Transcription profiling of mouse hypomorphic for ATG16L1 (implicated in Crohns disease) protein expression reveals a key role for autophagy and the autophagy gene Atg16l1 in mouse and human intestinal Paneth cells

ABSTRACT: Susceptibility to Crohn's disease, a complex inflammatory disease involving the small intestine, is controlled by over 30 loci. One Crohn's disease risk allele is in ATG16L1, a gene homologous to the essential yeast autophagy gene ATG16 (ref. 2). It is not known how ATG16L1 or autophagy contributes to intestinal biology or Crohn's disease pathogenesis. To address these questions, we generated and characterized mice that are hypomorphic for ATG16L1 protein expression, and validated conclusions on the basis of studies in these mice by analysing intestinal tissues that we collected from Crohn's disease patients carrying the Crohn's disease risk allele of ATG16L1. Here we show that ATG16L1 is a bona fide autophagy protein. Within the ileal epithelium, both ATG16L1 and a second essential autoph

ORGANISM(S): Mus musculus

SUBMITTER: Thaddeus Stappenbeck 

PROVIDER: E-GEOD-13512 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress