METRN

Protein-coding gene in the species Homo sapiens
METRN
Identifiers
AliasesMETRN, C16orf23, c380A1.2, meteorin, glial cell differentiation regulator
External IDsOMIM: 610998; MGI: 1917333; HomoloGene: 11432; GeneCards: METRN; OMA:METRN - orthologs
Gene location (Human)
Chromosome 16 (human)
Chr.Chromosome 16 (human)[1]
Chromosome 16 (human)
Genomic location for METRN
Genomic location for METRN
Band16p13.3Start715,118 bp[1]
End719,655 bp[1]
Gene location (Mouse)
Chromosome 17 (mouse)
Chr.Chromosome 17 (mouse)[2]
Chromosome 17 (mouse)
Genomic location for METRN
Genomic location for METRN
Band17|17 A3.3Start26,012,195 bp[2]
End26,016,110 bp[2]
RNA expression pattern
Bgee
HumanMouse (ortholog)
Top expressed in
  • C1 segment

  • right uterine tube

  • caudate nucleus

  • nucleus accumbens

  • amygdala

  • right frontal lobe

  • putamen

  • anterior cingulate cortex

  • ventral tegmental area

  • anterior pituitary
Top expressed in
  • optic nerve

  • cerebellar cortex

  • somite

  • cerebellar vermis

  • lobe of cerebellum

  • median eminence

  • interventricular septum

  • superior frontal gyrus

  • lumbar subsegment of spinal cord

  • visual cortex
More reference expression data
BioGPS
n/a
Gene ontology
Molecular function
  • hormone activity
Cellular component
  • extracellular region
  • extracellular space
Biological process
  • multicellular organism development
  • cell differentiation
  • glial cell differentiation
  • positive regulation of axonogenesis
  • nervous system development
  • signal transduction
Sources:Amigo / QuickGO
Orthologs
SpeciesHumanMouse
Entrez

79006

70083

Ensembl

ENSG00000103260

ENSMUSG00000002274

UniProt

Q9UJH8

Q8C1Q4

RefSeq (mRNA)

NM_024042

NM_133719

RefSeq (protein)

NP_076947

NP_598480

Location (UCSC)Chr 16: 0.72 – 0.72 MbChr 17: 26.01 – 26.02 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Meteorin, glial cell differentiation regulator is a protein that in humans is encoded by the METRN gene. [5]

Function

Meteorin regulates glial cell differentiation and promotes the formation of axonal networks during neurogenesis. Aligned with its neurotrophic properties Meteorin promotes neurotic outgrowth of cultured dorsal root ganglion sensory neurons via a mechanism that involves satellite glial cells.[6] Meteorin also has been shown to have profound and extremely long-lasting analgesic effects in animal models of inflammatory and neuropathic pain.[7][8]

The human variant of the protein is currently being developed by the Danish biotechnology company, Hoba Therapeutics,[9] for the treatment of neuropathic pain in humans.

References

  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000103260 – Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000002274 – Ensembl, May 2017
  3. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. ^ "Entrez Gene: Meteorin, glial cell differentiation regulator". Retrieved 2016-02-25.
  6. ^ Nishino J, Yamashita K, Hashiguchi H, Fujii H, Shimazaki T, Hamada H (May 2004). "Meteorin: a secreted protein that regulates glial cell differentiation and promotes axonal extension". The EMBO Journal. 23 (9): 1998–2008. doi:10.1038/sj.emboj.7600202. PMC 404322. PMID 15085178.
  7. ^ Jørgensen JR, Xu XJ, Arnold HM, Munro G, Hao JX, Pepinsky B, Huang C, Gong BJ, Wiesenfeld-Hallin Z, Wahlberg LU, Johansen TE (October 2012). "Meteorin reverses hypersensitivity in rat models of neuropathic pain". Experimental Neurology. 237 (2): 260–6. doi:10.1016/j.expneurol.2012.06.027. PMID 22766205. S2CID 20074608.
  8. ^ Xie JY, Qu C, Munro G, Petersen KA, Porreca F (August 2019). "Antihyperalgesic effects of Meteorin in the rat chronic constriction injury model: a replication study". Pain. 160 (8): 1847–1855. doi:10.1097/j.pain.0000000000001569. PMC 6687406. PMID 31335652.
  9. ^ "HB-086 (recombinant human meteorin)". Hoba Therapeutics.

Further reading

This article incorporates text from the United States National Library of Medicine, which is in the public domain.


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