Brandl, Katharina and Tomisato, Wataru and Li, Xiaohong and Neppl, Christina and Pirie, Elaine and Falk, Werner and Xia, Yu and Moresco, Eva Marie Y. and Baccala, Roberto and Theofilopoulos, Argyrios N. and Schnabl, Bernd and Beutler, Bruce (2012) Yip1 domain family, member 6 (Yipf6) mutation induces spontaneous intestinal inflammation in mice. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 109 (31). pp. 12650-12655. ISSN 0027-8424,
Full text not available from this repository. (Request a copy)Abstract
Using an environmentally sensitized genetic screen we identified mutations that cause inflammatory colitis in mice. The X-linked Klein-Zschocher (KLZ) mutation created a null allele of Yipf6, a member of a gene family believed to regulate vesicular transport in yeast, but without known functions in mammals. Yipf6 is a five transmembrane-spanning protein associated with Golgi compartments. Klein-Zschocher mutants were extremely sensitive to colitis induced by dextran sodium sulfate (DSS) and developed spontaneous ileitis and colitis after 16 mo of age in specific pathogen-free housing conditions. Electron microscopy, gene expression, and immunocytochemistry analyses provided evidence that impaired intestinal homeostasis stemmed from defective formation and secretion of large secretory granules from Paneth and goblet cells. These studies support a tissue- and organ-specific function for Yipf6 in the maintenance of intestinal homeostasis and implicate the orthologous human gene as a disease susceptibility locus.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | BOWEL-DISEASE; CHRONIC ENTEROCOLITIS; ADAM17 DELETION; COLITIS; IDENTIFICATION; MOUSE; CELLS; STAT3; LINKS; ER; |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Innere Medizin I |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 11 May 2020 05:35 |
| Last Modified: | 11 May 2020 05:35 |
| URI: | https://pred.uni-regensburg.de/id/eprint/18423 |
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