M
Michael C. Wei
Researcher at Genentech
Publications - 61
Citations - 13643
Michael C. Wei is an academic researcher from Genentech. The author has contributed to research in topics: Medicine & Internal medicine. The author has an hindex of 20, co-authored 40 publications receiving 12967 citations. Previous affiliations of Michael C. Wei include Boston University & Washington University in St. Louis.
Papers
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Journal ArticleDOI
Proapoptotic BAX and BAK: A Requisite Gateway to Mitochondrial Dysfunction and Death
Michael C. Wei,Michael C. Wei,Wei-Xing Zong,Emily H. Cheng,Tullia Lindsten,Vily Panoutsakopoulou,Andrea J. Ross,Kevin A. Roth,Grant R. MacGregor,Craig B. Thompson,Stanley J. Korsmeyer +10 more
TL;DR: In this article, the authors found that doubly deficient cells are resistant to multiple apoptotic stimuli that act through disruption of mitochondrial function: staurosporine, ultraviolet radiation, growth factor deprivation, etoposide, and the endoplasmic reticulum stress stimuli thapsigargin and tunicamycin.
Journal ArticleDOI
BCL-2, BCL-XL Sequester BH3 Domain-Only Molecules Preventing BAX- and BAK-Mediated Mitochondrial Apoptosis
Emily H. Cheng,Michael C. Wei,Solly Weiler,Richard A. Flavell,Tak W. Mak,Tullia Lindsten,Stanley J. Korsmeyer +6 more
TL;DR: In mammals, BH3 domain-only molecules activate multidomain proapoptotic members to trigger a mitochondrial pathway, which both releases cytochrome c to activate caspases and initiates caspase-independent mitochondrial dysfunction.
Journal ArticleDOI
The combined functions of proapoptotic Bcl-2 family members bak and bax are essential for normal development of multiple tissues.
Tullia Lindsten,Andrea J. Ross,Ayala King,Wei-Xing Zong,Jeffrey C. Rathmell,Helena Shiels,Eugen Ulrich,Katrina G. Waymire,Patryce L. Mahar,Kenneth A. Frauwirth,Yifeng Chen,Michael C. Wei,Vicki M. Eng,David M. Adelman,M. Celeste Simon,Averil Ma,Jeffrey A. Golden,Gerard I. Evan,Stanley J. Korsmeyer,Grant R. MacGregor,Craig B. Thompson +20 more
TL;DR: Bax and Bak have overlapping roles in the regulation of apoptosis during mammalian development and tissue homeostasis and are found to be developmentally normal and reproductively fit.
Journal ArticleDOI
tBID, a membrane-targeted death ligand, oligomerizes BAK to release cytochrome c
Michael C. Wei,Tullia Lindsten,Vamsi K. Mootha,Solly Weiler,Atan Gross,Mona Ashiya,Craig B. Thompson,Stanley J. Korsmeyer +7 more
TL;DR: It is demonstrated that tBID functions as a membrane-targeted death ligand in which an intact BH3 domain is required for cytochrome c release, but not for targeting.
Journal ArticleDOI
Enforced dimerization of BAX results in its translocation, mitochondrial dysfunction and apoptosis.
TL;DR: It is demonstrated that a physiologic death stimulus, the withdrawal of interleukin‐3 (IL‐3), resulted in the translocation of monomeric BAX from the cytosol to the mitochondria where it could be cross‐linked as a BAX homodimer and enforced dimerization of BAX overrode the protection by BCL‐XL and IL‐3 to kill cells.