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TRIM32:一种多功能蛋白,参与肌肉动态平衡、葡萄糖代谢和肿瘤发生。

TRIM32: A Multifunctional Protein Involved in Muscle Homeostasis, Glucose Metabolism, and Tumorigenesis.

机构信息

Department of Biochemistry and Molecular Biophysics, Kansas State University, Manhattan, KS 66506, USA.

Department of Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, 20156 Milan, Italy.

出版信息

Biomolecules. 2021 Mar 10;11(3):408. doi: 10.3390/biom11030408.

DOI:10.3390/biom11030408
PMID:33802079
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7999776/
Abstract

Human tripartite motif family of proteins 32 (TRIM32) is a ubiquitous multifunctional protein that has demonstrated roles in differentiation, muscle physiology and regeneration, and tumor suppression. Mutations in TRIM32 result in two clinically diverse diseases. A mutation in the B-box domain gives rise to Bardet-Biedl syndrome (BBS), a disease whose clinical presentation shares no muscle pathology, while mutations in the NHL (NCL-1, HT2A, LIN-41) repeats of TRIM32 causes limb-girdle muscular dystrophy type 2H (LGMD2H). TRIM32 also functions as a tumor suppressor, but paradoxically is overexpressed in certain types of cancer. Recent evidence supports a role for TRIM32 in glycolytic-mediated cell growth, thus providing a possible mechanism for TRIM32 in the accumulation of cellular biomass during regeneration and tumorigenesis, including in vitro and in vivo approaches, to understand the broad spectrum of TRIM32 functions. A special emphasis is placed on the utility of the model, a unique system to study glycolysis and anabolic pathways that contribute to the growth and homeostasis of both normal and tumor tissues.

摘要

人类三联基序蛋白家族 32(TRIM32)是一种普遍存在的多功能蛋白,已被证明在分化、肌肉生理学和再生以及肿瘤抑制中发挥作用。TRIM32 的突变导致两种临床表现不同的疾病。B 盒结构域的突变导致 Bardet-Biedl 综合征(BBS),该病的临床表现与肌肉病理学无关,而 NHL(NCL-1、HT2A、LIN-41)重复结构域的突变导致肢带型肌营养不良 2H(LGMD2H)。TRIM32 还作为一种肿瘤抑制因子,但奇怪的是在某些类型的癌症中过度表达。最近的证据支持 TRIM32 在糖酵解介导的细胞生长中的作用,从而为 TRIM32 在再生和肿瘤发生过程中积累细胞生物量提供了一种可能的机制,包括体外和体内方法,以了解 TRIM32 的广泛功能。特别强调了模型的实用性,这是一个独特的系统,用于研究糖酵解和合成代谢途径,这些途径有助于正常和肿瘤组织的生长和稳态。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c00/7999776/a733762b0983/biomolecules-11-00408-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c00/7999776/0af838073f26/biomolecules-11-00408-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c00/7999776/86580b3ba8e0/biomolecules-11-00408-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c00/7999776/926c619a4287/biomolecules-11-00408-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c00/7999776/01fad3e0aa66/biomolecules-11-00408-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c00/7999776/308dadc84d1d/biomolecules-11-00408-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c00/7999776/a733762b0983/biomolecules-11-00408-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c00/7999776/0af838073f26/biomolecules-11-00408-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c00/7999776/86580b3ba8e0/biomolecules-11-00408-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c00/7999776/926c619a4287/biomolecules-11-00408-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c00/7999776/01fad3e0aa66/biomolecules-11-00408-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c00/7999776/308dadc84d1d/biomolecules-11-00408-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c00/7999776/a733762b0983/biomolecules-11-00408-g006.jpg

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2
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Mol Biol Cell. 2021 Feb 1;32(3):260-273. doi: 10.1091/mbc.E20-07-0453. Epub 2020 Dec 9.
3
Activin signaling promotes muscle growth through InR/TORC1-dependent and -independent processes.
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MedComm (2020). 2024 Nov 11;5(11):e790. doi: 10.1002/mco2.790. eCollection 2024 Nov.
4
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PLoS Pathog. 2024 Nov 11;20(11):e1012312. doi: 10.1371/journal.ppat.1012312. eCollection 2024 Nov.
5
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iScience. 2024 Oct 9;27(11):111118. doi: 10.1016/j.isci.2024.111118. eCollection 2024 Nov 15.
6
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