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Article

ULK1‐mediated phosphorylation of ATG16L1 promotes xenophagy, but destabilizes the ATG16L1 Crohn's mutant

24 May 2019

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Share to Adenosine and Purinergic Signaling
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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Identifiers

PMID: 31267703
DOI: 10.15252/embr.201846885

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ULK1‐mediated phosphorylation of ATG16L1 promotes xenophagy, but destabilizes the ATG16L1 Crohn's mutantPMID 31267703Read ↗

The role of ATG16L2 in autophagy and diseaseSemantic proximity Read ↗

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Distinct Tissue-Specific Roles for the Disease-Associated Autophagy Genes ATG16L2 and ATG16L1Semantic proximity Read ↗

A Deficiency in the Autophagy Gene Atg16L1 Enhances Resistance to Enteric Bacterial InfectionSemantic proximity Read ↗

The T300A Crohn's disease risk polymorphism impairs function of the WD40 domain of ATG16L1.Semantic proximity Read ↗

ATG16L1 Crohn's disease risk stresses the endoplasmic reticulum of Paneth cells.Semantic proximity Read ↗

An alteration in ATG16L1 stability in Crohn disease.Semantic proximity Read ↗

Structure and function of the ULK1 complex in autophagySemantic proximity Read ↗

Differential Involvement of Atg16L1 in Crohn Disease and Canonical AutophagySemantic proximity Read ↗

Autophagy and Crohns Disease: At the Crossroads of Infection, Inflammation, Immunity, and CancerSemantic proximity Read ↗

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