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

. 2021 Mar 23;9:633305. doi: 10.3389/fcell.2021.633305

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

Copyright © 2021 Sobanski, Rose, Suraweera, O’Byrne, Richard and Bolderson.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

PMC Copyright notice

A schematic representation of the Ataxia-Telangiectasia Mutated- (ATM) and DNA-Dependent Kinase- (DNA-PK) mediated regulation of metabolic processes after DNA Damage. ATM activates multiple downstream proteins regulating cell cycle arrest, DNA repair and cellular metabolism. ATM activates the tumor suppressor p53 which decreases GLUT recruitment, glycolysis, and dNTP production. ATM non-canonical function is essential for repairing mitochondrial genome defects to maintain mitochondrial homeostasis. For maintenance of energy production ATM activates AKT to promote glucose recruitment to the nucleus via GLUT4-mediated transport. ATM also activates G6PD though Hsp27, as an alternative mechanism to produce nucleotides for DNA metabolism. DNA-PK following energy depletion or metabolic rewiring promotes glycolysis through AMP signaling. This figure was created with BioRender.com.