S
Stanley J. Korsmeyer
Researcher at Harvard University
Publications - 316
Citations - 116613
Stanley J. Korsmeyer is an academic researcher from Harvard University. The author has contributed to research in topics: Apoptosis & Programmed cell death. The author has an hindex of 151, co-authored 316 publications receiving 113691 citations. Previous affiliations of Stanley J. Korsmeyer include University of Vienna & Washington University in St. Louis.
Papers
More filters
Journal ArticleDOI
Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programed cell death
TL;DR: Overexpressed Bax accelerates apoptotic death induced by cytokine deprivation in an IL-3-dependent cell line and counters the death repressor activity of B cl-2, suggesting a model in which the ratio of Bcl-2 to Bax determines survival or death following an apoptotic stimulus.
Journal ArticleDOI
Cell Death: Critical Control Points
TL;DR: The identification of critical control points in the cell death pathway has yielded fundamental insights for basic biology, as well as provided rational targets for new therapeutics.
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 is an inner mitochondrial membrane protein that blocks programmed cell death
TL;DR: It is demonstrated that Bcl-2 is an integral inner mitochondrial membrane protein of relative molecular mass 25,000 (25k) being localized to mitochondria and interfering with programmed cell death independent of promoting cell division.
Journal ArticleDOI
BCL-2 family members and the mitochondria in apoptosis
TL;DR: As the BCL-2 family members reside upstream of irreversible cellular damage and focus much of their efforts at the level of mitochondria, they play a pivotal role in deciding whether a cell will live or die, and it is argued that the amphipathic a-helical BH3 domain serves as a critical death domain in the pro-apoptotic members.