M. Wei

发表

Pro-apoptotic cascade activates BID, which oligomerizes BAK or BAX into pores that result in the release of cytochrome c

S. Korsmeyer, M. Wei, M. Saito, 2000, Cell Death and Differentiation.

BCL-2, BCL-X(L) sequester BH3 domain-only molecules preventing BAX- and BAK-mediated mitochondrial apoptosis.

S. Korsmeyer, T. Mak, E. Cheng, 2001, Molecular cell.

A reversible component of mitochondrial respiratory dysfunction in apoptosis can be rescued by exogenous cytochrome c

V. Mootha, S. Korsmeyer, C. Mannella, 2001, The EMBO journal.

Proapoptotic BAX and BAK: A Requisite Gateway to Mitochondrial Dysfunction and Death

S. Korsmeyer, E. Cheng, W. Zong, 2001, Science.

The combined functions of proapoptotic Bcl-2 family members bak and bax are essential for normal development of multiple tissues.

S. Korsmeyer, J. Golden, G. Evan, 2000, Molecular cell.

tBID, a membrane-targeted death ligand, oligomerizes BAK to release cytochrome c.

V. Mootha, S. Korsmeyer, M. Ashiya, 2000, Genes & development.

Enforced dimerization of BAX results in its translocation, mitochondrial dysfunction and apoptosis

S. Korsmeyer, M. Wei, J. Jockel, 1998, The EMBO journal.

Caspase Cleaved BID Targets Mitochondria and Is Required for Cytochrome c Release, while BCL-XL Prevents This Release but Not Tumor Necrosis Factor-R1/Fas Death*

S. Korsmeyer, H. Erdjument-Bromage, P. Tempst, 1999, The Journal of Biological Chemistry.

Death and survival signals determine active/inactive conformations of pro-apoptotic BAX, BAD, and BID molecules.

S. Korsmeyer, J. Zha, M. Wei, 1999, Cold Spring Harbor symposia on quantitative biology.

Rapid Detection of an ABT-737-Sensitive Primed for Death State in Cells Using Microplate-Based Respirometry

M. Wei, Stuart S. Martin, Hegang Chen, 2012, PloS one.

Posttranslational N-myristoylation of BID as a molecular switch for targeting mitochondria and apoptosis.

S. Korsmeyer, J. Zha, M. Wei, 2000, Science.