Sodium- and chloride-dependent glycine transporter 2

Protein-coding gene in the species Homo sapiens From Wikipedia, the free encyclopedia

Sodium- and chloride-dependent glycine transporter 2, also known as glycine transporter 2 (GlyT2), is a protein that in humans is encoded by the SLC6A5 gene.[5]

AliasesSLC6A5, GLYT-2, GLYT2, HKPX3, NET1, Glycine transporter 2, solute carrier family 6 member 5
End20,659,285 bp[1]
Quick facts SLC6A5, Identifiers ...
SLC6A5
Identifiers
AliasesSLC6A5, GLYT-2, GLYT2, HKPX3, NET1, Glycine transporter 2, solute carrier family 6 member 5
External IDsOMIM: 604159; MGI: 105090; HomoloGene: 37901; GeneCards: SLC6A5; OMA:SLC6A5 - orthologs
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_004211
NM_001318369

NM_001146013
NM_148931

RefSeq (protein)

NP_001305298
NP_004202

n/a

Location (UCSC)Chr 11: 20.6 – 20.66 MbChr 7: 49.56 – 49.61 Mb
PubMed search[3][4]
Wikidata
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The glycine transporter 2 is a membrane protein which recaptures glycine, a major inhibitory transmitter in the spinal cord and brainstem. GlyT2 is a specific marker of glycinergic neurons and a member of the Na+ and Cl-coupled transporter family SLC6. Glycine uptake mediated by GlyT2 is electrogenic, coupled to three Na+ and one Cl (i.e. two positive charges per glycine). In humans, GlyT2 is encoded by the SLC6A5 gene. Inactivation of GlyT2 in knockout mice is lethal during the second post-natal week as the absence of GlyT2 disrupts inhibitory transmission by reducing glycine release. Mutations in SLC6A5 gene are responsible for a presynaptic form of hyperekplexia, a genetic disease causing increased startle reflex. GlyT2 main physiological role is to recapture glycine released in the synaptic cleft and to maintain high glycine concentration in the presynaptic neuron. Therefore, chronic inhibition of GlyT2 will deplete intracellular storage of glycine and limit its accumulation in synaptic vesicles.[5][6]

Inhibitors

See also

References

Further reading

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