Format:
Online-Ressource
ISSN:
1469-3178
Content:
The Bcl2 pro‐survival protein family has long been recognized for its important contributions to cancer. At elevated levels relative to pro‐apoptotic effector members, the survival proteins prevent cancer cells from initiating apoptosis in the face of many intrinsic tumour‐suppressing pathways and extrinsic therapeutic treatments aimed at controlling tumorigenesis. Recent studies, including genome‐wide analyses, have begun to focus attention on a particularly enigmatic member of the family—myeloid cell leukaemia 1 (Mcl1). For reasons that are not clear, Mcl1 in cancer cells is turned over rapidly, eliminated primarily through the ubiquitin–proteasome pathway. Moreover, the mechanistic aspects of this constitutive membrane‐associated protein have not been fully elucidated. As the pro‐cancer activity of Mcl1 requires elevated expression levels of the protein, the cancer genome adapts to ensure either high levels of synthesis or evasion of degradation, or both. Here, we focus on the complex strategies at play and their therapeutic implications.
Content:
The pro‐survival members of the Bcl2 family have been recognized for their ability to save cancer cells from undergoing apoptosis. This review discusses recent progress in understanding the complex biology of one of those proteins, Mcl1, the multiple mechanisms available for re‐programming Mcl1 expression by cancer cells, and how this knowledge can be exploited for therapeutic applications.
In:
volume:14
In:
number:4
In:
year:2013
In:
pages:328-336
In:
extent:9
In:
European Molecular Biology Organization, EMBO reports, Heidelberg : EMBO Press, [200]-, 14, Heft 4 (2013), 328-336 (gesamt 9), 1469-3178
Language:
English
DOI:
10.1038/embor.2013.20
URN:
urn:nbn:de:101:1-2023020306022026426220
URL:
https://doi.org/10.1038/embor.2013.20
URL:
https://nbn-resolving.org/urn:nbn:de:101:1-2023020306022026426220
URL:
https://d-nb.info/1279957360/34
URL:
https://doi.org/10.1038/embor.2013.20
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