RNase-L Deficiency Exacerbates Experimental Colitis and Colitis-associated Cancer
Author(s) -
Tiha M. Long,
Arindam Chakrabarti,
Heather J. Ezelle,
Sarah E. Brennan-Laun,
Jean-Pierre Raufman,
I. V. Polyakova,
Robert H. Silverman,
Bret A. Hassel
Publication year - 2013
Publication title -
inflammatory bowel diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.932
H-Index - 146
eISSN - 1536-4844
pISSN - 1078-0998
DOI - 10.1097/mib.0b013e318281f2fd
Subject(s) - colitis , rnase p , endoribonuclease , immunology , immune system , interferon , innate immune system , cancer , ulcerative colitis , biology , receptor , inflammatory bowel disease , cancer research , medicine , rna , biochemistry , gene , disease
The endoribonuclease RNase-L is a type-I interferon (IFN)-regulated component of the innate immune response that functions in antiviral, antibacterial, and antiproliferative activities. RNase-L produces RNA agonists of RIG-I-like receptors, sensors of cytosolic pathogen-associated RNAs that induce cytokines including IFN-β. IFN-β and RIG-I-like receptors signaling mediate protective responses against experimental colitis and colitis-associated cancer and contribute to gastrointestinal homeostasis. Therefore, we investigated a role for RNase-L in murine colitis and colitis-associated cancer and its association with RIG-I-like receptors signaling in response to bacterial RNA.
Accelerating Research
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom
Address
John Eccles HouseRobert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom