2025
Transcriptional adaptation after deletion of Cdc42 in primary T cells
Rochussen A, Y. C, Griffiths G. Transcriptional adaptation after deletion of Cdc42 in primary T cells. Journal Of Cell Science 2025, 138: jcs263826. PMID: 40613419, PMCID: PMC12377712, DOI: 10.1242/jcs.263826.Peer-Reviewed Original ResearchTranscriptional adaptationRho family GTPasesPrimary T cellsNonsense-mediated decay mechanismWild-type cellsInhibition of Cdc42Deletion of Cdc42Study protein functionCRISPR-mediated deletionFamily GTPasesRho GTPasesEssential genesCytotoxic T lymphocytesCytoskeletal regulationGenetic compensationPolarised secretionCdc42 deletionProtein functionCdc42 proteinCdc42Cell polarityPromoter regionTranscriptional changesGene deletionChemical inhibition
2024
SH2 domain protein E and ABL signaling regulate blood vessel size
Schumacher J, Wright Z, Florat D, Anand S, Dasyani M, Batta S, Laverde V, Ferrari K, Klimkaite L, Bredemeier N, Gurung S, Koller G, Aguera K, Chadwick G, Johnson R, Davis G, Sumanas S. SH2 domain protein E and ABL signaling regulate blood vessel size. PLOS Genetics 2024, 20: e1010851. PMID: 38190417, PMCID: PMC10798624, DOI: 10.1371/journal.pgen.1010851.Peer-Reviewed Original ResearchZebrafish embryosDorsal aortaSrc homology 2 domainMutant phenotypeVascular tubulogenesisCell numberNegative regulatorBiological roleMolecular mechanismsProtein EChemical inhibitionUmbilical vein cellsE proteinEndothelial cell proliferationHuman endothelial cell culturesCell proliferationVein cellsProteinMutantsVascular tubesSpecific overexpressionTubulogenesisEndothelial cell culturesTight junctionsABL
2023
BRD4‐PRC2 represses transcription of T‐helper 2‐specific negative regulators during T‐cell differentiation
Zhao L, Wang Y, Jaganathan A, Sun Y, Ma N, Li N, Han X, Sun X, Yi H, Fu S, Han F, Li X, Xiao K, Walsh M, Zeng L, Zhou M, Cheung K. BRD4‐PRC2 represses transcription of T‐helper 2‐specific negative regulators during T‐cell differentiation. The EMBO Journal 2023, 42: embj2022111473. PMID: 36719036, PMCID: PMC10015369, DOI: 10.15252/embj.2022111473.Peer-Reviewed Original ResearchConceptsPolycomb repressive complex 2Cell lineage differentiationTranscriptional repressionPolycomb repressive complex 2 complexHistone H3 lysine 27 trimethylationH3 lysine 27 trimethylationTranscriptional de-repressionTarget gene lociCell type-specific mannerGene transcriptional repressionLysine 27 trimethylationLineage differentiationGene repressionTranscription factor GATA3Gene locusTranscriptional activityTranscriptional programsNegative regulatorLineage-specific differentiationTranscriptional downregulationProtein degradationChemical inhibitionTranscript expressionBrd4's roleBRD4
2022
KCNJ8/ABCC9-containing K-ATP channel modulates brain vascular smooth muscle development and neurovascular coupling
Ando K, Tong L, Peng D, Vázquez-Liébanas E, Chiyoda H, He L, Liu J, Kawakami K, Mochizuki N, Fukuhara S, Grutzendler J, Betsholtz C. KCNJ8/ABCC9-containing K-ATP channel modulates brain vascular smooth muscle development and neurovascular coupling. Developmental Cell 2022, 57: 1383-1399.e7. PMID: 35588738, DOI: 10.1016/j.devcel.2022.04.019.Peer-Reviewed Original ResearchConceptsK-ATP channel functionVascular smooth muscle cell differentiationChannel functionSmooth muscle cell differentiationMuscle cell differentiationVascular smooth muscle developmentSmooth muscle developmentVSMC developmentHuman central nervous system disordersMuscle developmentVSMC differentiationCentral nervous system disordersCell differentiationChemical inhibitionVoltage-dependent calcium channelsATP-sensitive potassium channelsFunction mutationsCell progenitorsK-ATP channelsCerebral blood flowCell culture modelMolecular causesNervous system disordersIntracellular CaVasoconstrictive capacity
2021
Inhibition of histone acetyltransferase function radiosensitizes CREBBP/EP300 mutants via repression of homologous recombination, potentially targeting a gain of function
