MIR96

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MIR96
Identifiers
AliasesMIR96, DFNA50, MIRN96, hsa-mir-96, miR-96, miRNA96, microRNA 96
External IDsOMIM: 611606 GeneCards: MIR96
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

n/a

n/a

RefSeq (protein)

n/a

n/a

Location (UCSC)Chr 7: 129.77 – 129.77 Mbn/a
PubMed search[2]n/a
Wikidata
View/Edit Human

MicroRNA 96 is a miRNA that in humans is encoded by the MIR96 gene.[3][4] It's a human variant of mir-96 microRNA.

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

  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000199158Ensembl, May 2017
  2. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  3. ^ "Entrez Gene: MicroRNA 96". Retrieved 2016-04-10.
  4. ^ "MIR96 gene on U.S. National Library of Medicine 2020-08-4".

Further reading

  • Mencía A, Modamio-Høybjør S, Redshaw N, Morín M, Mayo-Merino F, Olavarrieta L, Aguirre LA, del Castillo I, Steel KP, Dalmay T, Moreno F, Moreno-Pelayo MA (2009). "Mutations in the seed region of human miR-96 are responsible for nonsyndromic progressive hearing loss". Nat. Genet. 41 (5): 609–13. doi:10.1038/ng.355. PMID 19363479. S2CID 11113852.

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