# USMG5

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**Up-regulated during skeletal muscle growth protein 5 (USMG5)**, also known as **ATP synthase membrane subunit DAPIT (ATP5MD)**, **Diabetes-associated protein in insulin-sensitive tissues**, or **HCV F-transactivated protein 2** is a [protein](/source/Protein) that in humans is encoded by the *USMG5* [gene](/source/Gene). [1][2][3]

## Structure

The *USMG5* gene is located on the [q arm](/source/Locus_(genetics)) of [chromosome 10](/source/Chromosome_10) at position 24.33 and it spans 7,463 base pairs.[1] The *USMG5* gene produces a 6.46 kDa protein composed of 58 [amino acids](/source/Amino_acids).[4][5] USMG5 is a small subunit of the [mitochondrial ATP synthase](/source/ATP_synthase) (complex V), as well as the [lysosomal](/source/Lysosome) [V-ATPase](/source/V-ATPase).[6] The protein is associated with the [ATP synthase](/source/ATP_synthase) in a [stoichiometric](/source/Stoichiometric) manner.[7] The structure of the protein contains a [putative transmembrane segment](/source/Transmembrane_domain) and a single presumed [α-helix](/source/%CE%91-helix) that spans from amino acid 23 to 45. The structure has been found to be similar to its [putative](/source/Putative) [yeast](/source/Yeast) [ortholog](/source/Ortholog).[8]

## Function

The human *USMG5* gene codes for a [protein](/source/Protein) with a role in maintaining and regulating the [ATP synthase](/source/ATP_synthase) population in the [mitochondria](/source/Mitochondria).[2][3][8] The protein is responsible for several minor roles that are expendable for the core function of [complex V](/source/ATP_synthase).[7] A knockdown of the protein has been shown to lead to reduced ATP synthesis rate and CV dimer expression, while the wild type has been shown to boost the [dimerization](/source/Dimer_(chemistry)) of [complex V](/source/ATP_synthase) as well as enhance the [ATP synthesis](/source/ATP_synthesis) rate.[9]

## Clinical Significance

Mutations in *USMG5* has been found to result in [mitochondrial deficiencies](/source/Mitochondrial_disease) and associated disorders of the [mitochondrial ATP synthase](/source/ATP_synthase) (complex V). [Homozygous](/source/Zygosity) splice-site [mutations](/source/Mutations) (c.87 + 1G>C) in the Ashkenazi Jewish population have been associated with cases of [leigh syndrome](/source/Leigh_syndrome) caused by the decrease of [Complex V](/source/ATP_synthase) dimerization and ATP synthesis. [Leigh syndrome](/source/Leigh_syndrome) is a heterogeneous mitochondrial oxidative phosphorylation (OXPHOS) disease that is characterized by [psychomotor retardation](/source/Psychomotor_retardation) and [necrotizing](/source/Necrosis) lesions in the brain.[9]

## Interactions

USMG5 is a component of the [ATP synthase complex](/source/ATP_synthase), and has co-complex interactions with [ATP5F1](/source/ATP5F1), [ATP5MC1](/source/ATP5MC1), [TP5F1E](/source/TP5F1E), [ATP5PD](/source/ATP5PD), [ATP5ME](/source/ATP5ME), [ATP5PF](/source/ATP5PF), [ATP5MF](/source/ATP5MF), and others.[2][3]

## References

1. ["Entrez Gene: ATP synthase membrane subunit DAPIT"](https://www.ncbi.nlm.nih.gov/gene/84833). Retrieved 2018-08-14.

1. ["USMG5 - Up-regulated during skeletal muscle growth protein 5 - Homo sapiens (Human) - USMG5 gene & protein"](https://www.uniprot.org/uniprot/P30049). Retrieved 2018-08-07.

