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{{Infobox gene}}
{{Infobox gene}}


'''Sodium- and chloride-dependent betaine transporter''', also known as '''Na(+)/Cl(-) betaine/GABA transporter''' ('''BGT-1'''), is a [[protein]] that in humans is encoded by the ''SLC6A12'' [[gene]]. (BGT1; '''SLC6A12''' is predominantly expressed in the [[liver]] (hepatocytes).<ref name="Zhou et al. 2012">{{cite journal |vauthors=Zhou Y, Holmseth S, Hua R, Lehre AC, Olofsson AM, Poblete-Naredo I, Kempson SA, Danbolt NC | title = The betaine-GABA transporter (BGT1, slc6a12) is predominantly expressed in the liver and at lower levels in the kidneys and at the brain surface | journal = Am J Physiol Renal Physiol | volume = 302 | issue = 3 | pages = F316-28 | year = 2012 | pmid = 22071246 | doi = 10.1152/ajprenal.00464.2011}}</ref> It is also expressed in the kidney<ref name="Zhou et al. 2012"/> where it is regulated by [[NFAT5#Osmotic stress|NFAT5]] during a response to [[osmotic]] stress.<ref>{{Cite journal |vauthors=Lee SD, Choi SY, Lim SW, Lamitina ST, Ho SN, Go WY, Kwon HM | doi = 10.1152/ajprenal.00227.2010 | title = TonEBP stimulates multiple cellular pathways for adaptation to hypertonic stress: Organic osmolyte-dependent and -independent pathways | journal = AJP: Renal Physiology | volume = 300 | issue = 3
'''Sodium- and chloride-dependent betaine transporter''', also known as '''Na(+)/Cl(-) betaine/GABA transporter''' ('''BGT-1'''), is a [[protein]] that in humans is encoded by the ''SLC6A12'' [[gene]]. BGT-1 is predominantly expressed in the [[liver]] (hepatocytes).<ref name="Zhou et al. 2012">{{cite journal |vauthors=Zhou Y, Holmseth S, Hua R, Lehre AC, Olofsson AM, Poblete-Naredo I, Kempson SA, Danbolt NC | title = The betaine-GABA transporter (BGT1, slc6a12) is predominantly expressed in the liver and at lower levels in the kidneys and at the brain surface | journal = Am J Physiol Renal Physiol | volume = 302 | issue = 3 | pages = F316-28 | year = 2012 | pmid = 22071246 | doi = 10.1152/ajprenal.00464.2011}}</ref> It is also expressed in the kidney<ref name="Zhou et al. 2012"/> where it is regulated by [[NFAT5#Osmotic stress|NFAT5]] during a response to [[osmotic]] stress.<ref>{{Cite journal |vauthors=Lee SD, Choi SY, Lim SW, Lamitina ST, Ho SN, Go WY, Kwon HM | doi = 10.1152/ajprenal.00227.2010 | title = TonEBP stimulates multiple cellular pathways for adaptation to hypertonic stress: Organic osmolyte-dependent and -independent pathways | journal = AJP: Renal Physiology | volume = 300 | issue = 3
| pages = F707–F715 | year = 2011 | pmid = 21209002 | pmc =3064130 }}</ref> Further, BGT1 is also present in the [[leptomeninges]] surrounding the brain.<ref name="Zhou et al. 2012"/> Deletion of the BGT1 gene in mice did not appear to have any impact on the tendency to develop epilepsy.<ref name="Lehre et al. 2011">{{cite journal |vauthors=Lehre AC, Rowley NM, Zhou Y, Holmseth S, Guo C, Holen T, Hua R, Laake P, Olofsson AM, Poblete-Naredo I, Rusakov DA, Madsen KK, Clausen RP, Schousboe A, White HS, Danbolt NC | title = Deletion of the betaine-GABA transporter (BGT1; slc6a12) gene does not affect seizure thresholds of adult mice | journal = Epilepsy Res | volume = 95 | issue = 1–2 | pages = 70–81 | year = 2011 | pmid = 21459558 | doi = 10.1016/j.eplepsyres.2011.02.014 | pmc=3376448}}</ref> This is to be expected considering that BGT1 is expressed at far lower levels than [[GABA transporter 1|GAT1]] and also has lower affinity for [[GABA]]. This implies that it is not likely to contribute significantly to the inactivation of the inhibitory neurotransmitter GABA.<ref name="Lehre et al. 2011"/>
| pages = F707–F715 | year = 2011 | pmid = 21209002 | pmc =3064130 }}</ref> Further, BGT1 is also present in the [[leptomeninges]] surrounding the brain.<ref name="Zhou et al. 2012"/> Deletion of the BGT1 gene in mice did not appear to have any impact on the tendency to develop epilepsy.<ref name="Lehre et al. 2011">{{cite journal |vauthors=Lehre AC, Rowley NM, Zhou Y, Holmseth S, Guo C, Holen T, Hua R, Laake P, Olofsson AM, Poblete-Naredo I, Rusakov DA, Madsen KK, Clausen RP, Schousboe A, White HS, Danbolt NC | title = Deletion of the betaine-GABA transporter (BGT1; slc6a12) gene does not affect seizure thresholds of adult mice | journal = Epilepsy Res | volume = 95 | issue = 1–2 | pages = 70–81 | year = 2011 | pmid = 21459558 | doi = 10.1016/j.eplepsyres.2011.02.014 | pmc=3376448}}</ref> This is to be expected considering that BGT1 is expressed at far lower levels than [[GABA transporter 1|GAT1]] and also has lower affinity for [[GABA]]. This implies that it is not likely to contribute significantly to the inactivation of the inhibitory neurotransmitter GABA.<ref name="Lehre et al. 2011"/>


