Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2024 Jan 23;10(1):9. doi: 10.1038/s41514-024-00135-7

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2024

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

PMC Copyright notice

Fig. 2 — After induction of DNA damage, ATR-CHK1 and ATM-CHK2 are recruited to the damaged position. These lead to an activation and increased presence of p53, by inhibiting MDM2/4. Activated p53 in turn either binds to FOXO4, inducing increased expression of p21, or interacts with PUMA and NOXA, which activates the apoptosis cascade. Besides activation of p53, ATR-CHK1 and ATM-CHK2 are also responsible for phosphorylation of p38MAPK and transcription of p16. These two proteins activate senescence in the cell.