microRNA 203a
MicroRNA 203a is a small RNA that in humans is encoded by the preMIR203A gene. [3]
| MIR203A | |||||||||||||||||||||||||||||||||||||||||||||||||||
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| Identifiers | |||||||||||||||||||||||||||||||||||||||||||||||||||
| Aliases | MIR203A, MIR203, MIRN203, hsa-mir-203a, miR-203, miRNA203, mir-203a, microRNA 203a | ||||||||||||||||||||||||||||||||||||||||||||||||||
| External IDs | OMIM: 611899 GeneCards: MIR203A | ||||||||||||||||||||||||||||||||||||||||||||||||||
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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 an 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: ENSG00000207568 - Ensembl, May 2017
- "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
- "Entrez Gene: MicroRNA 203a". Retrieved 2017-07-03.
Further reading
- Sonkoly E, Wei T, Janson PC, Sääf A, Lundeberg L, Tengvall-Linder M, Norstedt G, Alenius H, Homey B, Scheynius A, Ståhle M, Pivarcsi A (2007). "MicroRNAs: novel regulators involved in the pathogenesis of psoriasis?". PLOS ONE. 2 (7): e610. Bibcode:2007PLoSO...2..610S. doi:10.1371/journal.pone.0000610. PMC 1905940. PMID 17622355.
- Lena AM, Shalom-Feuerstein R, Rivetti di Val Cervo P, Aberdam D, Knight RA, Melino G, Candi E (2008). "miR-203 represses 'stemness' by repressing DeltaNp63". Cell Death Differ. 15 (7): 1187–95. doi:10.1038/cdd.2008.69. PMID 18483491.
- Greither T, Grochola LF, Udelnow A, Lautenschläger C, Würl P, Taubert H (2010). "Elevated expression of microRNAs 155, 203, 210 and 222 in pancreatic tumors is associated with poorer survival". Int. J. Cancer. 126 (1): 73–80. doi:10.1002/ijc.24687. PMID 19551852.
- Sonkoly E, Wei T, Pavez Loriè E, Suzuki H, Kato M, Törmä H, Ståhle M, Pivarcsi A (2010). "Protein kinase C-dependent upregulation of miR-203 induces the differentiation of human keratinocytes". J. Invest. Dermatol. 130 (1): 124–34. doi:10.1038/jid.2009.294. PMID 19759552.
- Furuta M, Kozaki KI, Tanaka S, Arii S, Imoto I, Inazawa J (2010). "miR-124 and miR-203 are epigenetically silenced tumor-suppressive microRNAs in hepatocellular carcinoma". Carcinogenesis. 31 (5): 766–76. doi:10.1093/carcin/bgp250. PMID 19843643.
- Melar-New M, Laimins LA (2010). "Human papillomaviruses modulate expression of microRNA 203 upon epithelial differentiation to control levels of p63 proteins". J. Virol. 84 (10): 5212–21. doi:10.1128/JVI.00078-10. PMC 2863797. PMID 20219920.
- Ikenaga N, Ohuchida K, Mizumoto K, Yu J, Kayashima T, Sakai H, Fujita H, Nakata K, Tanaka M (2010). "MicroRNA-203 expression as a new prognostic marker of pancreatic adenocarcinoma". Ann. Surg. Oncol. 17 (12): 3120–8. doi:10.1245/s10434-010-1188-8. PMID 20652642. S2CID 24422912.
- Wei T, Orfanidis K, Xu N, Janson P, Ståhle M, Pivarcsi A, Sonkoly E (2010). "The expression of microRNA-203 during human skin morphogenesis" (PDF). Exp. Dermatol. 19 (9): 854–6. doi:10.1111/j.1600-0625.2010.01118.x. PMID 20698882. S2CID 30026838.
- McKenna DJ, McDade SS, Patel D, McCance DJ (2010). "MicroRNA 203 expression in keratinocytes is dependent on regulation of p53 levels by E6". J. Virol. 84 (20): 10644–52. doi:10.1128/JVI.00703-10. PMC 2950558. PMID 20702634.
This article incorporates text from the United States National Library of Medicine, which is in the public domain.