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The Trim39 ubiquitin ligase inhibits APC/CCdh1-mediated degradation of the Bax activator MOAP-1.

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Date
2012-04-30
Authors
Huang, Nai-Jia
Zhang, Liguo
Tang, Wanli
Chen, Chen
Yang, Chih-Sheng
Kornbluth, Sally
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Abstract
Proapoptotic Bcl-2 family members, such as Bax, promote release of cytochrome c from mitochondria, leading to caspase activation and cell death. It was previously reported that modulator of apoptosis protein 1 (MOAP-1), an enhancer of Bax activation induced by DNA damage, is stabilized by Trim39, a protein of unknown function. In this paper, we show that MOAP-1 is a novel substrate of the anaphase-promoting complex (APC/C(Cdh1)) ubiquitin ligase. The influence of Trim39 on MOAP-1 levels stems from the ability of Trim39 (a RING domain E3 ligase) to directly inhibit APC/C(Cdh1)-mediated protein ubiquitylation. Accordingly, small interfering ribonucleic acid-mediated knockdown of Cdh1 stabilized MOAP-1, thereby enhancing etoposide-induced Bax activation and apoptosis. These data identify Trim39 as a novel APC/C regulator and provide an unexpected link between the APC/C and apoptotic regulation via MOAP-1.
Type
Journal article
Subject
Adaptor Proteins, Signal Transducing
Adenomatous Polyposis Coli Protein
Apoptosis
Apoptosis Regulatory Proteins
Blotting, Western
Cadherins
Carrier Proteins
DNA Damage
Flow Cytometry
G1 Phase
HeLa Cells
Humans
Immunoprecipitation
RNA, Small Interfering
Recombinant Proteins
Ubiquitin
Ubiquitination
bcl-2-Associated X Protein
Permalink
https://hdl.handle.net/10161/8382
Published Version (Please cite this version)
10.1083/jcb.201111141
Publication Info
Huang, Nai-Jia; Zhang, Liguo; Tang, Wanli; Chen, Chen; Yang, Chih-Sheng; & Kornbluth, Sally (2012). The Trim39 ubiquitin ligase inhibits APC/CCdh1-mediated degradation of the Bax activator MOAP-1. J Cell Biol, 197(3). pp. 361-367. 10.1083/jcb.201111141. Retrieved from https://hdl.handle.net/10161/8382.
This is constructed from limited available data and may be imprecise. To cite this article, please review & use the official citation provided by the journal.
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Scholars@Duke

Kornbluth

Sally A. Kornbluth

Jo Rae Wright University Distinguished Professor
Our lab studies the regulation of complex cellular processes, including cell cycle progression and programmed cell death (apoptosis). These tightly orchestrated processes are critical for appropriate cell proliferation and cell death, and when they go awry can result in cancer and degenerative disorders. Within these larger fields, we have focused on understanding the cellular mechanisms that prevent the onset of mitosis prior to the completion of DNA replication, the process
Zhang

Liguo Zhang

Academic Dean, Dku Undergrad Students
Alphabetical list of authors with Scholars@Duke profiles.
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