about
Fas-mediated neutrophil apoptosis is accelerated by Bid, Bak, and Bax and inhibited by Bcl-2 and Mcl-1Bcl-xL-inhibitory BH3 mimetics can induce a transient thrombocytopathy that undermines the hemostatic function of platelets.Megakaryocytes possess a functional intrinsic apoptosis pathway that must be restrained to survive and produce platelets.Caspase-9 mediates the apoptotic death of megakaryocytes and platelets, but is dispensable for their generation and function.Platelet production proceeds independently of the intrinsic and extrinsic apoptosis pathways.Effect of thrombopoietin receptor agonists on the apoptotic profile of platelets in patients with chronic immune thrombocytopenia.Individual and overlapping roles of BH3-only proteins Bim and Bad in apoptosis of lymphocytes and platelets and in suppression of thymic lymphoma developmentMitochondrial apoptosis is dispensable for NLRP3 inflammasome activation but non-apoptotic caspase-8 is required for inflammasome primingApoptotic caspases suppress mtDNA-induced STING-mediated type I IFN production.Apoptotic processes in megakaryocytes and platelets.Two distinct pathways regulate platelet phosphatidylserine exposure and procoagulant function.Stressed mitochondria sound the alarm.Mcl-1 and Bcl-xL coordinately regulate megakaryocyte survivalPlatelet Life Span and Apoptosis
P50
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P50
description
medical biologist
@en
wetenschapper
@nl
հետազոտող
@hy
name
Michael J White
@ast
Michael J White
@nl
Michael J White
@sl
Michael J. White
@en
Michael J. White
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type
label
Michael J White
@ast
Michael J White
@nl
Michael J White
@sl
Michael J. White
@en
Michael J. White
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prefLabel
Michael J White
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Michael J White
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Michael J White
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Michael J. White
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Michael J. White
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P1053
K-1824-2013
P106
P2038
Michael_White18
P21
P31
P3829
P496
0000-0001-9472-7806