Rab11FIP1-deficient mice develop spontaneous inflammation and show increased susceptibility to colon damage-Reference-Cited by-同舟云学术

Rab11FIP1-deficient mice develop spontaneous inflammation and show increased susceptibility to colon damage

Published:2022-09-01 Issue:3 Volume:323 Page:G239-G254
ISSN:0193-1857
Container-title:American Journal of Physiology-Gastrointestinal and Liver Physiology
language:en
Short-container-title:American Journal of Physiology-Gastrointestinal and Liver Physiology

Author:

Rathan-Kumar Sudiksha¹²,Roland Joseph T.¹²,Momoh Michael¹²,Goldstein Anna¹²,Lapierre Lynne A.¹²,Manning Elizabeth¹²,Mitchell Louise³,Norman Jim³,Kaji Izumi¹²^ORCID,Goldenring James R.¹²⁴⁵^ORCID

Affiliation:

1. Section of Surgical Sciences, Vanderbilt University Medical Center, Nashville, Tennessee

2. Epithelial Biology Center, Vanderbilt University Medical Center, Nashville, Tennessee

3. Cancer Research UK Beatson Institute, Glasgow, Scotland, United Kingdom

4. Department of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, Tennessee

5. Nashville Veterans Affairs Medical Center, Nashville, Tennessee

Abstract

Although Rab11FIP1 is important in membrane trafficking in epithelial cells, the gastrointestinal phenotype of Rab11FIP1 knockout (KO) mice had never been reported. This study demonstrated that Rab11FIP1 loss induces mistrafficking of Rab14 and MUC13 and decreases in colonic goblet cells, resulting in impaired mucosal integrity.

Funder

Cancer Research UK

HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases

Christine Volpe Fund

Vanderbilt University Medical Center

Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center

HHS | NIH | National Cancer Institute

U.S. Department of Veterans Affairs

HHS | NIH | National Eye Institute

Publisher

American Physiological Society

Subject