MIR503
MicroRNA 503 is a non-coding RNA molecule that in humans is encoded by the MIR503 gene. [3]
MIR503 | |||||||||||||||||||||||||||||||||||||||||||||||||||
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Aliases | MIR503, MIRN503, hsa-mir-503, mir-503, microRNA 503 | ||||||||||||||||||||||||||||||||||||||||||||||||||
External IDs | OMIM: 300865 GeneCards: MIR503 | ||||||||||||||||||||||||||||||||||||||||||||||||||
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Function
microRNAs (miRNAs) are short (20-24 nt) non-coding RNAs that are involved in post-transcriptional regulation of gene expression in multicellular organisms by affecting both the stability and translation of mRNAs. miRNAs are transcribed by RNA polymerase II as part of capped and polyadenylated primary transcripts (pri-miRNAs) that can be either protein-coding or non-coding.
The primary transcript is cleaved by the Drosha ribonuclease III enzyme to produce an approximately 70-nt stem-loop precursor miRNA (pre-miRNA), which is further cleaved by the cytoplasmic Dicer ribonuclease to generate the mature miRNA and antisense miRNA star (miRNA*) products.
The mature miRNA is incorporated into a RNA-induced silencing complex (RISC), which recognizes target mRNAs through imperfect base pairing with the miRNA and most commonly results in translational inhibition or destabilization of the target mRNA. The RefSeq represents the predicted microRNA stem-loop.
References
- GRCh38: Ensembl release 89: ENSG00000208005 - Ensembl, May 2017
- "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
- "Entrez Gene: MicroRNA 503". Retrieved 2017-05-30.
Further reading
- Jiang Q, Feng MG, Mo YY (2009). "Systematic validation of predicted microRNAs for cyclin D1". BMC Cancer. 9: 194. doi:10.1186/1471-2407-9-194. PMC 2728105. PMID 19538740.
- Sarkar S, Dey BK, Dutta A (2010). "MiR-322/424 and -503 are induced during muscle differentiation and promote cell cycle quiescence and differentiation by down-regulation of Cdc25A". Mol. Biol. Cell. 21 (13): 2138–49. doi:10.1091/mbc.E10-01-0062. PMC 2893979. PMID 20462953.
- Caporali A, Meloni M, Völlenkle C, Bonci D, Sala-Newby GB, Addis R, Spinetti G, Losa S, Masson R, Baker AH, Agami R, le Sage C, Condorelli G, Madeddu P, Martelli F, Emanueli C (2011). "Deregulation of microRNA-503 contributes to diabetes mellitus-induced impairment of endothelial function and reparative angiogenesis after limb ischemia". Circulation. 123 (3): 282–91. doi:10.1161/CIRCULATIONAHA.110.952325. PMID 21220732.
- Zhou J, Wang W (2011). "Analysis of microRNA expression profiling identifies microRNA-503 regulates metastatic function in hepatocellular cancer cell". J Surg Oncol. 104 (3): 278–83. doi:10.1002/jso.21941. PMID 21495032. S2CID 23582191.
- Cheng G, Sun S, Wang Z, Jin S (2012). "Investigation of the interaction between the MIR-503 and CD40 genes in irradiated U937 cells". Radiat Oncol. 7: 38. doi:10.1186/1748-717X-7-38. PMC 3325872. PMID 22429276.
- Roy P, Bhattacharya G, Lahiri A, Dasgupta UB, Banerjee D, Chandra S, Das M (2012). "hsa-miR-503 is downregulated in β thalassemia major". Acta Haematol. 128 (3): 187–9. doi:10.1159/000339492. PMID 22890417. S2CID 5328558.
- Kim J, Kang Y, Kojima Y, Lighthouse JK, Hu X, Aldred MA, McLean DL, Park H, Comhair SA, Greif DM, Erzurum SC, Chun HJ (2013). "An endothelial apelin-FGF link mediated by miR-424 and miR-503 is disrupted in pulmonary arterial hypertension". Nat. Med. 19 (1): 74–82. doi:10.1038/nm.3040. PMC 3540168. PMID 23263626.
- Zhou B, Ma R, Si W, Li S, Xu Y, Tu X, Wang Q (2013). "MicroRNA-503 targets FGF2 and VEGFA and inhibits tumor angiogenesis and growth". Cancer Lett. 333 (2): 159–69. doi:10.1016/j.canlet.2013.01.028. PMID 23352645.
- Zhou R, Gong AY, Chen D, Miller RE, Eischeid AN, Chen XM (2013). "Histone deacetylases and NF-kB signaling coordinate expression of CX3CL1 in epithelial cells in response to microbial challenge by suppressing miR-424 and miR-503". PLOS ONE. 8 (5): e65153. Bibcode:2013PLoSO...865153Z. doi:10.1371/journal.pone.0065153. PMC 3665534. PMID 23724129.
This article incorporates text from the United States National Library of Medicine, which is in the public domain.