MIR562 microRNA 562 [Homo sapiens (human)] - Gene

Summary

Official Symbol: MIR562provided by HGNC
Official Full Name: microRNA 562provided by HGNC
Primary source: HGNC:HGNC:32818
See related: Ensembl:ENSG00000207626 miRBase:MI0003568; AllianceGenome:HGNC:32818
Gene type: ncRNA
RefSeq status: PROVISIONAL
Organism: Homo sapiens
Lineage: Eukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi; Mammalia; Eutheria; Euarchontoglires; Primates; Haplorrhini; Catarrhini; Hominidae; Homo
Also known as: MIRN562; hsa-mir-562
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:: 2q37.1

Exon count:: 1

Annotation release	Status	Assembly	Chr	Location
RS_2023_10	current	GRCh38.p14 (GCF_000001405.40)	2	NC_000002.12 (232172653..232172747)
RS_2023_10	current	T2T-CHM13v2.0 (GCF_009914755.1)	2	NC_060926.1 (232659232..232659326)
105.20220307	previous assembly	GRCh37.p13 (GCF_000001405.25)	2	NC_000002.11 (233037363..233037457)

Chromosome 2 - NC_000002.12 Genomic Context describing neighboring genes

Genomic regions, transcripts, and products

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Genomic Sequence:

Go to nucleotide: Graphics FASTA GenBank

Bibliography

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GeneRIFs: Gene References Into Functions

What's a GeneRIF?

Hsa_circ_0093741 competes with FRS2 for miR-562 binding sites to promote nephroblastoma progression.
Title: Hsa_circ_0093741 competes with FRS2 for miR-562 binding sites to promote nephroblastoma progression.
This data suggests that ANXA1-regulated miR26b* and miR562 may play a role in wound healing and tumor-induced endothelial cell tube formation by targeting NF-kappaB expression and point towards a potential therapeutic target for breast cancer.
Title: Annexin-A1 regulates microRNA-26b* and microRNA-562 to directly target NF-κB and angiogenesis in breast cancer cells.
miR-562 expression is reduced in Wilms' tumor and may contribute to tumorigenesis by deregulating target gene EYA1.
Title: Loss of heterozygosity at 2q37 in sporadic Wilms' tumor: putative role for miR-562.

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Phenotypes

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Review eQTL and phenotype association data in this region using PheGenI

Variation

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See variants in ClinVar

See studies and variants in dbVar

See Variation Viewer (GRCh37.p13)

See Variation Viewer (GRCh38)

General gene information

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Gene Ontology Provided by GOA

Function	Evidence Code	Pubs
enables mRNA base-pairing translational repressor activity	IDA Inferred from Direct Assay more info	PubMed

Process	Evidence Code	Pubs
involved_in miRNA-mediated gene silencing by mRNA destabilization	IDA Inferred from Direct Assay more info	PubMed
involved_in miRNA-mediated post-transcriptional gene silencing	IEA Inferred from Electronic Annotation 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.