MicroRNA 210

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Identifiers
Aliases
External IDs	GeneCards: [1]
Orthologs
Species	Human	Mouse
Entrez	n/a	n/a
Ensembl	n/a	n/a
UniProt	n/a	n/a
RefSeq (mRNA)	n/a	n/a
RefSeq (protein)	n/a	n/a
Location (UCSC)	n/a	n/a
PubMed search	n/a	n/a
Wikidata
View/Edit Human

MicroRNA 210 is a protein that in humans is encoded by the MIR210 gene.

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. [provided by RefSeq, Sep 2009].

Further reading

• Greither T, Grochola LF, Udelnow A, Lautenschläger C, Würl P, Taubert H (January 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.
• Zhang Z, Sun H, Dai H, Walsh RM, Imakura M, Schelter J, Burchard J, Dai X, Chang AN, Diaz RL, Marszalek JR, Bartz SR, Carleton M, Cleary MA, Linsley PS, Grandori C (September 2009). "MicroRNA miR-210 modulates cellular response to hypoxia through the MYC antagonist MNT". Cell Cycle. 8 (17): 2756–68. doi:10.4161/cc.8.17.9387. PMID 19652553.
• Bianchi N, Zuccato C, Lampronti I, Borgatti M, Gambari R (August 2009). "Expression of miR-210 during erythroid differentiation and induction of gamma-globin gene expression". BMB Rep. 42 (8): 493–9. PMID 19712585.
• Huang X, Ding L, Bennewith KL, Tong RT, Welford SM, Ang KK, Story M, Le QT, Giaccia AJ (September 2009). "Hypoxia-inducible mir-210 regulates normoxic gene expression involved in tumor initiation". Mol. Cell. 35 (6): 856–67. doi:10.1016/j.molcel.2009.09.006. PMC 2782615. PMID 19782034.
• Chan SY, Zhang YY, Hemann C, Mahoney CE, Zweier JL, Loscalzo J (October 2009). "MicroRNA-210 controls mitochondrial metabolism during hypoxia by repressing the iron-sulfur cluster assembly proteins ISCU1/2". Cell Metab. 10 (4): 273–84. doi:10.1016/j.cmet.2009.08.015. PMC 2759401. PMID 19808020.
• Bostjancic E, Zidar N, Glavac D (2009). "MicroRNA microarray expression profiling in human myocardial infarction". Dis. Markers. 27 (6): 255–68. doi:10.3233/DMA-2009-0671. PMC 3834671. PMID 20075508.
• Gee HE, Camps C, Buffa FM, Patiar S, Winter SC, Betts G, Homer J, Corbridge R, Cox G, West CM, Ragoussis J, Harris AL (May 2010). "hsa-mir-210 is a marker of tumor hypoxia and a prognostic factor in head and neck cancer". Cancer. 116 (9): 2148–58. doi:10.1002/cncr.25009. PMID 20187102.
• Biswas S, Roy S, Banerjee J, Hussain SR, Khanna S, Meenakshisundaram G, Kuppusamy P, Friedman A, Sen CK (April 2010). "Hypoxia inducible microRNA 210 attenuates keratinocyte proliferation and impairs closure in a murine model of ischemic wounds". Proc. Natl. Acad. Sci. U.S.A. 107 (15): 6976–81. doi:10.1073/pnas.1001653107. PMC 2872456. PMID 20308562.
• Favaro E, Ramachandran A, McCormick R, Gee H, Blancher C, Crosby M, Devlin C, Blick C, Buffa F, Li JL, Vojnovic B, Pires das Neves R, Glazer P, Iborra F, Ivan M, Ragoussis J, Harris AL (April 2010). "MicroRNA-210 regulates mitochondrial free radical response to hypoxia and krebs cycle in cancer cells by targeting iron sulfur cluster protein ISCU". PLoS ONE. 5 (4): e10345. doi:10.1371/journal.pone.0010345. PMC 2859946. PMID 20436681.

This article incorporates text from the United States National Library of Medicine, which is in the public domain.