Virus-plus-susceptibility gene interaction determines Crohn's disease gene Atg16L1 phenotypes in intestine.
Cadwell, Ken; Patel, Khushbu K; Maloney, Nicole S; Liu, Ta-Chiang; Ng, Aylwin C Y; Storer, Chad E; Head, Richard D; Xavier, Ramnik; Stappenbeck, Thaddeus S; Virgin, Herbert W.
; 141(7): 1135-45, 2010 Jun 25.
Artigo em Inglês | MEDLINE | ID: mdl-20602997
XBP1 links ER stress to intestinal inflammation and confers genetic risk for human inflammatory bowel disease.
Crohn's disease: loss of tolerance or a disorder of autophagy?
Caspase-8 regulates TNF-α-induced epithelial necroptosis and terminal ileitis.
Type I interferon signalling in the intestinal epithelium affects Paneth cells, microbial ecology and epithelial regeneration.
Association of a functional variant in the Wnt co-receptor LRP6 with early onset ileal Crohn's disease.
Cellular and molecular mechanisms underlying NOD2 risk-associated polymorphisms in Crohn's disease.
Histone deacetylase 3 coordinates commensal-bacteria-dependent intestinal homeostasis.
Genomic ATG16L1 risk allele-restricted Paneth cell ER stress in quiescent Crohn's disease.
Paneth Cell Alterations in the Development and Phenotype of Crohn's Disease.
A key role for autophagy and the autophagy gene Atg16l1 in mouse and human intestinal Paneth cells.