Cited 14 time in webofscience Cited 15 time in scopus

BNIP3 is degraded by ULK1-dependent autophagy via MTORC1 and AMPK

Title
BNIP3 is degraded by ULK1-dependent autophagy via MTORC1 and AMPK
Authors
Park, CW[Park, Chang Wook]Hong, SM[Hong, Sun Mi]Kim, ES[Kim, Eung-Sam]Kwon, JH[Kwon, Jung Hee]Kim, KT[Kim, Kyong-Tai]Nam, HG[Nam, Hong Gil]Choi, KY[Choi, Kwan Yong]
DGIST Authors
Nam, HG[Nam, Hong Gil]
Issue Date
2013-03
Citation
Autophagy, 9(3), 345-360
Type
Article
Article Type
Article
Keywords
AMPKAutophagyBECN1BNIP3Controlled StudyDown-RegulationEnzyme RegulationFemaleGenetic TranscriptionHumanHuman CellHydroxymethylglutaryl Coenzyme A Reductase KinaseHypoxiaHypoxia-Inducible Factor-1 AlphaKwashiorkorMacroautophagyMammalian Target of Rapamycin Complex 1Microtubule Associated Protein 1MitochondrionMTORPhosphotransferaseProteasomeProtein BNip3Protein DegradationSignal TransductionStarvationTorin1ULK1UNC 51 Like KinaseUnclassified Drug
ISSN
1554-8627
Abstract
BNIP3 (BCL2/adenovirus E1B 19 kDa interacting protein 3) is an atypical BH3-only protein that is induced by hypoxiainducible factor 1 (HI F1) under hypoxia. BNIP3 is primarily regulated at the transcriptional level. However, little is known about the underlying mechanism of BNIP3 degradation. In this study, we found that BNIP3 was downregulated when hypoxia was accompanied by amino acid starvation. The BNIP3 downregulation did not occur at the transcription level and was independent of HI F1A. BNIP3 was primarily degraded by the proteasome, but BNIP3 was subjected to both proteasomal and autophagic degradation in response to starvation. The autophagic degradation of BNIP3 was dependent on ATG7 and MAP1LC3. We determined that autophagic degradation of BNIP3 was specifically regulated by ULK1 via the MTOR-AMPK pathway. Moreover, we confirmed that BNIP3 could play a protective role in tumor cells under hypoxia, and the treatment with Torin1, an MTOR inhibitor, decreased the BNIP3 level and enhanced the death of hypoxic tumor cells. © 2013 Landes Bioscience.
URI
http://hdl.handle.net/20.500.11750/1607
DOI
10.4161/auto.23072
Publisher
Taylor and Francis Inc.
Related Researcher
Files:
There are no files associated with this item.
Collection:
New BiologyETC1. Journal Articles


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