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Elizabeth Yang

Researcher at Children's National Medical Center

Publications -  44
Citations -  12940

Elizabeth Yang is an academic researcher from Children's National Medical Center. The author has contributed to research in topics: Cell cycle & Apoptosis. The author has an hindex of 23, co-authored 42 publications receiving 11862 citations. Previous affiliations of Elizabeth Yang include Washington University in St. Louis & Vanderbilt University.

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Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy

Daniel J. Klionsky, +1287 more
- 01 Apr 2012 - 
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Serine Phosphorylation of Death Agonist BAD in Response to Survival Factor Results in Binding to 14-3-3 Not BCL-XL

Jiping Zha, +4 more
- 15 Nov 1996 - 
TL;DR: The rapid phosphorylation of BAD following IL-3 connects a proximal survival signal with the BCL-2 family, modulating this checkpoint for apoptosis and enhanced BAD's death-promoting activity.
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Bad, a heterodimeric partner for Bcl-xL and Bcl-2, displaces bax and promotes cell death

Elizabeth Yang, +5 more
- 27 Jan 1995 - 
TL;DR: A novel interacting protein, Bad, whose homology to Bcl-2 is limited to the BH1 and BH2 domains is identified, whose role in the mammalian cell death pathway is determined by these competing dimerizations in which levels of Bad influence the effectiveness of BCl-2 versus B cl-xL in repressing death.
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Molecular thanatopsis: a discourse on the BCL2 family and cell death

Elizabeth Yang, +1 more
- 15 Jul 1996 - 
TL;DR: The author’s website is www.hematologylibrary.org, which can be found online at http://bloodjournal.org/site/misc/rights.xhtml.
Journal ArticleDOI

Multiple Bcl-2 family members demonstrate selective dimerizations with Bax

Thomas W. Sedlak, +6 more
- 15 Aug 1995 - 
TL;DR: The susceptibility to apoptosis is determined by multiple competing dimerizations in which Bax may be a common partner, and a Gly-159-->Ala substitution in BH1 of Bcl-xL disrupted its heterodimerization with Bax and abrogated its inhibition of apoptosis in mammalian cells.