miR-17-92a-1 cluster host gene
Last updated 14 Apr 2023
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The MIR17HG gene provides instructions for making the miR-17~92 microRNA (miRNA) cluster. MiRNAs are short pieces of RNA, a chemical cousin of DNA. These molecules control gene expression by blocking protein production. The miR-17~92 cluster includes six miRNAs: miR-17, miR-18a, miR-19a, miR-19b-1, miR-20a, and miR-92a-1. MiRNAs in this cluster control the expression of hundreds of genes. These miRNAs help regulate signaling pathways that direct several cellular processes involved in growth and development, including cell growth and division (proliferation), cell maturation (differentiation), and the self-destruction of cells (apoptosis). Studies suggest that the miR-17~92 cluster is necessary for normal development of the skeleton, heart, kidneys, lungs, and nervous system.
Normal function
The MIR17HG gene provides instructions for making the miR-17~92 microRNA (miRNA) cluster. MiRNAs are short pieces of RNA, a chemical cousin of DNA. These molecules control gene expression by blocking protein production. The miR-17~92 cluster includes six miRNAs: miR-17, miR-18a, miR-19a, miR-19b-1, miR-20a, and miR-92a-1. MiRNAs in this cluster control the expression of hundreds of genes. These miRNAs help regulate signaling pathways that direct several cellular processes involved in growth and development, including cell growth and division (proliferation), cell maturation (differentiation), and the self-destruction of cells (apoptosis). Studies suggest that the miR-17~92 cluster is necessary for normal development of the skeleton, heart, kidneys, lungs, and nervous system.
The MIR17HG gene belongs to a class of genes known as oncogenes. When mutated, oncogenes have the potential to cause normal cells to become cancerous.
Conditions referring to this gene or chromosome
Other names
C13orf25
FGLDS2
FLJ14178
LINC00048
MIHG1
miR-17-92
MIRH1
MIRHG1
NCRNA00048
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Further reading and references
- miR-17-92a-1 cluster host gene; MedlinePlus, National Library of Medicine.
- de Pontual L, Yao E, Callier P, Faivre L, Drouin V, Cariou S, Van Haeringen A, Genevieve D, Goldenberg A, Oufadem M, Manouvrier S, Munnich A, Vidigal JA, Vekemans M, Lyonnet S, Henrion-Caude A, Ventura A, Amiel J. Germline deletion of the miR-17 approximately 92 cluster causes skeletal and growth defects in humans. Nat Genet. 2011 Sep 4;43(10):1026-30. doi: 10.1038/ng.915.
- Fang LL, Wang XH, Sun BF, Zhang XD, Zhu XH, Yu ZJ, Luo H. Expression, regulation and mechanism of action of the miR-17-92 cluster in tumor cells (Review). Int J Mol Med. 2017 Dec;40(6):1624-1630. doi: 10.3892/ijmm.2017.3164. Epub 2017 Sep 29.
- Grote LE, Repnikova EA, Amudhavalli SM. Expanding the phenotype of feingold syndrome-2. Am J Med Genet A. 2015 Dec;167A(12):3219-25. doi: 10.1002/ajmg.a.37368. Epub 2015 Sep 11.
- Hemmat M, Rumple MJ, Mahon LW, Strom CM, Anguiano A, Talai M, Nguyen B, Boyar FZ. Short stature, digit anomalies and dysmorphic facial features are associated with the duplication of miR-17 ~ 92 cluster. Mol Cytogenet. 2014 Apr 16;7:27. doi: 10.1186/1755-8166-7-27. eCollection 2014.
- Kannu P, Campos-Xavier AB, Hull D, Martinet D, Ballhausen D, Bonafe L. Post-axial polydactyly type A2, overgrowth and autistic traits associated with a chromosome 13q31.3 microduplication encompassing miR-17-92 and GPC5. Eur J Med Genet. 2013 Aug;56(8):452-7. doi: 10.1016/j.ejmg.2013.06.001. Epub 2013 Jun 20.
- Mirzamohammadi F, Kozlova A, Papaioannou G, Paltrinieri E, Ayturk UM, Kobayashi T. Distinct molecular pathways mediate Mycn and Myc-regulated miR-17-92 microRNA action in Feingold syndrome mouse models. Nat Commun. 2018 Apr 10;9(1):1352. doi: 10.1038/s41467-018-03788-7.
- Mogilyansky E, Rigoutsos I. The miR-17/92 cluster: a comprehensive update on its genomics, genetics, functions and increasingly important and numerous roles in health and disease. Cell Death Differ. 2013 Dec;20(12):1603-14. doi: 10.1038/cdd.2013.125.
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