Kumar M, Molkentine D, Molkentine J, Bridges K, Xie T, Yang L, Hefner A, Gao M, Bahri R, Dhawan A, Frederick MJ, Seth S, Abdelhakiem M, Beadle BM, Johnson F, Wang J, Shen L, Heffernan T, Sheth A, Ferris RL, Myers JN, Pickering CR, Skinner HD. Inhibition of histone acetyltransferase function radiosensitizes CREBBP/EP300 mutants via repression of homologous recombination, potentially targeting a gain of function. Nature Communications 2021, 12: 6340. PMID: 34732714, PMCID: PMC8566594, DOI: 10.1038/s41467-021-26570-8.Peer-Reviewed Original ResearchMeSH KeywordsAcetylationAnimalsApoptosisBiomarkers, TumorBRCA1 ProteinCell Line, TumorCREB-Binding ProteinE1A-Associated p300 ProteinGain of Function MutationHistone AcetyltransferasesHomologous RecombinationHumansMaleMice, NudeMutationNeoplasmsProtein DomainsSquamous Cell Carcinoma of Head and NeckXenograft Model Antitumor Assays
2019
A Unique SUMO-Interacting Motif of Trx2 Is Critical for Its Mitochondrial Presequence Processing and Anti-oxidant Activity
Chen C, Wang K, Zhang H, Zhou HJ, Chen Y, Min W. A Unique SUMO-Interacting Motif of Trx2 Is Critical for Its Mitochondrial Presequence Processing and Anti-oxidant Activity. Frontiers In Physiology 2019, 10: 1089. PMID: 31555141, PMCID: PMC6727865, DOI: 10.3389/fphys.2019.01089.Peer-Reviewed Original ResearchSUMO-interacting motifMitochondrial processing peptidaseReactive oxygen speciesMitochondrial intermediate peptidaseStress-induced cellular senescenceOxidative stress-induced cellular senescenceMitochondrial redox proteinsMitochondrial thioredoxin 2Excess reactive oxygen speciesMitochondrial processingPresequence processingProcessing peptidaseTrx2 proteinMitochondrial targetingMassive reactive oxygen speciesAntisenescence activityCellular senescenceThioredoxin 2Chemical inhibitionMature formRedox proteinsUnprocessed formProteinTrx2Catalytic siteInterferon‐regulated suprabasin is essential for stress‐induced stem‐like cell conversion and therapy resistance of human malignancies
Hubackova S, Pribyl M, Kyjacova L, Moudra A, Dzijak R, Salovska B, Strnad H, Tambor V, Imrichova T, Svec J, Vodicka P, Vaclavikova R, Rob L, Bartek J, Hodny Z. Interferon‐regulated suprabasin is essential for stress‐induced stem‐like cell conversion and therapy resistance of human malignancies. Molecular Oncology 2019, 13: 1467-1489. PMID: 30919591, PMCID: PMC6599850, DOI: 10.1002/1878-0261.12480.Peer-Reviewed Original ResearchConceptsMitogen-activated protein kinase/ERK kinaseSiRNA-mediated knockdownSBSN expressionERK pathwayProtein kinase/ERK kinaseHundreds of genesExtracellular signal-regulated kinase 1/2Signal-regulated kinase 1/2MEK/ERK pathwayCancer cellsPhenotypic plasticityTranscript profilesStress resistanceTherapy resistanceERK kinaseStem-like cellsActive NotchStem cell markersMolecular mechanismsAnoikis resistanceKinase 1/2Cancer evolutionChemical inhibitionCancer cell linesHuman clinical specimens
2016
Inhibiting poly(ADP-ribosylation) improves axon regeneration
Byrne AB, McWhirter RD, Sekine Y, Strittmatter SM, Miller DM, Hammarlund M. Inhibiting poly(ADP-ribosylation) improves axon regeneration. ELife 2016, 5: e12734. PMID: 27697151, PMCID: PMC5050021, DOI: 10.7554/elife.12734.Peer-Reviewed Original ResearchConceptsNovel intrinsic regulatorAxon regenerationDLK functionChemical inhibitionIntrinsic regulatorRegeneration pathwayPARG expressionIntrinsic regenerative potentialDLK signalingCritical functionsPARGRegenerative potentialPARP inhibitorsProteinPARPMammalian cortical neuronsRegenerationMotor neuronsGABA neuronsPolymeraseCortical neuronsSignalingRegulatorSpeciesNeurons
2015
Chemical inhibition of DNA repair kinases as a promising tool in oncology
Durisova K, Salovska B, Pejchal J, Tichy A. Chemical inhibition of DNA repair kinases as a promising tool in oncology. Biomedical Papers 2015, 160: 11-19. PMID: 26498210, DOI: 10.5507/bp.2015.046.Peer-Reviewed Original ResearchConceptsDNA-dependent protein kinaseDNA repair pathwaysRepair pathwaysDNA repairSpecific DNA repair pathwaysKey DNA repairDNA-damaging agentsSmall molecule inhibitorsATM-Rad3Protein kinaseAtaxia telangiectasiaChemical inhibitionKinaseMolecule inhibitorsSpecific inhibitorPathwayPotent inhibitorInhibitorsRecent studiesTumor resistanceTumor cellsMajor roleRadiotherapy efficiencyRepairCells
