Abstract
Apoptosis is an evolutionarily conserved form of programed cell death (PCD) that has a vital effect on early embryonic development, tissue homeostasis and clearance of damaged cells. Dysregulation of apoptosis can lead to many diseases, such as Alzheimer's disease, cancer, AIDS and heart disease. The anti-apoptotic protein MCL1, a member of the BCL2 family, plays important roles in these physiological and pathological processes. Its high expression is closely related to drug resistances in the treatment of tumor. This review summarizes the structure and function of MCL1, the types of post-translational modifications of MCL1 and their effects on the functions of MCL1, as well as the treatment strategies targeting MCL1 in cancer therapy. The research on the fine regulation of MCL1 will be favorable to the provision of a promising future for the design and screening of MCL1 inhibitors.
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