Mir124a-1hg Mir124-1 host gene (non-protein coding) [Mus musculus (house mouse)] - Gene

Summary

Official Symbol: Mir124a-1hgprovided by MGI
Official Full Name: Mir124-1 host gene (non-protein coding)provided by MGI
Primary source: MGI:MGI:2442197
See related: Ensembl:ENSMUSG00000097545 AllianceGenome:MGI:2442197
Gene type: ncRNA
RefSeq status: VALIDATED
Organism: Mus musculus
Lineage: Eukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi; Mammalia; Eutheria; Euarchontoglires; Glires; Rodentia; Myomorpha; Muroidea; Muridae; Murinae; Mus; Mus
Also known as: Rncr3; mir-3078; mir-124-1; A930011O12Rik
Summary: Acts upstream of or within several processes, including gene silencing by miRNA; long-term synaptic potentiation; and sensory perception of sound. Is expressed in brain subventricular zone; brain ventricular layer; and spinal cord. [provided by Alliance of Genome Resources, Apr 2022]
Expression: Biased expression in cerebellum adult (RPKM 109.3), CNS E14 (RPKM 72.2) and 5 other tissues See more
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Genomic context

Location:: 14 D1; 14 33.77 cM

Exon count:: 4

Annotation release	Status	Assembly	Chr	Location
RS_2024_02	current	GRCm39 (GCF_000001635.27)	14	NC_000080.7 (64825564..64831410)
108.20200622	previous assembly	GRCm38.p6 (GCF_000001635.26)	14	NC_000080.6 (64588115..64593961)

Chromosome 14 - NC_000080.7 Genomic Context describing neighboring genes

Genomic regions, transcripts, and products

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Genomic Sequence:

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Expression

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See details

Project title: Mouse ENCODE transcriptome data
Description: RNA profiling data sets generated by the Mouse ENCODE project.
BioProject: PRJNA66167
Publication: PMID 25409824
Analysis date: n/a

Bibliography

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GeneRIFs: Gene References Into Functions

What's a GeneRIF?

Mechanism of Dcp2/RNCR3/Dkc1/Snora62 axis regulating neuronal apoptosis in chronic cerebral ischemia.
Title: Mechanism of Dcp2/RNCR3/Dkc1/Snora62 axis regulating neuronal apoptosis in chronic cerebral ischemia.
Role of miR-124-3p in regulatory mechanisms of Gpm6a expression in the hippocampus of chronically stressed rats.
Title: Role of miR-124-3p in regulatory mechanisms of Gpm6a expression in the hippocampus of chronically stressed rats.
miR-124-3p sabotages lncRNA MALAT1 stability to repress chondrocyte pyroptosis and relieve cartilage injury in osteoarthritis.
Title: miR-124-3p sabotages lncRNA MALAT1 stability to repress chondrocyte pyroptosis and relieve cartilage injury in osteoarthritis.
Microglia-Derived Small Extracellular Vesicles Reduce Glioma Growth by Modifying Tumor Cell Metabolism and Enhancing Glutamate Clearance through miR-124.
Title: Microglia-Derived Small Extracellular Vesicles Reduce Glioma Growth by Modifying Tumor Cell Metabolism and Enhancing Glutamate Clearance through miR-124.
These results show that antagonizing let-7 and increasing levels of miR-25 and miR-124 using miRNA mimics is useful in reprogramming Muller glial cells to retinal neurons in vitro and could help in stimulating regeneration in this system.
Title: MicroRNAs miR-25, let-7 and miR-124 regulate the neurogenic potential of Müller glia in mice.
Synchronizing the expression of miR-124, miR-128, and miR-137 in a gene therapy approach displays significant anticancer synergism, abrogates this epigenesis-mediated, multi-protein tumor survival mechanism and results in a 5-fold increase in survival when combined with chemotherapy in murine glioblastoma models.
Title: The functional synergism of microRNA clustering provides therapeutically relevant epigenetic interference in glioblastoma.
Knockdown of miR-124 exerts cardioprotection via preventing apoptosis and ameliorating mitochondrial dysfunction following MI by targeting STAT3.
Title: Inhibition of MicroRNA-124 Reduces Cardiomyocyte Apoptosis Following Myocardial Infarction via Targeting STAT3.
Rap2a is a common target of both miR-9 and miR-124. miR-9 and miR-124 together, but neither miRNA alone, strongly suppressed Rap2a, thereby promoting neuronal differentiation of neural stem cells and dendritic branching of differentiated neurons.
Title: miR-9 and miR-124 synergistically affect regulation of dendritic branching via the AKT/GSK3β pathway by targeting Rap2a.
OSBP may be a target and downstream effector of miR-124 for regulating neurite outgrowth and elongation.
Title: MicroRNA124 Regulated Neurite Elongation by Targeting OSBP.
RNCR3 has an atheroprotective role in atherosclerosis.
Title: Role of long non-coding RNA-RNCR3 in atherosclerosis-related vascular dysfunction.

Submit: New GeneRIF Correction See all GeneRIFs (22)

Variation

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Alleles

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

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

General gene information

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Markers

Mirn124a-1 (e-PCR), detects polymorphism
- UniSTS:516535

Gene Ontology Provided by MGI

Function	Evidence Code	Pubs
enables molecular_function	ND No biological Data available more info

Process	Evidence Code	Pubs
acts_upstream_of_or_within female sex differentiation	IEP Inferred from Expression Pattern more info	PubMed
acts_upstream_of_or_within long-term synaptic potentiation	IEP Inferred from Expression Pattern more info	PubMed
acts_upstream_of_or_within miRNA-mediated post-transcriptional gene silencing	IDA Inferred from Direct Assay more info	PubMed
acts_upstream_of_or_within negative regulation of gene expression	IDA Inferred from Direct Assay more info	PubMed
acts_upstream_of_or_within negative regulation of gene expression	IMP Inferred from Mutant Phenotype more info	PubMed
acts_upstream_of_or_within sensory perception of sound	IEP Inferred from Expression Pattern more info	PubMed

Component	Evidence Code	Pubs
is_active_in cellular_component	ND No biological Data available more info

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.