2014
N-Glycosylation Determines the Abundance of the Transient Receptor Potential Channel TRPP2*
Hofherr A, Wagner C, Fedeles S, Somlo S, Köttgen M. N-Glycosylation Determines the Abundance of the Transient Receptor Potential Channel TRPP2*. Journal Of Biological Chemistry 2014, 289: 14854-14867. PMID: 24719335, PMCID: PMC4031537, DOI: 10.1074/jbc.m114.562264.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAsparagineBinding SitesBlotting, WesternCell LineCells, CulturedGlucosidasesGlycosylationHEK293 CellsHeLa CellsHumansIntracellular Signaling Peptides and ProteinsLysosomesMass SpectrometryMiceMice, KnockoutMicroscopy, FluorescenceMutationPolycystic Kidney, Autosomal DominantProtein Serine-Threonine KinasesProteolysisPyruvate Dehydrogenase Acetyl-Transferring KinaseConceptsGlucosidase IINon-catalytic β-subunitsProtein expressionFirst extracellular loopAutosomal dominant polycystic liver diseaseEfficient biogenesisGenetic interactionsMembrane proteinsBiochemical approachesN-glycosylationGenetic approachesTRPP2Glycosylation sitesBiological roleLysosomal degradationΒ-subunitChemical inhibitionBiogenesisExtracellular loopNonselective cation channelsIon channelsBiological importanceGlycosylationCation channelsProtein levels
2013
Phosphatidylcholine Transfer Protein Interacts with Thioesterase Superfamily Member 2 to Attenuate Insulin Signaling
Ersoy B, Tarun A, D’Aquino K, Hancer N, Ukomadu C, White M, Michel T, Manning B, Cohen D. Phosphatidylcholine Transfer Protein Interacts with Thioesterase Superfamily Member 2 to Attenuate Insulin Signaling. Science Signaling 2013, 6: ra64. PMID: 23901139, PMCID: PMC3959124, DOI: 10.1126/scisignal.2004111.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsGlucoseHEK293 CellsHomeostasisHumansInhibitory Concentration 50InsulinLiverMechanistic Target of Rapamycin Complex 1MiceMice, TransgenicMultiprotein ComplexesPhospholipid Transfer ProteinsPhosphorylationSignal TransductionThiolester HydrolasesTOR Serine-Threonine KinasesTuberous Sclerosis Complex 2 ProteinTumor Suppressor ProteinsConceptsThioesterase superfamily member 2Insulin receptor substrate 2Phosphatidylcholine transfer proteinTSC1-TSC2 complexGenetic ablationRapamycin complex 1Transfer proteinSteady-state amountsMember 2Hepatic glucose homeostasisPhospholipid-binding proteinProtein exhibitInsulin signalingChemical inhibitionKey effectorsSubstrate 2Mammalian targetDiet-induced diabetesProteinTSC2KnockdownGlucose homeostasisPhospholipid-dependent mechanismsActivationComplexes 1
2012
Ucp2 Induced by Natural Birth Regulates Neuronal Differentiation of the Hippocampus and Related Adult Behavior
Simon-Areces J, Dietrich MO, Hermes G, Garcia-Segura LM, Arevalo MA, Horvath TL. Ucp2 Induced by Natural Birth Regulates Neuronal Differentiation of the Hippocampus and Related Adult Behavior. PLOS ONE 2012, 7: e42911. PMID: 22905184, PMCID: PMC3414493, DOI: 10.1371/journal.pone.0042911.Peer-Reviewed Original ResearchConceptsUCP2 expressionCellular stressHippocampal neuronsChemical inhibitionMitochondrial bioenergeticsNeuronal differentiationGenetic ablationNatural birthProtein 2Adult behaviorCell proliferationCritical roleAdult brainNeuronal numberExpressionBioenergeticsNeuronsBirthDifferentiationRegulationProliferationSynaptogenesisVitroNeuroprotectionHippocampusP190B RhoGAP Regulates Chromosome Segregation in Cancer Cells
Hwang M, Peddibhotla S, McHenry P, Chang P, Yochum Z, Park K, Sears J, Vargo-Gogola T. P190B RhoGAP Regulates Chromosome Segregation in Cancer Cells. Cancers 2012, 4: 475-489. PMID: 22582143, PMCID: PMC3348653, DOI: 10.3390/cancers4020475.Peer-Reviewed Original ResearchChromosome segregationMicrotubule-kinetochore attachmentsDisruption of mitosisRegulator of mitosisDeficient MCF-7 cellsP190B Rho GTPaseCancer cellsMitotic defectsRho proteinsRho GTPasesRac GTPaseRho GTPaseRac activityKnockdown cellsCell cycle analysisDeficient cellsChemical inhibitionNovel roleMitosisP190BS transitionS phaseHeLa cellsAltered expressionMCF-7 cells
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