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BibTex format

@article{Brandl:2009:10.1073/pnas.0813036106,
author = {Brandl, K and Rutschmann, S and Li, X and Du, X and Xiao, N and Schnabl, B and Brenner, DA and Beutler, B},
doi = {10.1073/pnas.0813036106},
journal = {Proc Natl Acad Sci U S A},
pages = {3300--3305},
title = {Enhanced sensitivity to DSS colitis caused by a hypomorphic Mbtps1 mutation disrupting the ATF6-driven unfolded protein response.},
url = {http://dx.doi.org/10.1073/pnas.0813036106},
volume = {106},
year = {2009}
}

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TY  - JOUR
AB  - Here, we describe an N-ethyl-N-nitrosourea (ENU)-induced missense error in the membrane-bound transcription factor peptidase site 1 (S1P)-encoding gene (Mbtps1) that causes enhanced susceptibility to dextran sodium sulfate (DSS)-induced colitis. S1P cleaves and activates cAMP response element binding protein/ATF transcription factors, the sterol regulatory element-binding proteins (SREBPs), and other proteins of both endogenous and viral origin. Because S1P has a nonredundant function in the ATF6-dependent unfolded protein response (UPR), woodrat mice show diminished levels of major endoplasmic reticulum chaperones GRP78 (BiP) and GRP94 in the colon upon DSS administration. Experiments with bone marrow chimeric mice reveal a requirement for S1P in nonhematopoietic cells, without which a diminished UPR and colitis develop.
AU  - Brandl,K
AU  - Rutschmann,S
AU  - Li,X
AU  - Du,X
AU  - Xiao,N
AU  - Schnabl,B
AU  - Brenner,DA
AU  - Beutler,B
DO  - 10.1073/pnas.0813036106
EP  - 3305
PY  - 2009///
SP  - 3300
TI  - Enhanced sensitivity to DSS colitis caused by a hypomorphic Mbtps1 mutation disrupting the ATF6-driven unfolded protein response.
T2  - Proc Natl Acad Sci U S A
UR  - http://dx.doi.org/10.1073/pnas.0813036106
UR  - https://www.ncbi.nlm.nih.gov/pubmed/19202076
VL  - 106
ER  -

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