The multiple mechanisms of MCL1 in the regulation of cell fate
| Autor: | William J. Placzek, Hayley Widden |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
DNA Repair
Cell division QH301-705.5 DNA damage Cell Medicine (miscellaneous) Cellular homeostasis Apoptosis Review Article Cell fate determination Biology General Biochemistry Genetics and Molecular Biology Mice Autophagy medicine Animals Humans MCL1 Biology (General) Cell Proliferation Cell growth Mitochondria Cell biology medicine.anatomical_structure Myeloid Cell Leukemia Sequence 1 Protein Calcium Signal transduction General Agricultural and Biological Sciences Cell signalling |
| Zdroj: | Communications Biology Communications Biology, Vol 4, Iss 1, Pp 1-12 (2021) |
| ISSN: | 2399-3642 |
| Popis: | MCL1 (myeloid cell leukemia-1) is a widely recognized pro-survival member of the Bcl-2 (B-cell lymphoma protein 2) family and a promising target for cancer therapy. While the role MCL1 plays in apoptosis is well defined, its participation in emerging non-apoptotic signaling pathways is only beginning to be appreciated. Here, we synthesize studies characterizing MCL1s influence on cell proliferation, DNA damage response, autophagy, calcium handling, and mitochondrial quality control to highlight the broader scope that MCL1 plays in cellular homeostasis regulation. Throughout this review, we discuss which pathways are likely to be impacted by emerging MCL1 inhibitors, as well as highlight non-cancerous disease states that could deploy Bcl-2 homology 3 (BH3)-mimetics in the future. In this review Widden and Placzek synthesize studies characterizing the influence that myeloid cell leukemia-1 (MCL1) has on cell proliferation, DNA damage response, autophagy, calcium handling, and mitochondrial quality control to highlight the broader scope that it plays in cellular homeostasis regulation. They discuss which pathways are likely to be impacted by emerging MCL1 inhibitors, as well as highlight non-cancerous disease states that could deploy BH3-mimetics in the future. |
| Databáze: | OpenAIRE |
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