This is an old revision of this page, as edited by ProteinBoxBot(talk | contribs) at 05:26, 20 May 2016(Updating to new gene infobox populated via wikidata). The present address (URL) is a permanent link to this revision, which may differ significantly from the current revision.
Revision as of 05:26, 20 May 2016 by ProteinBoxBot(talk | contribs)(Updating to new gene infobox populated via wikidata)
Glycine transporter 2 (GlyT2) also known as the sodium- and chloride-dependent glycine transporter 2 or solute carrier family 6 member 5 is a protein that in humans is encoded by the SLC6A5gene.[5]
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 SLC6A5gene. 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]
^"Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^"Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^ abMorrow JA, Collie IT, Dunbar DR, Walker GB, Shahid M, Hill DR (November 1998). "Molecular cloning and functional expression of the human glycine transporter GlyT2 and chromosomal localisation of the gene in the human genome". FEBS Lett. 439 (3): 334–40. doi:10.1016/S0014-5793(98)01390-8. PMID9845349.{{cite journal}}: CS1 maint: multiple names: authors list (link)