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. 2021 Oct 8;13(19):5025. doi: 10.3390/cancers13195025

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© 2021 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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Schematic representation of the model of RBL1/p107 regulation by calpain and CaMKs. In cycling cells RBL1/p107 is phosphorylated by cyclin-CDK complexes, promoting RBL1/p107 cytoplasmic localization (left panel). Calpain inhibition or CaMK inhibition promote RBL1/p107 dephosphorylation and nuclear accumulation by directly or indirectly affecting its stability or the activity/levels of cyclins and CDKs. RBL1/p107 nuclear accumulation might increase the localization of transcriptional repressors at the promoters of genes controlling cell cycle progression, contributing to cell cycle arrest (right panel).