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Protein-coding gene in the species Homo sapiens

LPAR6

LPAR6
All data from the card 17
Aliases
LPAR6, ARWH1, HYPT8, LAH3, P2RY5, P2Y5, lysophosphatidic acid receptor 6, LPA-6
External IDs
OMIM: 609239; MGI: 1914418; GeneCards: LPAR6
Chr.
Chromosome 13 (human)
Band
13q14.2
End
48,444,704 bp
Chr.
Chromosome 14 (mouse)
Band
14|14 D3
End
73,480,734 bp
BioGPS
More reference expression data
Databases
NCBI: entry; OMA: entry
Species
Human
Entrez
10161
Ensembl
ENSG00000139679
UniProt
P43657
RefSeq (mRNA)
NM_005767NM_001162497NM_001162498NM_001377316NM_001377317
RefSeq (protein)
NP_001155969NP_001155970NP_005758NP_001364245NP_001364246
Location (UCSC)
Chr 13: 48.39 – 48.44 Mb

Lysophosphatidic acid receptor 6, also known as LPA6 and P2RY5, is a protein that in humans is encoded by the LPAR6 gene. LPA6 is a G protein-coupled receptor that binds the lipid signaling molecule lysophosphatidic acid (LPA).

The protein encoded by this gene belongs to the family of G-protein coupled receptors, that are preferentially activated by adenosine and uridine nucleotides. This gene aligns with an internal intron of the retinoblastoma susceptibility gene in the reverse orientation.

Role in hair growth/loss

In February 2008, researchers at the University of Bonn announced they have found the genetic basis of two distinct forms of inherited hair loss, opening a broad path to treatments for baldness. They found that mutations in the gene P2RY5 causes a rare, inherited form of hair loss called hypotrichosis simplex. It is the first receptor in humans known to play a role in hair growth. The fact that any receptor plays a specific role in hair growth was previously unknown to scientists, and with this new knowledge a focus on finding more of these genes may be able to lead to therapies for many different types of hair loss.

In 2013, it was found that mutations in LPAR6 give rise to the Cornish Rex cat breed, which has a form of ectodermal dysplasia characterised by short woolly hair which is susceptible to loss.

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Text from Wikipedia, CC BY-SA 4.0 · Source article