Serotonin transporter 480669 224252936 2008-07-08T00:30:50Z ProteinBoxBot 3991663 Replaced protein Box Template with PBB Template for easy viewing. {{PBB|geneid=6532}} The '''[[serotonin]] transporter''' (SERT) is a [[monoamine transporter]] [[protein]]. <!-- The PBB_Summary template is automatically maintained by Protein Box Bot. See Template:PBB_Controls to Stop updates. --> {{PBB_Summary | section_title = | summary_text = This protein is an integral membrane protein that transports the neurotransmitter serotonin from synaptic spaces into presynaptic neurons. This transport of serotonin by the SERT protein terminates the action of serotonin and recycles it in a sodium-dependent manner. This protein is a target of psychomotor stimulants, such as amphetamines and cocaine, and is a member of the sodium:neurotransmitter symporter family. A repeat length polymorphism in the promoter of this gene has been shown to affect the rate of serotonin uptake and may play a role in sudden infant death syndrome, aggressive behavior in Alzheimer disease patients, [[post-traumatic stress disorder]] and depression-susceptibility in people experiencing emotional trauma.<ref>{{cite web | title = Entrez Gene: SLC6A4 solute carrier family 6 (neurotransmitter transporter, serotonin), member 4| url = http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=6532| accessdate = }}</ref> }} ==Function== It reuptakes serotonin in the synaptic cleft and terminates its function. It allows [[neuron]]s, [[platelet]]s, and other cells to accumulate the chemical [[neurotransmitter]] [[serotonin]], which affects [[emotion]]s and drives. Neurons communicate by using chemical messages like serotonin between cells. The [[transporter protein]], by recycling serotonin, regulates its concentration in a gap, or [[synapse]], and thus its effects on a receiving neuron’s [[receptor (biochemistry)|receptor]]. Medical studies have shown that changes in serotonin transporter metabolism appear to be associated with many different phenomena, including [[alcoholism]], [[clinical depression]], [[obsessive-compulsive disorder]] (OCD), [[romantic love]]<ref>{{Cite journal | author = [[Donatella Marazziti]], H.S. Akiskal, A. Rossi, G.B. Cassano | title = Alteration of the platelet serotonin transporter in romantic love | journal = [[Psychological Medicine]] | year = 1999 | month = May | volume = 29 | issue = 3 | pages = 741–745 | pmid = 10405096 | url = http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=26031 | doi = 10.1017/S0033291798007946 }}</ref>, [[hypertension]] and [[generalized social phobia]]<ref>{{Cite journal | author = van der Wee et al. | title = Increased Serotonin and Dopamine Transporter Binding in Psychotropic Medication–Naïve Patients with Generalized Social Anxiety Disorder Shown by 123I-β-(4-Iodophenyl)-Tropane SPECT | journal = The Journal of Nuclear Medecine | year = 2008 | month = May | volume = 49 | issue = 5 | pages = 757–763 | pmid = 18413401 | url = http://www.ncbi.nlm.nih.gov/pubmed/18413401?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum | doi = 10.2967/jnumed.107.045518 }}</ref>. <gallery> Image:Serotonin (5-HT).svg|[[Serotonin]] </gallery> ==Pharmacology== SERT spans the plasma membrane 12 times. It belongs to NE, DA, SERT monoamine transporter family. Transporters are important sites for agents that treat [[psychiatric disorder]]s. Drugs that reduce the binding of serotonin to transporters ([[selective serotonin reuptake inhibitor]]s, or SSRIs) are used to treat mental disorders. About half of patients with OCD are treated with SSRIs. [[Fluoxetine]] is an example of a [[selective serotonin reuptake inhibitor]]. ==Genetics== [[image:Chromosome_17.svg|125px|thumb|[[Chromosome 17 (human)|Chromosome&nbsp;17]].]] The [[gene]] that encodes the serotonin transporter is called ''solute carrier family 6 neurotransmitter transporter, serotonin), member 4'' (SLC6A4). (See [[Solute carrier family]]). In [[human]]s the gene is found on [[chromosome 17]] on location 17q11.1&ndash;q12.<ref name="NakamuraM2000Human">{{Cite journal | author = M. Nakamura, S. Ueno, A. Sano & H. Tanabe | title = The human serotonin transporter gene linked polymorphism (5-HTTLPR) shows ten novel allelic variants | journal = [[Molecular Psychiatry]] | year = 2000 | volume = 5 | pages = 32&ndash;38 | doi = 10.1038/sj.mp.4000698 }}</ref> Mutations associated with the gene may result in changes in serotonin transporter function, and experiments with [[mouse|mice]] have identified more the 50 different phenotypic changes as a result of genetic variation. These phenotypic changes may, e.g., be increased [[anxiety]] and [[gut]] dysfunction.