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Positive feedback look identified with ATM via NF-κB pathway back to cellular senescence

As always, it's complicated, but controlling levels of ATM could be part of a therapy to combat ageing

02-Apr-2020

Key points from article :

When DNA is damaged it signals for help - including using Ataxia-telangiectasia mutated (ATM) kinase.

Clear biochemical link between ATM and the inflammatory NF-κB pathway identified.

NF-κB pathway linked to other age-related diseases, including atherosclerosis, osteoporosis, and Type 2 diabetes.

Also linked to cellular senescence itself.

ATM-deficient mice exhibited fewer signs of cellular senescence, including SASP factors.

Used an ATM kinase inhibitor, KU-55933, to rescue cells from cellular senescence.

However, it also reduced Poly [ADP-ribose] polymerase 1 (PARP1), which is used in DNA repair.

Research by Scripps Research, University of Minnesota Medical School and University of Pittsburgh School of Medicine published in Aging.

Mentioned in this article:

Click on resource name for more details.

Scripps Research Institute

Medical research facility with focus on research and education in the biomedical sciences.

University of Minnesota Medical School

Medical care and educational institution.

University of Pittsburgh

Public state-related research university

Topics mentioned on this page:
Senescent Cells