Mir17hg Mir17 host gene (non-protein coding) [Mus musculus (house mouse)] - Gene

Summary

Official Symbol: Mir17hgprovided by MGI
Official Full Name: Mir17 host gene (non-protein coding)provided by MGI
Primary source: MGI:MGI:1923207
See related: AllianceGenome:MGI:1923207
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: Mirhg1; mir-17-92; 5033413D16Rik
Summary: Acts upstream of or within response to wounding. Human ortholog(s) of this gene implicated in Feingold syndrome. Orthologous to human MIR17HG (miR-17-92a-1 cluster host gene). [provided by Alliance of Genome Resources, Apr 2022]
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Genomic context

Location:: 14 E4; 14 59.4 cM

Exon count:: 1

Annotation release	Status	Assembly	Chr	Location
RS_2024_02	current	GRCm39 (GCF_000001635.27)	14	NC_000080.7 (115281822..115284160)
108.20200622	previous assembly	GRCm38.p6 (GCF_000001635.26)	14	NC_000080.6 (115044390..115046728)

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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Bibliography

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GeneRIFs: Gene References Into Functions

What's a GeneRIF?

Long Non-Coding RNA Mir17hg Positively Regulates Melanogenesis by Inhibiting TGFbeta Receptor 2 under Psychological Stress.
Title: Long Non-Coding RNA Mir17hg Positively Regulates Melanogenesis by Inhibiting TGFβ Receptor 2 under Psychological Stress.
Long non-coding RNA MIR17HG impedes FOSL2-mediated transcription activation of HIC1 to maintain a pro-inflammatory phenotype of microglia during intracerebral haemorrhage.
Title: Long non-coding RNA MIR17HG impedes FOSL2-mediated transcription activation of HIC1 to maintain a pro-inflammatory phenotype of microglia during intracerebral haemorrhage.
Exosomal miR-17-92 derived from human mesenchymal stem cells promotes wound healing by enhancing angiogenesis and inhibiting endothelial cell ferroptosis.
Title: Exosomal miR-17-92 derived from human mesenchymal stem cells promotes wound healing by enhancing angiogenesis and inhibiting endothelial cell ferroptosis.
Endothelial-Derived miR-17 approximately 92 Promotes Angiogenesis to Protect against Renal Ischemia-Reperfusion Injury.
Title: Endothelial-Derived miR-17∼92 Promotes Angiogenesis to Protect against Renal Ischemia-Reperfusion Injury.
These findings provide mechanistic insight into the role of the lncRNA MIR17HG and its miRNA members in regulating colorectal cancer carcinogenesis and progression.
Title: Long Noncoding RNA MIR17HG Promotes Colorectal Cancer Progression via miR-17-5p.
miR-17-92 ameliorates renal ischemia reperfusion injury.
Title: miR-17-92 ameliorates renal ischemia reperfusion injury.
Interestingly, deletion or overexpression of miR-17- 92 cluster in keratinocytes, or deletion of miR-17- 92 in T cells did not significantly affect IMQ-induced psoriasis-like dermatitis development in the mutant mice compared with wild-type littermates. Thus, miRNA miR-17- 92 cluster may not be a key factor regulating imiqumod-induced psoriasis-like dermatitis.
Title: miRNA miR-17-92 cluster is differentially regulated in the imiqumod-treated skin but is not required for imiqumod-induced psoriasis-like dermatitis in mice.
Data show that the induction of BIM in the MYC- and RAS-driven leukemia is mediated by the downregulation of miR-17-92, and suggest that induction of BIM-mediated apoptosis may be a therapeutic approach for acute lymphoblastic leukemia (ALL).
Title: BIM mediates oncogene inactivation-induced apoptosis in multiple transgenic mouse models of acute lymphoblastic leukemia.
miR-17-92-dependent tuning of LKB1 levels regulates both the metabolic potential of Myc+ lymphomas and tumor growth in vivo.
Title: The miR-17∼92 microRNA Cluster Is a Global Regulator of Tumor Metabolism.
The results of this study suggest that miR-17-92 promotes neuronal differentiation of grafted NSCs under neuroinflammatory condition via inhibition of multiple proteins in JAK-STAT pathway.
Title: miR-17-92 facilitates neuronal differentiation of transplanted neural stem/precursor cells under neuroinflammatory conditions.

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General gene information

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Other Names

Mir17 host gene 1 (non-protein coding)
microRNA host gene 1 (non-protein coding)

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 response to wounding	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.