The REGγ-proteasome forms a regulatory circuit with IκBɛ and NFκB in experimental colitis.

Abstract:

:Increasing incidence of inflammatory bowel disorders demands a better understanding of the molecular mechanisms underlying its multifactorial aetiology. Here we demonstrate that mice deficient for REGγ, a proteasome activator, show significantly attenuated intestinal inflammation and colitis-associated cancer in dextran sodium sulfate model. Bone marrow transplantation experiments suggest that REGγ's function in non-haematopoietic cells primarily contributes to the phenotype. Elevated expression of REGγ exacerbates local inflammation and promotes a reciprocal regulatory loop with NFκB involving ubiquitin-independent degradation of IκBɛ. Additional deletion of IκBɛ restored colitis phenotypes and inflammatory gene expression in REGγ-deficient mice. In sum, this study identifies REGγ-mediated control of IκBɛ as a molecular mechanism that contributes to NFκB activation and promotes bowel inflammation and associated tumour formation in response to chronic injury.

journal_name

Nat Commun

journal_title

Nature communications

authors

Xu J,Zhou L,Ji L,Chen F,Fortmann K,Zhang K,Liu Q,Li K,Wang W,Wang H,Xie W,Wang Q,Liu J,Zheng B,Zhang P,Huang S,Shi T,Zhang B,Dang Y,Chen J,O'Malley BW,Moses RE,Wang P,Li L,Xiao J,Hoffmann A,Li X

doi

10.1038/ncomms10761

subject

Has Abstract

pub_date

2016-02-22 00:00:00

pages

10761

issn

2041-1723

pii

ncomms10761

journal_volume

7

pub_type

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