2024
A TRilogy of ATR’s Non-Canonical Roles Throughout the Cell Cycle and Its Relation to Cancer
Joo Y, Ramirez C, Kabeche L. A TRilogy of ATR’s Non-Canonical Roles Throughout the Cell Cycle and Its Relation to Cancer. Cancers 2024, 16: 3536. PMID: 39456630, PMCID: PMC11506335, DOI: 10.3390/cancers16203536.Peer-Reviewed Original ResearchDNA damage responseNon-canonical rolesCell cyclePromote faithful chromosome segregationDetect mechanical forcesDNA damage response pathwayFaithful chromosome segregationDNA damage checkpointRad3-related proteinNuclear membrane integrityCancer therapy targetATR inhibitorsChromosome segregationDamage checkpointDamage responseApical kinaseDamaged DNAMembrane integrityAtaxia telangiectasiaNon-canonicalCancer cellsDNAClinical trialsCancer therapyClinical relevance
2023
ATR protects centromere identity by promoting DAXX association with PML nuclear bodies
Trier I, Black E, Joo Y, Kabeche L. ATR protects centromere identity by promoting DAXX association with PML nuclear bodies. Cell Reports 2023, 42: 112495. PMID: 37163376, DOI: 10.1016/j.celrep.2023.112495.Peer-Reviewed Original ResearchConceptsCentromere identityInterphase centromeresNuclear bodiesDNA damage-independent mannerPromyelocytic leukemia nuclear bodiesMitotic chromosome segregationCentromere protein AATR inhibitionDNA damage responsePML nuclear bodiesATR-dependent phosphorylationAcute ATR inhibitionChaperone DAXXGenome stabilityChromosome segregationPML-NBsDamage responseUnperturbed cellsMaster regulatorAtaxia telangiectasiaC-terminusFormation defectsCentromeresCENPAberrant increase
2017
A mitosis-specific and R loop–driven ATR pathway promotes faithful chromosome segregation
Kabeche L, Nguyen HD, Buisson R, Zou L. A mitosis-specific and R loop–driven ATR pathway promotes faithful chromosome segregation. Science 2017, 359: 108-114. PMID: 29170278, PMCID: PMC5875943, DOI: 10.1126/science.aan6490.Peer-Reviewed Original ResearchConceptsFaithful chromosome segregationChromosome segregationR-loopsATR pathwayCyclin-dependent kinase 1 (CDK1) activityWhole chromosome missegregationReplication stress responseReplication protein ADNA damage responseCentromere protein FKinase 1 activityATR functionAurora BDamage responseChromosome instabilityCentromeresProtein FAtaxia telangiectasiaAurora AUnexpected roleStress responseDNA damageDNA synthesisATRProtein A
2014
DNA-Damage Response during Mitosis Induces Whole-Chromosome Missegregation
Bakhoum SF, Kabeche L, Murnane JP, Zaki BI, Compton DA. DNA-Damage Response during Mitosis Induces Whole-Chromosome Missegregation. Cancer Discovery 2014, 4: 1281-1289. PMID: 25107667, PMCID: PMC4221427, DOI: 10.1158/2159-8290.cd-14-0403.Peer-Reviewed Original ResearchConceptsDNA damage responseNumerical chromosomal instabilityDNA damageChromosome segregationChromosomal instabilityWhole chromosomal instabilityChromosome segregation defectsDefective chromosome segregationWhole chromosome missegregationChromosome segregation errorsPersistent DNA damageS-CINW-CINSegregation defectsMicrotubule attachmentDDR proteinsEntire chromosomesPlk1 kinaseCell divisionSegregation errorsMitotic processesChromosomesMitosisStructural rearrangementsCancer cells
2012
Cdk1 and Plk1 mediate a CLASP2 phospho-switch that stabilizes kinetochore–microtubule attachments
Maia AR, Garcia Z, Kabeche L, Barisic M, Maffini S, Macedo-Ribeiro S, Cheeseman IM, Compton DA, Kaverina I, Maiato H. Cdk1 and Plk1 mediate a CLASP2 phospho-switch that stabilizes kinetochore–microtubule attachments. Journal Of Cell Biology 2012, 199: 285-301. PMID: 23045552, PMCID: PMC3471233, DOI: 10.1083/jcb.201203091.Peer-Reviewed Original ResearchConceptsSpindle assembly checkpointKT-MT attachmentsChromosome alignmentAccurate chromosome segregationC-terminal phosphorylationKinetochore-microtubule attachmentsUnderlying regulatory mechanismsPlk1 recruitmentMitosis reliesChromosome segregationChromosome movementMT attachmentPlk1 kinaseSpindle bipolarityMicrotubule interfaceMT dynamicsRegulatory mechanismsCLASP2Plk1CDK1PhosphorylationAttachment stabilityKinetochoresMitosisKinase