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 Communjournal_title
Nature communicationsauthors
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 Xdoi
10.1038/ncomms10761subject
Has Abstractpub_date
2016-02-22 00:00:00pages
10761issn
2041-1723pii
ncomms10761journal_volume
7pub_type
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