1. "UniProt: the universal protein knowledgebase". *Nucleic Acids Research*. **45** (D1): D158–D169. January 2017. [doi:10.1093/nar/gkw1099](https://doi.org/10.1093/nar/gkw1099). [PMC 5210571](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5210571). [PMID 27899622](https://pubmed.ncbi.nlm.nih.gov/27899622)

1. Zong NC, Li H, Li H, Lam MP, Jimenez RC, Kim CS, Deng N, Kim AK, Choi JH, Zelaya I, Liem D, Meyer D, Odeberg J, Fang C, Lu HJ, Xu T, Weiss J, Duan H, Uhlen M, Yates JR, Apweiler R, Ge J, Hermjakob H, Ping P (October 2013). "Integration of cardiac proteome biology and medicine by a specialized knowledgebase". *Circulation Research*. **113** (9): 1043–1053. [doi:10.1161/CIRCRESAHA.113.301151](https://doi.org/10.1161/CIRCRESAHA.113.301151). [PMC 4076475](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4076475). [PMID 23965338](https://pubmed.ncbi.nlm.nih.gov/23965338)

1. ["Up-regulated during skeletal muscle growth protein 5"](https://web.archive.org/web/20180815024618/https://amino.heartproteome.org/web/protein/Q96IX5). *Cardiac Organellar Protein Atlas Knowledgebase (COPaKB)*. Archived from [the original](https://amino.heartproteome.org/web/protein/Q96IX5) on 2018-08-15. Retrieved 2018-08-14.

1. Kontro H, Hulmi JJ, Rahkila P, Kainulainen H (May 2012). "Cellular and tissue expression of DAPIT, a phylogenetically conserved peptide". *European Journal of Histochemistry*. **56** (2): e18. [doi:10.4081/ejh.2012.18](https://doi.org/10.4081/ejh.2012.18). [PMC 3428967](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3428967). [PMID 22688299](https://pubmed.ncbi.nlm.nih.gov/22688299)

1. Ohsakaya S, Fujikawa M, Hisabori T, Yoshida M (June 2011). "Knockdown of DAPIT (diabetes-associated protein in insulin-sensitive tissue) results in loss of ATP synthase in mitochondria". *The Journal of Biological Chemistry*. **286** (23): 20292–20296. [doi:10.1074/jbc.M110.198523](https://doi.org/10.1074/jbc.M110.198523). [PMC 3121504](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3121504). [PMID 21345788](https://pubmed.ncbi.nlm.nih.gov/21345788)

1. Kontro H, Hulmi JJ, Rahkila P, Kainulainen H (May 2012). "Cellular and tissue expression of DAPIT, a phylogenetically conserved peptide". *European Journal of Histochemistry*. **56** (2): e18. [doi:10.4081/ejh.2012.18](https://doi.org/10.4081/ejh.2012.18). [PMC 3428967](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3428967). [PMID 22688299](https://pubmed.ncbi.nlm.nih.gov/22688299)

1. Barca E, Ganetzky RD, Potluri P, Juanola-Falgarona M, Gai X, Li D, Jalas C, Hirsch Y, Emmanuele V, Tadesse S, Ziosi M, Akman HO, Chung WK, Tanji K, McCormick EM, Place E, Consugar M, Pierce EA, Hakonarson H, Wallace DC, Hirano M, Falk MJ (October 2018). "USMG5 Ashkenazi Jewish founder mutation impairs mitochondrial complex V dimerization and ATP synthesis". *Human Molecular Genetics*. **27** (19): 3305–3312. [doi:10.1093/hmg/ddy231](https://doi.org/10.1093/hmg/ddy231). [PMC 6140788](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6140788). [PMID 29917077](https://pubmed.ncbi.nlm.nih.gov/29917077)

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Adapted from the Wikipedia article [USMG5](https://en.wikipedia.org/wiki/USMG5) by Wikipedia contributors ([contributor history](https://en.wikipedia.org/wiki/USMG5?action=history)). Available under [Creative Commons Attribution-ShareAlike 4.0 International](https://creativecommons.org/licenses/by-sa/4.0/). Changes may have been made.