Myeloid cell leukemia-1 as a therapeutic target.
Apoptosis, or programmed cell death, is essential for normal development and homeostasis. Insufficient apoptosis may contribute to the pathogenesis of malignancy and acute and chronic inflammation. Apoptosis may be induced by the death receptor or the mitochondrial pathways. Myeloid cell leukemia (Mcl)-1 is a member of the Bcl-2 family that contributes to the control of mitochondrial integrity, which is critical for maintaining cell viability. Mcl-1 has been shown to be essential for the development and survival of a variety of cell types. This review characterizes the role of Mcl-1 in the regulation of apoptosis and the promotion of disease, and defines novel strategies that have been identified to target this molecule.
Mandelin
Arthur M
AM
Division of Rheumatology, Northwestern University, Feinberg School of Medicine, Chicago, IL, USA.
Pope
Richard M
RM
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D000970:Antineoplastic Agents / Q000627:therapeutic use; D017209:Apoptosis; D006801:Humans; D007249:Inflammation / Q000188:drug therapy* / Q000378:metabolism; D064549:Myeloid Cell Leukemia Sequence 1 Protein; D009363:Neoplasm Proteins / Q000037:antagonists & inhibitors* / Q000276:immunology / Q000378:metabolism; D009369:Neoplasms / Q000188:drug therapy* / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000037:antagonists & inhibitors* / Q000276:immunology / Q000378:metabolism
D000893:Anti-Inflammatory Agents; D000970:Antineoplastic Agents; D064549:Myeloid Cell Leukemia Sequence 1 Protein; D009363:Neoplasm Proteins; D019253:Proto-Oncogene Proteins c-bcl-2