Cell biology: Stressful genetics in Crohn's disease

Arthur Kaser; Richard S Blumberg

doi:10.1038/nature13060

Cell biology: Stressful genetics in Crohn's disease

Nature. 2014 Feb 27;506(7489):441-2. doi: 10.1038/nature13060. Epub 2014 Feb 19.

Authors

Arthur Kaser¹, Richard S Blumberg²

Affiliations

¹ Division of Gastroenterology and Hepatology, Department of Medicine, Addenbrooke's Hospital, University of Cambridge, Cambridge CB2 0QQ, UK.
² Division of Gastroenterology, Hepatology and Endoscopy, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.

Abstract

A common variant of the autophagy protein ATG16L1 is a risk factor for Crohn’s disease. But the genetic alteration is revealed only when the protein is cleaved by the enzyme caspase 3 during cellular stress.

Publication types

Comment

MeSH terms

Animals
Autophagy-Related Proteins
Carrier Proteins / genetics*
Carrier Proteins / metabolism*
Caspase 3 / metabolism*
Crohn Disease / genetics*
Female
Humans
Male
Polymorphism, Single Nucleotide / genetics*
Proteolysis*

Substances

ATG16L1 protein, human
Autophagy-Related Proteins
Carrier Proteins
CASP3 protein, human
Caspase 3

Abstract

Publication types

MeSH terms

Substances

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