mir-17 microRNA precursor family

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mir-17 microRNA precursor family
RF00051.jpg
Predicted secondary structure and sequence conservation of mir-17
Identifiers
Symbol mir-17
Rfam RF00051
miRBase MI0000071
miRBase family MIPF0000001
Other data
RNA type Gene; miRNA
Domain(s) Eukaryota
GO 0035195 0035068
SO 0001244

The miR-17 microRNA precursor family are a group of related small non-coding RNA genes called microRNAs that regulate gene expression. The microRNA precursor miR-17 family, includes miR-20a/b, miR-93, and miR-106a/b. With the exception of miR-93, these microRNAs are produced from several microRNA gene clusters, which apparently arose from a series of ancient evolutionary genetic duplication events, and also include members of the miR-19, and miR-25 families.[1] These clusters are transcribed as long non-coding RNA transcripts that are processed to form ~70 nucleotide microRNA precursors, that are subsequently processed by the Dicer enzyme to give a ~22 nucleotide products. The mature microRNA products are thought to regulate expression levels of other genes through complementarity to the 3' UTR of specific target messenger RNA.[2][3]

The paralogous miRNA gene clusters that give rise to miR-17 family microRNAs (miR-17~92, miR-106a~363, and miR-106b~25) have been implicated in a wide variety of malignancies and are sometimes referred to as oncomirs.[4] The oncogenic potential of these non-protein encoding genes was first identified in mouse viral tumorigenesis screens.[5][6][7] In humans, the activating mutations of miR-17~92 have been identified in non-Hodgkin's lymphoma, whereas the miRNA constituents of the clusters are overexpressed in a multiple cancer types.[8][9][10] High level expression of miR-17 family members induces cell proliferation, whereas deletion of the miR-17~92 cluster, in mice, is lethal and causes lung and lymphoid cell developmental defects.[11] In addition, in the nasopharyngeal carcinoma cell line, miR-20a and miR-20b has been shown to target the 3’ UTR of vascular endothelial growth factor (VEGF) and repress the expression of VEGF, which is an important angiogenic factor. [12][13]

References[edit]

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  8. ^ Ota A, Tagawa H, Karnan S, Tsuzuki S, Karpas A, Kira S, Yoshida Y, Seto M (2004). "Identification and characterization of a novel gene, C13orf25, as a target for 13q31-q32 amplification in malignant lymphoma.". Cancer Res. 64 (9): 3087–95. doi:10.1158/0008-5472.CAN-03-3773. PMID 15126345. 
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  10. ^ Mendell JT (2008). "miRiad roles for the miR-17-92 cluster in development and disease.". Cell. 133 (2): 217–22. doi:10.1016/j.cell.2008.04.001. PMC 2732113. PMID 18423194. 
  11. ^ Ventura A, Young AG, Winslow MM, Lintault L, Meissner A, Erkeland SJ, Newman J, Bronson RT, Crowley D, Stone JR, et al (2008). "Targeted deletion reveals essential and overlapping functions of the miR-17~92 family of miRNA clusters.". Cell. 132 (5): 875–86. doi:10.1016/j.cell.2008.02.019. PMC 2323338. PMID 18329372. 
  12. ^ Hua Z, Lv Q, Ye W, Wong CK, Cai G, Gu D, Ji Y, Zhao C, Wang J, Yang BB, Zhang Y (Dec 27, 2006). "MiRNA-directed regulation of VEGF and other angiogenic factors under hypoxia". PLOS ONE 1 (1): e116. doi:10.1371/journal.pone.0000116. PMC 1762435. PMID 17205120. 
  13. ^ Ye W, Lv Q, Wong CK, Hu S, Fu C, Hua Z, Cai G, Li G, Yang BB, Zhang Y (Mar 5, 2008). "The effect of central loops in miRNA:MRE duplexes on the efficiency of miRNA-mediated gene regulation". PLOS ONE 3 (3): e1719. doi:10.1371/journal.pone.0001719. PMC 2248708. PMID 18320040. 

Further reading[edit]

[1] [2] [3] [4] [5] [6] [7] [8] [9] [10] [11] [12] [13] [14] [15] [16] [17] [18] [19] [20] [21] [22] [23] [24] [25] [26] [27] [28] [29] [30] [31] [32] [33] [34] [35] [36] [37] [38] [39] [40] [41] [42] [43] [44] [45] [46] [47] [48] [49] [50] [51] [52] [53] [54] [55] [56] [57] [58] [59] [60] [61] [62] [63] [64] [65]

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