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COMMD1 expression is controlled by critical residues that determine XIAP binding

Maine, Gabriel N., Mao, Xicheng, Muller, Patricia A., Komarck, Christine M., Klomp, Leo W. J., Burstein, Ezra·2009·Biochemical Journal
DOI 10.1042/bj20080854PMC PMC2606926
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Abstract

COMMD {COMM [copper metabolism Murr1 (mouse U2af1-rs1 region 1)] domain-containing} proteins participate in several cellular processes, ranging from NF-κB (nuclear factor κB) regulation, copper homoeostasis, sodium transport and adaptation to hypoxia. The best-studied member of this family is COMMD1, but relatively little is known about its regulation, except that XIAP [X-linked IAP (inhibitor of apoptosis)] functions as its ubiquitin ligase. In the present study, we identified that the COMM domain of COMMD1 is required for its interaction with XIAP, and other COMMD proteins can similarly interact with IAPs. Two conserved leucine repeats within the COMM domain were found to be critically required for XIAP binding. A COMMD1 mutant which was unable to bind to XIAP demonstrated a complete loss of basal ubiquitination and great stabilization of the protein. Underscoring the importance of IAP-mediated ubiquitination, we found that long-term expression of wild-type COMMD1 results in nearly physiological protein levels as a result of increased ubiquitination, but this regulatory event is circumvented when a mutant form that cannot bind XIAP is expressed. In summary, our findings indicate that COMMD1 expression is controlled primarily by protein ubiquitination, and its interaction with IAP proteins plays an essential role.

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  • The fact that the endosomal recycling process is primarily regulated at the post-translational (protein) level supports the hypothesis that the CCDC93 variant (rs17512204) encodes a protein with improved function.

    “This can be explained by the fact that this process is primarily regulated at the post-translational (protein) level, 12,13,40 which, in turn, supports our hypothesis that the CCDC93 variant (rs17512204) encodes a protein with improved function.”

    From A common variant in CCDC93 protects against myocardial infarction and cardiovascular mortality by regulating endosomal trafficking of low-density lipoprotein receptor (2020) · cites this paper as [40]

    The Results section, “COMMD1 ubiquitination controls basal levels of expression” (page unavailable), says COMMD1 protein levels are regulated primarily through a post-transcriptional mechanism involving ubiquitination. It does not establish that endosomal recycling as a process is primarily regulated at the protein level. The CCDC93 variant’s improved function is presented as the citing authors’ hypothesis, not a finding attributed to this source. (LLM, conf=0.84)

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Research works printed but not linked: 26

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Metadata

Authors
Maine, G. N., Mao, X., Muller, P. A., Komarck, C. M., Klomp, L. W. J., & Burstein, E.
Affiliations
  • Department of Internal Medicine, University of Michigan Medical School, 109 Zina Pitcher Place - SPC 2200, Ann Arbor, MI 48109, U.S.A.
  • Laboratory of Metabolic and Endocrine Diseases, University of Utrecht, Room KC.02.069.1, Lundlaan 6, 3584 EA, Utrecht, The Netherlands
Venue
Biochemical Journal
Publisher
Portland Press Ltd.
Published
2008-12-23
Volume
417
Issue
2
Pages
601-609
ISSN
  • 0264-6021
  • 1470-8728
DOI
10.1042/bj20080854
PMC
PMC2606926
Cited by
57
References
1
Language
en

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