CNTNAP3 associated ATG16L1 expression and Crohn's disease.
Yu Qi QiaoMei Lan HuangQing ZhengTian Rong WangAn Tao XuYuan CaoDi ZhaoZhi Hua RanJun ShenPublished in: Mediators of inflammation (2015)
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.
Keyphrases
- cell death
- endoplasmic reticulum stress
- oxidative stress
- poor prognosis
- signaling pathway
- end stage renal disease
- newly diagnosed
- ejection fraction
- peritoneal dialysis
- binding protein
- prognostic factors
- gene expression
- long non coding rna
- stem cells
- cell therapy
- dna methylation
- transcription factor
- nk cells
- genome wide identification