Mir216a microRNA 216a [Mus musculus (house mouse)] - Gene

Summary

Official Symbol: Mir216aprovided by MGI
Official Full Name: microRNA 216aprovided by MGI
Primary source: MGI:MGI:2676892
See related: Ensembl:ENSMUSG00000065539 miRBase:MI0000699; AllianceGenome:MGI:2676892
Gene type: ncRNA
RefSeq status: PROVISIONAL
Organism: Mus musculus
Lineage: Eukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi; Mammalia; Eutheria; Euarchontoglires; Glires; Rodentia; Myomorpha; Muroidea; Muridae; Murinae; Mus; Mus
Also known as: Mirn216; Mirn216a; mir-216a; mmu-mir-216
Summary: 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]
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Genomic context

Location:: 11 A3.3; 11 16.23 cM

Exon count:: 1

Annotation release	Status	Assembly	Chr	Location
RS_2024_02	current	GRCm39 (GCF_000001635.27)	11	NC_000077.7 (28707012..28707083)
108.20200622	previous assembly	GRCm38.p6 (GCF_000001635.26)	11	NC_000077.6 (28757012..28757083)

Chromosome 11 - NC_000077.7 Genomic Context describing neighboring genes

Genomic regions, transcripts, and products

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Genomic Sequence:

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Bibliography

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GeneRIFs: Gene References Into Functions

What's a GeneRIF?

MicroRNA-216a is essential for cardiac angiogenesis.
Title: MicroRNA-216a is essential for cardiac angiogenesis.
Deletion of pancreas-specific miR-216a reduces beta-cell mass and inhibits pancreatic cancer progression in mice.
Title: Deletion of pancreas-specific miR-216a reduces beta-cell mass and inhibits pancreatic cancer progression in mice.
MiR-216a-5p ameliorates learning-memory deficits and neuroinflammatory response of Alzheimer's disease mice via regulation of HMGB1/NF-kappaB signaling.
Title: MiR-216a-5p ameliorates learning-memory deficits and neuroinflammatory response of Alzheimer's disease mice via regulation of HMGB1/NF-κB signaling.
Targeting HMGB1-TLR4 signaling by miR-216a-5p elevation alleviates the inflammatory behavioral hypersensitivity.
Title: Targeting HMGB1-TLR4 signaling by miR-216a-5p elevation alleviates the inflammatory behavioral hypersensitivity.
MiR-216a-5p alleviates chronic constriction injury-induced neuropathic pain in rats by targeting KDM3A and inactivating Wnt/beta-catenin signaling pathway.
Title: MiR-216a-5p alleviates chronic constriction injury-induced neuropathic pain in rats by targeting KDM3A and inactivating Wnt/β-catenin signaling pathway.
Microvesicles containing microRNA-216a secreted by tubular epithelial cells participate in renal interstitial fibrosis through activating PTEN/AKT pathway.
Title: Microvesicles containing microRNA-216a secreted by tubular epithelial cells participate in renal interstitial fibrosis through activating PTEN/AKT pathway.
In the carotid atherosclerotic plaques from miR-216a-treated apolipoprotein E(-/-) mice, the numbers of M1 macrophages were increased whereas M2 cells reduced, accompanying with inhibited Smad3 expression and upregulated inflammatory markers and TERT activity.
Title: MicroRNA-216a promotes M1 macrophages polarization and atherosclerosis progression by activating telomerase via the Smad3/NF-κB pathway.
The miR216a antagomir attenuated, whereas the miR216a agomir promoted TGFbetainduced myofibroblast transdifferentiation. Mechanistically, miR216a accelerated myofibroblast transdifferentiation via the AKT/glycogen synthase kinase 3beta signaling pathway, independent of the canonical Smad3 pathway.
Title: miR‑216a exacerbates TGF‑β‑induced myofibroblast transdifferentiation via PTEN/AKT signaling.
Circulating miR-216a may serve as a potential biomarker for severe acute pancreatitis
Title: Circulating microRNA 216 as a Marker for the Early Identification of Severe Acute Pancreatitis.
TGF-beta and miR-216a were involved the progress of acute pancreatitis through PI3K/Akt signaling pathway and TGF-beta pathway by targeting PTEN and SMAD7.
Title: Transforming growth factor (TGF)-β-induced microRNA-216a promotes acute pancreatitis via Akt and TGF-β pathway in mice.

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Variation

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Alleles

Alleles of this type are documented at Mouse Genome Informatics (MGI)

Endonuclease-mediated (2) 1 citation
Targeted (1) 1 citation

General gene information

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Gene Ontology Provided by MGI

Process	Evidence Code	Pubs
acts_upstream_of_or_within cellular response to leukemia inhibitory factor	IEP Inferred from Expression Pattern more info	PubMed
involved_in gene expression	IMP Inferred from Mutant Phenotype more info	PubMed
involved_in mesonephric duct formation	IMP Inferred from Mutant Phenotype more info	PubMed

NCBI Reference Sequences (RefSeq)

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RefSeqs maintained independently of Annotated Genomes

These reference sequences exist independently of genome builds. Explain

These reference sequences are curated independently of the genome annotation cycle, so their versions may not match the RefSeq versions in the current genome build. Identify version mismatches by comparing the version of the RefSeq in this section to the one reported in Genomic regions, transcripts, and products above.