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词条 Mir-17 microRNA precursor family
释义

  1. References

  2. Further reading

  3. External links

{{Infobox rfam
| Name = mir-17 microRNA precursor family
| image = RF00051.jpg
| width =
| caption = Predicted secondary structure and sequence conservation of mir-17
| Symbol = mir-17
| AltSymbols =
| Rfam = RF00051
| miRBase = MI0000071
| miRBase_family = MIPF0000001
| RNA_type = Gene; miRNA
| Tax_domain = Eukaryota
| GO = {{GO|0035195}} {{GO|0035068}}
| SO = {{SO|0001244}}
| CAS_number =
| EntrezGene =
| HGNCid =
| OMIM =
| PDB =
| RefSeq =
| Chromosome =
| Arm =
| Band =
| LocusSupplementaryData =
}}

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

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Further reading

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External links

  • {{Rfam|id=RF00051|name=mir-17 microRNA precursor family}}
{{miRNA precursor families}}

2 : MicroRNA|MicroRNA precursor families

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