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CNTNAP3 Associated ATG16L1 Expression and Crohn's Disease
Autophagy is a common physiological process in cell homeostasis and regulation. Autophagy-related gene mutations and autophagy disorders are important in Crohn's disease (CD). The nucleotide oligomerization domain 2–autophagy genes autophagy 16-like 1 (NOD2–ATG16L1) signaling axis disorder cont...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4391322/ https://www.ncbi.nlm.nih.gov/pubmed/25883416 http://dx.doi.org/10.1155/2015/404185 |
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author | Qiao, Yu Qi Huang, Mei Lan Zheng, Qing Wang, Tian Rong Xu, An Tao Cao, Yuan Zhao, Di Ran, Zhi Hua Shen, Jun |
author_facet | Qiao, Yu Qi Huang, Mei Lan Zheng, Qing Wang, Tian Rong Xu, An Tao Cao, Yuan Zhao, Di Ran, Zhi Hua Shen, Jun |
author_sort | Qiao, Yu Qi |
collection | PubMed |
description | Autophagy is a common physiological process in cell homeostasis and regulation. Autophagy-related gene mutations and autophagy disorders are important in Crohn's disease (CD). The nucleotide oligomerization domain 2–autophagy genes autophagy 16-like 1 (NOD2–ATG16L1) signaling axis disorder contributes to the dysfunction of autophagy. This paper is focused on the relationship between contactin associated protein-like 3 (CNTNAP3) and ATG16L1 expression in Crohn's disease. The results indicated that the expression of ATG16L1 is higher in some CD patients compared to normal controls. ATG16L1 was well correlated with the C-reactive protein (CRP) in some CD patients. In vitro study revealed that CNTNAP3 could upregulate the expression of ATG16L1 and increase autophagy vacuoles. |
format | Online Article Text |
id | pubmed-4391322 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-43913222015-04-16 CNTNAP3 Associated ATG16L1 Expression and Crohn's Disease Qiao, Yu Qi Huang, Mei Lan Zheng, Qing Wang, Tian Rong Xu, An Tao Cao, Yuan Zhao, Di Ran, Zhi Hua Shen, Jun Mediators Inflamm Research Article Autophagy is a common physiological process in cell homeostasis and regulation. Autophagy-related gene mutations and autophagy disorders are important in Crohn's disease (CD). The nucleotide oligomerization domain 2–autophagy genes autophagy 16-like 1 (NOD2–ATG16L1) signaling axis disorder contributes to the dysfunction of autophagy. This paper is focused on the relationship between contactin associated protein-like 3 (CNTNAP3) and ATG16L1 expression in Crohn's disease. The results indicated that the expression of ATG16L1 is higher in some CD patients compared to normal controls. ATG16L1 was well correlated with the C-reactive protein (CRP) in some CD patients. In vitro study revealed that CNTNAP3 could upregulate the expression of ATG16L1 and increase autophagy vacuoles. Hindawi Publishing Corporation 2015 2015-03-26 /pmc/articles/PMC4391322/ /pubmed/25883416 http://dx.doi.org/10.1155/2015/404185 Text en Copyright © 2015 Yu Qi Qiao et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Qiao, Yu Qi Huang, Mei Lan Zheng, Qing Wang, Tian Rong Xu, An Tao Cao, Yuan Zhao, Di Ran, Zhi Hua Shen, Jun CNTNAP3 Associated ATG16L1 Expression and Crohn's Disease |
title | CNTNAP3 Associated ATG16L1 Expression and Crohn's Disease |
title_full | CNTNAP3 Associated ATG16L1 Expression and Crohn's Disease |
title_fullStr | CNTNAP3 Associated ATG16L1 Expression and Crohn's Disease |
title_full_unstemmed | CNTNAP3 Associated ATG16L1 Expression and Crohn's Disease |
title_short | CNTNAP3 Associated ATG16L1 Expression and Crohn's Disease |
title_sort | cntnap3 associated atg16l1 expression and crohn's disease |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4391322/ https://www.ncbi.nlm.nih.gov/pubmed/25883416 http://dx.doi.org/10.1155/2015/404185 |
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