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Linking membrane trafficking and intestinal homeostasis

A major challenge for the human body is to maintain symbiotic relationships with bacterial communities that colonize their intestines. Although several molecules important for intestinal homeostasis have been discovered, the vast array still needs to be identified. We approached this task using a fo...

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Detalles Bibliográficos
Autores principales: Moresco, Eva Marie Y., Brandl, Katharina
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Landes Bioscience 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3875636/
https://www.ncbi.nlm.nih.gov/pubmed/24665373
http://dx.doi.org/10.4161/tisb.23119
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author Moresco, Eva Marie Y.
Brandl, Katharina
author_facet Moresco, Eva Marie Y.
Brandl, Katharina
author_sort Moresco, Eva Marie Y.
collection PubMed
description A major challenge for the human body is to maintain symbiotic relationships with bacterial communities that colonize their intestines. Although several molecules important for intestinal homeostasis have been discovered, the vast array still needs to be identified. We approached this task using a forward genetic approach, which revealed several molecules essential for intestinal homeostasis. One recently identified molecule is Ypt1p-interacting protein 1 domain family, member 6 (Yipf6). Mice with a null mutation in Yipf6 are hypersensitive to dextran sulfate sodium (DSS) induced colitis and develop spontaneous intestinal inflammation. Members of the Yip1 family are believed to be involved in ER to Golgi membrane transport.   In this review we summarize recent advances in the understanding of genes involved in intestinal homeostasis with a specific focus on the Yip family members. We speculate on how deficiency or dysfunction of Yip molecules may dysregulate intestinal homeostasis leading to pathogenic states.
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spelling pubmed-38756362014-02-19 Linking membrane trafficking and intestinal homeostasis Moresco, Eva Marie Y. Brandl, Katharina Tissue Barriers Commentary A major challenge for the human body is to maintain symbiotic relationships with bacterial communities that colonize their intestines. Although several molecules important for intestinal homeostasis have been discovered, the vast array still needs to be identified. We approached this task using a forward genetic approach, which revealed several molecules essential for intestinal homeostasis. One recently identified molecule is Ypt1p-interacting protein 1 domain family, member 6 (Yipf6). Mice with a null mutation in Yipf6 are hypersensitive to dextran sulfate sodium (DSS) induced colitis and develop spontaneous intestinal inflammation. Members of the Yip1 family are believed to be involved in ER to Golgi membrane transport.   In this review we summarize recent advances in the understanding of genes involved in intestinal homeostasis with a specific focus on the Yip family members. We speculate on how deficiency or dysfunction of Yip molecules may dysregulate intestinal homeostasis leading to pathogenic states. Landes Bioscience 2013-01-01 2013-01-01 /pmc/articles/PMC3875636/ /pubmed/24665373 http://dx.doi.org/10.4161/tisb.23119 Text en Copyright © 2013 Landes Bioscience http://creativecommons.org/licenses/by-nc/3.0/ This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.
spellingShingle Commentary
Moresco, Eva Marie Y.
Brandl, Katharina
Linking membrane trafficking and intestinal homeostasis
title Linking membrane trafficking and intestinal homeostasis
title_full Linking membrane trafficking and intestinal homeostasis
title_fullStr Linking membrane trafficking and intestinal homeostasis
title_full_unstemmed Linking membrane trafficking and intestinal homeostasis
title_short Linking membrane trafficking and intestinal homeostasis
title_sort linking membrane trafficking and intestinal homeostasis
topic Commentary
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3875636/
https://www.ncbi.nlm.nih.gov/pubmed/24665373
http://dx.doi.org/10.4161/tisb.23119
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