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 contribut...
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| Main Authors: | , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2015-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2015/404185 |
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| _version_ | 1841524732238757888 |
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| author | Yu Qi Qiao Mei Lan Huang Qing Zheng Tian Rong Wang An Tao Xu Yuan Cao Di Zhao Zhi Hua Ran Jun Shen |
| author_facet | Yu Qi Qiao Mei Lan Huang Qing Zheng Tian Rong Wang An Tao Xu Yuan Cao Di Zhao Zhi Hua Ran Jun Shen |
| author_sort | Yu Qi Qiao |
| collection | DOAJ |
| 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 | Article |
| id | doaj-art-7ee732fcf246438daf7703ce5c2b8fa5 |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2015-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-7ee732fcf246438daf7703ce5c2b8fa52025-02-03T05:47:31ZengWileyMediators of Inflammation0962-93511466-18612015-01-01201510.1155/2015/404185404185CNTNAP3 Associated ATG16L1 Expression and Crohn’s DiseaseYu Qi Qiao0Mei Lan Huang1Qing Zheng2Tian Rong Wang3An Tao Xu4Yuan Cao5Di Zhao6Zhi Hua Ran7Jun Shen8Division of Gastroenterology and Hepatology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, ChinaDivision of Gastroenterology and Hepatology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, ChinaDivision of Gastroenterology and Hepatology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, ChinaDivision of Gastroenterology and Hepatology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, ChinaDivision of Gastroenterology and Hepatology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, ChinaDivision of Gastroenterology and Hepatology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, ChinaDivision of Gastroenterology and Hepatology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, ChinaDivision of Gastroenterology and Hepatology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, ChinaDivision of Gastroenterology and Hepatology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, ChinaAutophagy 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.http://dx.doi.org/10.1155/2015/404185 |
| spellingShingle | Yu Qi Qiao Mei Lan Huang Qing Zheng Tian Rong Wang An Tao Xu Yuan Cao Di Zhao Zhi Hua Ran Jun Shen CNTNAP3 Associated ATG16L1 Expression and Crohn’s Disease Mediators of Inflammation |
| 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 |
| url | http://dx.doi.org/10.1155/2015/404185 |
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