Mir382 microRNA 382 [Mus musculus (house mouse)] - Gene

Summary

Official Symbol: Mir382provided by MGI
Official Full Name: microRNA 382provided by MGI
Primary source: MGI:MGI:3619392
See related: Ensembl:ENSMUSG00000065428 miRBase:MI0000799; AllianceGenome:MGI:3619392
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: Mirn382; mir-382; mmu-mir-382
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:: 12 F1; 12 60.56 cM

Exon count:: 1

Annotation release	Status	Assembly	Chr	Location
RS_2024_02	current	GRCm39 (GCF_000001635.27)	12	NC_000078.7 (109700205..109700280)
108.20200622	previous assembly	GRCm38.p6 (GCF_000001635.26)	12	NC_000078.6 (109733771..109733846)

Chromosome 12 - NC_000078.7 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?

Aerobic exercise improves cognitive impairment in mice with type 2 diabetes by regulating the MALAT1/miR-382-3p/BDNF signaling pathway in serum-exosomes.
Title: Aerobic exercise improves cognitive impairment in mice with type 2 diabetes by regulating the MALAT1/miR-382-3p/BDNF signaling pathway in serum-exosomes.
MicroRNA-382 Promotes M2-Like Macrophage via the SIRP-alpha/STAT3 Signaling Pathway in Aristolochic Acid-Induced Renal Fibrosis.
Title: MicroRNA-382 Promotes M2-Like Macrophage via the SIRP-α/STAT3 Signaling Pathway in Aristolochic Acid-Induced Renal Fibrosis.
Modulation of miR-382-5p reduces apoptosis of myocardial cells after acute myocardial infarction.
Title: Modulation of miR-382-5p reduces apoptosis of myocardial cells after acute myocardial infarction.
MiR-382-5p suppresses M1 macrophage polarization and inflammatory response in response to bronchopulmonary dysplasia through targeting CDK8: Involving inhibition of STAT1 pathway.
Title: MiR-382-5p suppresses M1 macrophage polarization and inflammatory response in response to bronchopulmonary dysplasia through targeting CDK8: Involving inhibition of STAT1 pathway.
The lncRNA Ftx/miR-382-5p/Nrg1 axis improves the inflammation response of microglia and spinal cord injury repair.
Title: The lncRNA Ftx/miR-382-5p/Nrg1 axis improves the inflammation response of microglia and spinal cord injury repair.
Upregulation of miR-382 contributes to renal fibrosis secondary to aristolochic acid-induced kidney injury via PTEN signaling pathway.
Title: Upregulation of miR-382 contributes to renal fibrosis secondary to aristolochic acid-induced kidney injury via PTEN signaling pathway.
Depleting miR-382 or miR-674 decelerates ependymal ciliary beating and mediates ventricular enlargement.
Title: Schizophrenia-related microdeletion causes defective ciliary motility and brain ventricle enlargement via microRNA-dependent mechanisms in mice.
Identify miR-382 as a promoter for hepatocyte proliferation and cell growth via targeting PTEN-Akt axis
Title: miR-382 targeting PTEN-Akt axis promotes liver regeneration.
miR-382 inhibits osteosarcoma metastasis and relapse by targeting YB-1 protein.
Title: miR-382 inhibits osteosarcoma metastasis and relapse by targeting Y box-binding protein 1.
Data support a completely novel mechanism in which miR-382 targets kallikrein 5 and contributes to the development of renal inner medullary interstitial fibrosis.
Title: MiR-382 targeting of kallikrein 5 contributes to renal inner medullary interstitial fibrosis.

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Variation

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Alleles

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

Endonuclease-mediated (1)

General gene information

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Gene Ontology Provided by MGI

Process	Evidence Code	Pubs
acts_upstream_of_or_within cellular response to amino acid stimulus	IDA Inferred from Direct Assay more info	PubMed
acts_upstream_of_or_within cellular response to leukemia inhibitory factor	IEP Inferred from Expression Pattern more info	PubMed
acts_upstream_of_or_within cellular response to phenylalanine	IEP Inferred from Expression Pattern more info	PubMed
involved_in energy homeostasis	IMP Inferred from Mutant Phenotype more info	PubMed
acts_upstream_of_or_within long-term synaptic potentiation	IEP Inferred from Expression Pattern more info	PubMed
involved_in metabolic process	IMP Inferred from Mutant Phenotype more info	PubMed
involved_in negative regulation of gene expression	IDA Inferred from Direct Assay more info	PubMed
acts_upstream_of_or_within regulation of SMAD protein signal transduction	IDA Inferred from Direct Assay 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.