Michael Wei, MD, PhD

Publications

• Nontuberculous mycobacteria infections in immunocompromised patients: single institution experience. Wei MC, Banaei N, Yakrus MA, Stoll T, Gutierrez KM, Agarwal R. J Pediatr Hematol Oncol. 2009; 31 (8): 556-60
• Nodular lymphocyte-predominant Hodgkin lymphoma presenting as fulminant hepatic failure in a pediatric patient: a case report with pathologic, immunophenotypic, and molecular findings. Woolf KM, Wei MC, Link MP, Arber DA, Warnke RA. Appl Immunohistochem Mol Morphol. 2008; 16 (2): 196-201
• CpG island methylator phenotype and childhood leukemia. Lacayo NJ, DiMartino JF, Wei MC, Dahl GV. Clin Cancer Res. 2006; 12 (16): 4787-9
• Bcl-2-related genes in lymphoid neoplasia. Wei MC, Int J Hematol. 2004; 80 (3): 205-9
• A reversible component of mitochondrial respiratory dysfunction in apoptosis can be rescued by exogenous cytochrome c. Mootha VK, Wei MC, Buttle KF, Scorrano L, Panoutsakopoulou V, Mannella CA, Korsmeyer SJ. EMBO J. 2001; 20 (4): 661-71
• BCL-2, BCL-X(L) sequester BH3 domain-only molecules preventing BAX- and BAK-mediated mitochondrial apoptosis. Cheng EH, Wei MC, Weiler S, Flavell RA, Mak TW, Lindsten T, Korsmeyer SJ. Mol Cell. 2001; 8 (3): 705-11
• Proapoptotic BAX and BAK: a requisite gateway to mitochondrial dysfunction and death. Wei MC, Zong WX, Cheng EH, Lindsten T, Panoutsakopoulou V, Ross AJ, Roth KA, MacGregor GR, Thompson CB, Korsmeyer SJ. Science. 2001; 292 (5517): 727-30
• Posttranslational N-myristoylation of BID as a molecular switch for targeting mitochondria and apoptosis. Zha J, Weiler S, Oh KJ, Wei MC, Korsmeyer SJ. Science. 2000; 290 (5497): 1761-5
• Pro-apoptotic cascade activates BID, which oligomerizes BAK or BAX into pores that result in the release of cytochrome c. Korsmeyer SJ, Wei MC, Saito M, Weiler S, Oh KJ, Schlesinger PH. Cell Death Differ. 2000; 7 (12): 1166-73
• tBID, a membrane-targeted death ligand, oligomerizes BAK to release cytochrome c. Wei MC, Lindsten T, Mootha VK, Weiler S, Gross A, Ashiya M, Thompson CB, Korsmeyer SJ. Genes Dev. 2000; 14 (16): 2060-71
• 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. Gross A, Yin XM, Wang K, Wei MC, Jockel J, Milliman C, Erdjument-Bromage H, Tempst P, Korsmeyer SJ. J Biol Chem. 1999; 274 (2): 1156-63
• Transduced p16INK4a peptides inhibit hypophosphorylation of the retinoblastoma protein and cell cycle progression prior to activation of Cdk2 complexes in late G1. Gius DR, Ezhevsky SA, Becker-Hapak M, Nagahara H, Wei MC, Dowdy SF. Cancer Res. 1999; 59 (11): 2577-80
• Enforced dimerization of BAX results in its translocation, mitochondrial dysfunction and apoptosis. Gross A, Jockel J, Wei MC, Korsmeyer SJ. EMBO J. 1998; 17 (14): 3878-85
• Hypo-phosphorylation of the retinoblastoma protein (pRb) by cyclin D:Cdk4/6 complexes results in active pRb. Ezhevsky SA, Nagahara H, Vocero-Akbani AM, Gius DR, Wei MC, Dowdy SF. Proc Natl Acad Sci U S A. 1997; 94 (20): 10699-704