Michael Wei, MD, PhD

Professional Education

Board Certification: Pediatrics, American Board of Pediatrics (2005)

Medical Education: Washington University School Of Medicine (2002) MO

Residency: Children's Hospital Boston (2005) MA

Board Certification: Pediatric Hematology-Oncology, American Board of Pediatrics (2009)

Fellowship: Lucile Packard Children's Hospital (2008) CA

BS, University of Illinois, Biology, Electrical Engineering (1995)

MD, PhD, Washington University, Molecular Cell Biology (2002)

Next-Generation NAMPT Inhibitors Identified by Sequential High-Throughput Phenotypic Chemical and Functional Genomic Screens.
Matheny, C. J., Wei, M. C., Bassik, M. C., Donnelly, A. J., Kampmann, M., & Cleary, M. L. (2013). Next-Generation NAMPT Inhibitors Identified by Sequential High-Throughput Phenotypic Chemical and Functional Genomic Screens. Chemistry & biology, 20(11), 1352-1363.

Nontuberculous Mycobacteria Infections in Immunocompromised Patients Single Institution Experience
Wei, M. C., Banaei, N., Yakrus, M. A., Stoll, T., Gutierrez, K. M., & Agarwal, R. (2009). Nontuberculous Mycobacteria Infections in Immunocompromised Patients Single Institution Experience. JOURNAL OF PEDIATRIC HEMATOLOGY ONCOLOGY, 31(8), 556-560.

Nodular lymphocyte-predominant Hodgkin lymphoma presenting as fulminant hepatic failure in a pediatric patient: A case report with pathologic, immunophenotypic, and molecular findings
Woolf, K. Mw., Wei, M. C., Link, M. P., Arber, D. A., & Warnke, R. A. (2008). Nodular lymphocyte-predominant Hodgkin lymphoma presenting as fulminant hepatic failure in a pediatric patient: A case report with pathologic, immunophenotypic, and molecular findings. APPLIED IMMUNOHISTOCHEMISTRY & MOLECULAR MORPHOLOGY, 16(2), 196-201.

CpG island methylator phenotype and childhood leukemia
Lacayo, N. J., Di Martino, J. F., Wei, M. C., & Dahl, G. V. (2006). CpG island methylator phenotype and childhood leukemia. CLINICAL CANCER RESEARCH, 12(16), 4787-4789.

Bcl-2-related genes in lymphoid neoplasia
Wei, M. C. (2004). Bcl-2-related genes in lymphoid neoplasia. INTERNATIONAL JOURNAL OF HEMATOLOGY, 80(3), 205-209.

BCL-2, BCL-X-L sequester BH3 domain-only molecules preventing BAX- and BAK-mediated mitochondrial apoptosis
Cheng, E. Hya., Wei, M. C., Weiler, S., Flavell, R. A., Mak, T. W., & Korsmeyer, S. J. (2001). BCL-2, BCL-X-L sequester BH3 domain-only molecules preventing BAX- and BAK-mediated mitochondrial apoptosis. MOLECULAR CELL, 8(3), 705-711.

Proapoptotic BAX and BAK: A requisite gateway to mitochondrial dysfunction and death
Wei, M. C., Zong, W. X., Cheng, E. Hy., LINDSTEN, T., Panoutsakopoulou, V., & Korsmeyer, S. J. (2001). Proapoptotic BAX and BAK: A requisite gateway to mitochondrial dysfunction and death. SCIENCE, 292(5517), 727-730.

A reversible component of mitochondrial respiratory dysfunction in apoptosis can be rescued by exogenous cytochrome c
Mootha, V. K., Wei, M. C., Buttle, K. F., Scorrano, L., Panoutsakopoulou, V., & Korsmeyer, S. J. (2001). A reversible component of mitochondrial respiratory dysfunction in apoptosis can be rescued by exogenous cytochrome c. EMBO JOURNAL, 20(4), 661-671.

Posttranslational N-myristoylation of BID as a molecular switch for targeting mitochondria and apoptosis
Zha, J. P., Weiler, S., Oh, K. J., Wei, M. C., & Korsmeyer, S. J. (2000). Posttranslational N-myristoylation of BID as a molecular switch for targeting mitochondria and apoptosis. SCIENCE, 290(5497), 1761-1765.

Pro-apoptotic cascade activates BID, which oligomerizes BAK or BAX into pores that result in the release of cytochrome c
Korsmeyer, S. J., Wei, M. C., Saito, M., Weller, S., Oh, K. J., & Schlesinger, P. H. (2000). Pro-apoptotic cascade activates BID, which oligomerizes BAK or BAX into pores that result in the release of cytochrome c. CELL DEATH AND DIFFERENTIATION, 7(12), 1166-1173.

tBID, a membrane-targeted death ligand, oligomerizes BAK to release cytochrome c
Wei, M. C., LINDSTEN, T., Mootha, V. K., Weiler, S., Gross, A., & Korsmeyer, S. J. (2000). tBID, a membrane-targeted death ligand, oligomerizes BAK to release cytochrome c. GENES & DEVELOPMENT, 14(16), 2060-2071.

Transduced p16(INK4a) peptides inhibit hypophosphorylation of the retinoblastoma protein and cell cycle progression prior to activation of Cdk2 complexes in late G(1)
Gius, D. R., Ezhevsky, S. A., Becker-Hapak, M., Nagahara, H., Wei, M. C., & Dowdy, S. F. (1999). Transduced p16(INK4a) peptides inhibit hypophosphorylation of the retinoblastoma protein and cell cycle progression prior to activation of Cdk2 complexes in late G(1). CANCER RESEARCH, 59(11), 2577-2580.

Caspase cleaved BID targets mitochondria and is required for cytochrome c release, while BCL-X-L prevents this release but not tumor necrosis factor-R1/Fas death
Gross, A., Yin, X. M., Wang, K., Wei, M. C., Jockel, J., & Korsmeyer, S. J. (1999). Caspase cleaved BID targets mitochondria and is required for cytochrome c release, while BCL-X-L prevents this release but not tumor necrosis factor-R1/Fas death. JOURNAL OF BIOLOGICAL CHEMISTRY, 274(2), 1156-1163.

Enforced dimerization of BAX results in its translocation, mitochondrial dysfunction and apoptosis
Gross, A., Jockel, J., Wei, M. C., & Korsmeyer, S. J. (1998). Enforced dimerization of BAX results in its translocation, mitochondrial dysfunction and apoptosis. EMBO JOURNAL, 17(14), 3878-3885.

Hypo-phosphorylation of the retinoblastoma protein (pRb) by cyclin D:Cdk4/6 complexes results in active pRb
Ezhevsky, S. A., Nagahara, H., VoceroAkbani, A. M., Gius, D. R., Wei, M. C., & Dowdy, S. F. (1997). Hypo-phosphorylation of the retinoblastoma protein (pRb) by cyclin D:Cdk4/6 complexes results in active pRb. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 94(20), 10699-10704.