2019
BOK promotes erythropoiesis in a mouse model of myelodysplastic syndrome
Kang SH, Perales O, Michaud M, Katz SG. BOK promotes erythropoiesis in a mouse model of myelodysplastic syndrome. Annals Of Hematology 2019, 98: 2089-2096. PMID: 31203423, PMCID: PMC6702064, DOI: 10.1007/s00277-019-03726-7.Peer-Reviewed Original ResearchConceptsUnfolded protein responseER stressPro-apoptotic membersBcl-2 familyNHD13 miceRT-qPCR analysisInduction of apoptosisProgenitor stem cellsHematopoietic progenitor cell assaysProtein responseDownstream effectorsGene knockoutMyelodysplastic syndromeCell stressProgenitor cell assaysEndoplasmic reticulumLower mean cell hemoglobin concentrationErythroid progenitorsNUP98-HOXD13 transgenic miceClonal hematopoietic stem cell disordersStem cellsSimilar overall survivalAcute myeloid leukemiaHematopoietic stem cell disordersMean cell hemoglobin concentrationMinocycline mitigates the effect of neonatal hypoxic insult on human brain organoids
Boisvert EM, Means RE, Michaud M, Madri JA, Katz SG. Minocycline mitigates the effect of neonatal hypoxic insult on human brain organoids. Cell Death & Disease 2019, 10: 325. PMID: 30975982, PMCID: PMC6459920, DOI: 10.1038/s41419-019-1553-x.Peer-Reviewed Original ResearchMeSH KeywordsBrainCell DeathHuman Embryonic Stem CellsHumansHypoxia, BrainHypoxia-Ischemia, BrainMinocyclineNeuronsOrganoidsProto-Oncogene Proteins c-bcl-2SOXB1 Transcription FactorsTime FactorsConceptsNeonatal hypoxic injuryBrain developmentEfficacy of minocyclineLow birth weightUse of minocyclineEffects of hypoxiaNormal brain developmentCerebral organoid modelHuman brain organoidsLater time pointsAnimal model systemsNeonatal hypoxicDevastating causeCerebral palsySignificant morbidityHuman brain developmentNeurological consequencesBirth weightHypoxic injuryNeuronal deathCortical neuronsInjury resultsGlial cellsForebrain markersPotential treatment
2018
Methods to Probe Calcium Regulation by BCL-2 Family Members
Carpio MA, Katz SG. Methods to Probe Calcium Regulation by BCL-2 Family Members. Methods In Molecular Biology 2018, 1877: 173-183. PMID: 30536006, DOI: 10.1007/978-1-4939-8861-7_12.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisBiological TransportCalciumCytosolEndoplasmic ReticulumHumansMitochondriaMitochondrial MembranesPermeabilityProto-Oncogene Proteins c-bcl-2ConceptsMitochondrial outer membrane permeabilizationBcl-2 family membersEndoplasmic reticulumOuter membrane permeabilizationProcess of apoptosisSuch important functionsMembrane permeabilizationDirect regulationFamily membersAdditional roleImportant functionsCalcium regulationApoptosisRegulationRelease of calciumMitochondriaPermeabilizationBiologyCytosolMembersReticulum
2017
Non-apoptotic functions of BCL-2 family proteins
Gross A, Katz SG. Non-apoptotic functions of BCL-2 family proteins. Cell Death & Differentiation 2017, 24: 1348-1358. PMID: 28234359, PMCID: PMC5520452, DOI: 10.1038/cdd.2017.22.Peer-Reviewed Original ResearchConceptsNon-apoptotic rolesBcl-2 family proteinsFamily proteinsApoptotic roleNon-apoptotic functionsWhole-cell metabolismCellular survival pathwaysMitochondrial physiologyCellular survivalSurvival pathwaysMajor regulatorNuclear processesApoptosis processProteinMechanism of actionPhysiologyImportant cluesRoleAutophagyRegulatorFascinating fieldRegulationPathwayMechanismMetabolism
2015
BCL-2 family member BOK promotes apoptosis in response to endoplasmic reticulum stress
Carpio MA, Michaud M, Zhou W, Fisher JK, Walensky LD, Katz SG. BCL-2 family member BOK promotes apoptosis in response to endoplasmic reticulum stress. Proceedings Of The National Academy Of Sciences Of The United States Of America 2015, 112: 7201-7206. PMID: 26015568, PMCID: PMC4466744, DOI: 10.1073/pnas.1421063112.Peer-Reviewed Original ResearchConceptsB-cell lymphoma 2 ovarian killerApoptotic defectsMultidomain proapoptotic proteins BaxApoptotic responseStress stimuliER stressBcl-2 family proteinsER stress agentsUnfolded protein responseMouse embryonic fibroblastsDefective apoptotic responseMitochondrial apoptotic pathwayProapoptotic protein BaxPredominant subcellular localizationThapsigargin-induced apoptosisEndoplasmic reticulum stressFamily proteinsDeath responseSubcellular localizationEmbryonic fibroblastsHigh homologyProtein responseApoptotic pathwayOvert phenotypeProtein Bax