMice, KnockoutMitosisMutationReceptor, Notch1Signal TransductionTriple Negative Breast NeoplasmsConceptsTriple-negative breast cancerEpithelial-mesenchymal transitionHuman breast cancer tissuesBRCA1 mutation carriersBreast cancer tissuesBRCA1-deficient miceActivation of Notch1Breast cancer formationRefractory diseaseForm of Notch1Breast cancerMutation carriersHigh riskCancer tissuesClinical optionG2/M cell cycle checkpointFatal diseaseCell cycle checkpointsM cell cycle checkpointNotch1 activationBRCA1 deficiencyPhosphorylation of ATRNotch1Cancer formationCycle checkpoints