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CNTNAP3 associated ATG16L1 expression and Crohn's disease.

Mediators of inflammation (2015-04-18)
Yu Qi Qiao, Mei Lan Huang, Qing Zheng, Tian Rong Wang, An Tao Xu, Yuan Cao, Di Zhao, Zhi Hua Ran, Jun Shen
ABSTRACT

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.

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Sigma-Aldrich
MISSION® esiRNA, targeting human CNTNAP3, CH17-296N19.1