AI Article Synopsis
- The cell cycle in eukaryotic cells is controlled by protein complexes made of cyclins and cyclin-dependent kinases (CDKs), which are inhibited by CDK inhibitors (CKIs), notably p27.
- The degradation of p27 is crucial for cells to re-enter the cell cycle from the resting G0 phase, which is facilitated by ubiquitination via specific ligase complexes and degradation through the proteasome.
- p27 has been shown to function as a tumor suppressor in mouse models and human tumor studies, making its regulation and degradation significant in the context of cancer development.
Article Abstract
The cell cycle of eukaryotic cells is regulated by a series of protein complexes composed of cyclins and cyclin-dependent kinases (CDKs), the activity of which is suppressed by a group of CDK inhibitors (CKIs). Among the CKIs, p27 plays a pivotal role in the control of cell proliferation. Degradation of p27 is a critical event for reentry of cells into the cell cycle from G0 phase and occurs through ubiquitination by two ubiquitin ligase complexes (KPC and SCFSkP2) and subsequent degradation by the 26S-proteasome. A tumor suppressing function of p27 has been demonstrated in mouse models and studies of human tumors. This review will focus on the regulation of p27 proteolysis and its consequences for tumorigenesis.
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