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. 2021 Jan 6;10(1):bio057232. doi: 10.1242/bio.057232

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© 2021. Published by The Company of Biologists Ltd

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.

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Fig. 4. — Ctdp1 deletion impairs MEF proliferation and promotes cell cycle arrest. (A) Ctdp1^+/+ and Ctdp1^flox/flox MEF proliferation after Lenti-Cre transduction. (B) Cell cycle analysis of the Ctdp1^+/+ and Ctdp1^flox/flox MEFs 5 days post Lenti-Cre transduction. Presented as mean±s.e.m., n=3. P-values ≤0.05 are displayed. (C–E) Western blot analysis of DNA damage response proteins (C), G1-S and G2-M transition related proteins (D), and RB phosphorylation (E) in Ctdp1^+/+ and Ctdp1^flox/flox MEFs with and without Lenti-Cre transduction. (F) Working model illustrating that Ctdp1 KO upregulates the CDK inhibitor p27 (red arrow), which functions to inhibit cell cycle progression through G1-S and G2-M transitions. Loss of Ctdp1 also downregulates (blue arrows) pRB, Cyclin B and pHistone H3 which promote G1-S transition, G2-M transition and M phase entry, respectively.