Journal
CELL RESEARCH
Volume 21, Issue 1, Pages 22-39Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/cr.2010.166
Keywords
deubiquitinases; NF-kappa B; IKK; A20; CYLD
Categories
Funding
- NIH [PO1CA128115, RO1CA135362, RO1GM083143]
- NATIONAL CANCER INSTITUTE [P01CA128115, R01CA135362] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM083143] Funding Source: NIH RePORTER
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Nuclear factor-kappa B (NF-kappa B) is a critical regulator of multiple biological functions including innate and adaptive immunity and cell survival. Activation of NF-kappa B is tightly regulated to preclude chronic signaling that may lead to persistent inflammation and cancer. Ubiquitination of key signaling molecules by E3 ubiquitin ligases has emerged as an important regulatory mechanism for NF-kappa B signaling. Deubiquitinases (DUBs) counteract E3 ligases and therefore play a prominent role in the downregulation of NF-kappa B signaling and homeostasis. Understanding the mechanisms of NF-kappa B downregulation by specific DUBs such as A20 and CYLD may provide therapeutic opportunities for the treatment of chronic inflammatory diseases and cancer.
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