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Enhanced sensitivity to DSS colitis caused by a hypomorphic Mbtps1 mutation disrupting the ATF6-driven unfolded protein response

Academic Article
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Overview

authors

  • Brandl, K.
  • Rutschmann, S.
  • Li, X. H.
  • Du, X.
  • Xiao, N. M.
  • Schnabl, B.
  • Brenner, D. A.
  • Beutler, Bruce

publication date

  • March 2009

journal

  • Proceedings of the National Academy of Sciences of the United States of America  Journal

abstract

  • 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.

subject areas

  • Activating Transcription Factor 6
  • Animals
  • Colitis
  • Dextran Sulfate
  • Endoplasmic Reticulum
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Mutation
  • Proprotein Convertases
  • Protein Folding
  • Serine Endopeptidases
  • Substrate Specificity
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Research

keywords

  • ER stress
  • UPR
  • inflammatory bowel disease
  • site 1 protease
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Identity

PubMed Central ID

  • PMC2651297

International Standard Serial Number (ISSN)

  • 0027-8424

Digital Object Identifier (DOI)

  • 10.1073/pnas.0813036106

PubMed ID

  • 19202076
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Additional Document Info

start page

  • 3300

end page

  • 3305

volume

  • 106

issue

  • 9

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