Revision as of 13:32, 20 April 2019

SLC6A12
Identifiers
AliasesSLC6A12, BGT-1, BGT1, GAT2, solute carrier family 6 member 12
External IDsOMIM: 603080; MGI: 95628; HomoloGene: 128225; GeneCards: SLC6A12; OMA:SLC6A12 - orthologs
Orthologs
SpeciesHumanMouse
Entrez

6539

14411

Ensembl

ENSG00000111181

ENSMUSG00000030109

UniProt

P48065

P31651

RefSeq (mRNA)

NM_001122847
NM_001122848
NM_001206931
NM_003044

RefSeq (protein)

NP_001116319
NP_001116320
NP_001193860
NP_003035

n/a

Location (UCSC)Chr 12: 0.19 – 0.21 MbChr 6: 121.32 – 121.34 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Sodium- and chloride-dependent betaine transporter, also known as Na(+)/Cl(-) betaine/GABA transporter (BGT-1), is a protein that in humans is encoded by the SLC6A12 gene. BGT-1 is predominantly expressed in the liver (hepatocytes).[5] It is also expressed in the kidney[5] where it is regulated by NFAT5 during a response to osmotic stress.[6] Further, BGT1 is also present in the leptomeninges surrounding the brain.[5] Deletion of the BGT1 gene in mice did not appear to have any impact on the tendency to develop epilepsy.[7] This is to be expected considering that BGT1 is expressed at far lower levels than GAT1 and also has lower affinity for GABA. This implies that it is not likely to contribute significantly to the inactivation of the inhibitory neurotransmitter GABA.[7]

See also

References

  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000111181 – Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000030109 – 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. ^ a b c Zhou Y, Holmseth S, Hua R, Lehre AC, Olofsson AM, Poblete-Naredo I, Kempson SA, Danbolt NC (2012). "The betaine-GABA transporter (BGT1, slc6a12) is predominantly expressed in the liver and at lower levels in the kidneys and at the brain surface". Am J Physiol Renal Physiol. 302 (3): F316-28. doi:10.1152/ajprenal.00464.2011. PMID 22071246.
  6. ^ Lee SD, Choi SY, Lim SW, Lamitina ST, Ho SN, Go WY, Kwon HM (2011). "TonEBP stimulates multiple cellular pathways for adaptation to hypertonic stress: Organic osmolyte-dependent and -independent pathways". AJP: Renal Physiology. 300 (3): F707–F715. doi:10.1152/ajprenal.00227.2010. PMC 3064130. PMID 21209002.
  7. ^ a b Lehre AC, Rowley NM, Zhou Y, Holmseth S, Guo C, Holen T, Hua R, Laake P, Olofsson AM, Poblete-Naredo I, Rusakov DA, Madsen KK, Clausen RP, Schousboe A, White HS, Danbolt NC (2011). "Deletion of the betaine-GABA transporter (BGT1; slc6a12) gene does not affect seizure thresholds of adult mice". Epilepsy Res. 95 (1–2): 70–81. doi:10.1016/j.eplepsyres.2011.02.014. PMC 3376448. PMID 21459558.


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