TRIM31 promotes Atg5/Atg7-independent autophagy in intestinal cells

While non-canonical, Atg5/Atg7-independent autophagy has been reported to occur, molecular details of alternative autophagy pathways remain unknown. Here, the authors report that the protein TRIM31 mediates alternative autophagy in intestinal cells, which protects against pathogenic bacteria.

Bibliographic Details
Main Authors: Eun A. Ra, Taeyun A. Lee, Seung Won Kim, Areum Park, Hyun jin Choi, Insook Jang, Sujin Kang, Jae Hee Cheon, Jin Won Cho, Ji Eun Lee, Sungwook Lee, Boyoun Park
Format: Article
Language:English
Published: Nature Publishing Group 2016-05-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/ncomms11726
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spelling doaj-105465ca7a7148d1ab2b63fadbbbcb8b2021-05-11T10:37:12ZengNature Publishing GroupNature Communications2041-17232016-05-017111510.1038/ncomms11726TRIM31 promotes Atg5/Atg7-independent autophagy in intestinal cellsEun A. Ra0Taeyun A. Lee1Seung Won Kim2Areum Park3Hyun jin Choi4Insook Jang5Sujin Kang6Jae Hee Cheon7Jin Won Cho8Ji Eun Lee9Sungwook Lee10Boyoun Park11Department of Systems Biology, College of Life Science and Biotechnology, Yonsei UniversityDepartment of Systems Biology, College of Life Science and Biotechnology, Yonsei UniversityDepartment of Internal Medicine and Institute of Gastroenterology, Yonsei University College of MedicineDepartment of Systems Biology, College of Life Science and Biotechnology, Yonsei UniversityDepartment of Systems Biology, College of Life Science and Biotechnology, Yonsei UniversityDepartment of Integrated OMICS for Biomedical Science, Yonsei UniversityDepartment of Systems Biology, College of Life Science and Biotechnology, Yonsei UniversityDepartment of Internal Medicine and Institute of Gastroenterology, Yonsei University College of MedicineDepartment of Integrated OMICS for Biomedical Science, Yonsei UniversityDepartment of Health Science and Technology, Samsung Advanced Institute for Health Sciences and Technology, Sungkyunkwan UniversityDepartment of Systems Biology, College of Life Science and Biotechnology, Yonsei UniversityDepartment of Systems Biology, College of Life Science and Biotechnology, Yonsei UniversityWhile non-canonical, Atg5/Atg7-independent autophagy has been reported to occur, molecular details of alternative autophagy pathways remain unknown. Here, the authors report that the protein TRIM31 mediates alternative autophagy in intestinal cells, which protects against pathogenic bacteria.https://doi.org/10.1038/ncomms11726
collection DOAJ
language English
format Article
sources DOAJ
author Eun A. Ra
Taeyun A. Lee
Seung Won Kim
Areum Park
Hyun jin Choi
Insook Jang
Sujin Kang
Jae Hee Cheon
Jin Won Cho
Ji Eun Lee
Sungwook Lee
Boyoun Park
spellingShingle Eun A. Ra
Taeyun A. Lee
Seung Won Kim
Areum Park
Hyun jin Choi
Insook Jang
Sujin Kang
Jae Hee Cheon
Jin Won Cho
Ji Eun Lee
Sungwook Lee
Boyoun Park
TRIM31 promotes Atg5/Atg7-independent autophagy in intestinal cells
Nature Communications
author_facet Eun A. Ra
Taeyun A. Lee
Seung Won Kim
Areum Park
Hyun jin Choi
Insook Jang
Sujin Kang
Jae Hee Cheon
Jin Won Cho
Ji Eun Lee
Sungwook Lee
Boyoun Park
author_sort Eun A. Ra
title TRIM31 promotes Atg5/Atg7-independent autophagy in intestinal cells
title_short TRIM31 promotes Atg5/Atg7-independent autophagy in intestinal cells
title_full TRIM31 promotes Atg5/Atg7-independent autophagy in intestinal cells
title_fullStr TRIM31 promotes Atg5/Atg7-independent autophagy in intestinal cells
title_full_unstemmed TRIM31 promotes Atg5/Atg7-independent autophagy in intestinal cells
title_sort trim31 promotes atg5/atg7-independent autophagy in intestinal cells
publisher Nature Publishing Group
series Nature Communications
issn 2041-1723
publishDate 2016-05-01
description While non-canonical, Atg5/Atg7-independent autophagy has been reported to occur, molecular details of alternative autophagy pathways remain unknown. Here, the authors report that the protein TRIM31 mediates alternative autophagy in intestinal cells, which protects against pathogenic bacteria.
url https://doi.org/10.1038/ncomms11726
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