期刊
TRENDS IN CELL BIOLOGY
卷 23, 期 1, 页码 22-29出版社
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tcb.2012.08.011
关键词
apoptosis; MCL-1; homeostasis; mitochondrial function; cancer; development.
类别
资金
- National Institute of Heart, Lung and Blood [R01HL102175]
- American Cancer Society [119130-RSG-10-255-01-LIB]
- Cancer Center [P30CA021765]
- American Lebanese Syrian Associated Charities of St Jude Children's Research Hospital
BCL-2 molecules are regulators of programmed cell death and defects in this pathway contribute to human diseases. One family member, MCL-1, is unique because its expression is tightly regulated and it is essential for promoting the survival of myriad cellular lineages. Additionally, MCL-1 promotes the maintenance of normal mitochondrial morphology and energy production. Dissection of these functions revealed recently that they depend on separate mitochondria! sublocalizations. MCL-1's antiapoptotic activity is restricted to the outer mitochondria! membrane (OMM), whereas its function in mitochondrial physiology requires localization to the matrix. These findings provide an attractive model for how MCL-1's diverse functions may contribute to normal cell homeostasis and function. MCL-1 is, highly amplified in human cancer, suggesting that these functions may contribute to malignant cell growth and evasion of apoptosis.
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