<ref name="MurphyD2008Targeting">{{Cite journal | author = Dennis L. Murphy & [[Klaus-Peter Lesch]] | title = Targeting the murine serotonin transporter: insights into human neurobiology | journal = [[Nature Reviews Neuroscience]] | volume = 9 | pages = 85&ndash;96 | month = February | year = 2008 | doi = 10.1038/nrn2284 }}</ref> Some of the human genetic variations associated with the gene are:<ref name="MurphyD2008Targeting"/> * Length variation in the serotonin-transporter-gene-linked polymorphic region ([[5-HTTLPR]]) * [[rs25531]] &mdash; a [[single nucleotide polymorphism]] (SNP) in the 5-HTTLPR * [[rs25532]] &mdash; another SNP in the 5-HTTLPR * STin2 &mdash; a [[variable number of tandem repeats]] (VNTR) in the functional [[intron]] 2 * G56A on the second [[exon]] * I425V on the ninth exon === Length variation in 5-HTTLPR === The [[promotor]] region of the SLC6A4 gene contains a [[Polymorphism (biology)|polymorphism]] with "short" and "long" repeats in a region: 5-HTT-linked polymorphic region ([[5-HTTLPR]] or ''SERTPR'').<ref>{{Cite journal | author = [[Armin Heils]], Andreas Teufel, Susanne Petri, Gerald Stöber, Peter Riederer, Dietmar Bengel, & [[Klaus-Peter Lesch]] | title = Allelic variation of human serotonin transporter gene expression | journal = [[Journal of Neurochemistry]] | volume = 66 | issue = 6 | pages = 2621&ndash;2624 | year = 1996 | month = June | pmid = 8632190 | doi = 10.1046/j.1471-4159.1996.66062621.x | doi_brokendate = 2008-06-21 }}</ref> The short variation has 14 repeats of a sequence while the long variation has 16 repeats.<ref name="NakamuraM2000Human"/> The short variation leads to less [[transcription (genetics)|transcription]] for SLC6A4, and it has been found that it can partly account for anxiety-related [[personality trait]]s.<ref>{{Cite journal | author = [[Klaus-Peter Lesch]], Dietmar Bengel, Armin Heils, Sue Z. Sabol, Benjamin D. Greenberg, Susanne Petri, Jonathan Benjamin, Clemens R. Müller, Dean H. Hamer, Dennis L. Murphy | doi = 10.1126/science.274.5292.1527 | issue = 5292 | journal = [[Science (journal)|Science]] | month = November | title = Association of Anxiety-Related Traits with a Polymorphism in the Serotonin Transporter Gene Regulatory Region | url = http://www.sciencemag.org/cgi/content/abstract/274/5292/1527 | volume = 274 | year = 1996 | pages = 1527 | pmid = 8929413 }}</ref> This polymorphism has been extensively investigated in over 300 scientific studies (as of 2006).<ref>{{Cite journal | title = Simultaneous genotyping of four functional loci of human SLC6A4, with a reappraisal of 5-HTTLPR and rs255531 | journal = Molecular Psychiatry | year = 2006 | pages = 1–3 | doi = 10.1038/sj.mp.4001789 | author = J.R. Wendland, B.J. Martin, M.R. Kruse, [[K.-P. Lesch]], D.L. Murphy | volume = 274 }}</ref> The 5-HTTLPR polymorphism may be subdivided further: One study published in 2000 found 14 [[allele|allelic]] variants (14-A, 14-B, 14-C, 14-D, 15, 16-A, 16-B, 16-C, 16-D, 16-E, 16-F, 19, 20 and 22) in a group of around 200 [[Japanese people|Japanese]] and [[Caucasian race|Caucasian]] people.<ref name="NakamuraM2000Human"/> The low-expression variant of the 5-HTTLPR polymorphism (the short version) increased risk of socalled "posthurricane" [[post-traumatic stress disorder]] (PTSD) and [[major depression]] but only under the conditions of high hurricane exposure and low social support after adjustment for sex, ancestry, and age. Similar effects were found for major depression. High-risk individuals (high hurricane exposure, the low-expression 5-HTTLPR variant, low social support) were at 4.5 times the risk of developing PTSD and major depression of low-risk individuals.<ref>{{Cite journal | author = [[Dean G. Kilpatrick]], Koenen KC, Ruggiero KJ, Acierno R, Galea S, Resnick HS, Roitzsch J, Boyle J, [[Joel Gelernter]] | year = [[2007]] | month = November | title = The serotonin transporter genotype and social support and moderation of posttraumatic stress disorder and depression in hurricane-exposed adults | journal = [[The American Journal of Psychiatry]] | volume = 164 | issue = 11 | pages = 1693&ndash;1699 | pmid = 17974934 | doi = 10.1176/appi.ajp.2007.06122007 }}</ref> In addition to altering the expression of SERT protein and concentrations of extracellular serotonin in the brain, the 5-HTTLPR variation is associated with changes in brain structure. One study found less [[grey matter]] in perigenual [[anterior cingulate cortex]] and [[amygdala]] for short allele carriers of the [[5-HTTLPR]] polymorphism compared to subjects with the long/long genotype.<ref>{{Cite journal | author = Lukas Pezawas, [[Andreas Meyer-Lindenberg]], Emily M. Drabant, Beth A. Verchinski, Karen E. Munoz, Bhaskar S. Kolachana, Michael F. Egan, Venkata S. Mattay, Ahmaad R. Hariri & [[Daniel R. Weinberger]] | title = 5-HTTLPR polymorphism impacts human cingulate-amygdala interactions: a genetic susceptibility mechanism for depression | journal = [[Nature Neuroscience]] | volume = 8 | issue = 6 | month = June | year = [[2005]] | doi = 10.1038/nn1463 | pages = 828 }}</ref> In another study, people who inherited two short [[allele]]s were found to have more neurons and a larger volume in the pulvinar and limbic regions of the thalamus. Enlargement of the thalamus and reduced cortical volume provides an anatomical basis for why people who inherit the 5-HTTLPRshort/short genotype are more vulnerable to major depression, post-traumatic stress disorder, and suicide.<ref>Young KA, Holcomb LA, Yazdani U, Bonkale W, Hicks PB and German DC. 5HTTLPR polymorphism and enlargement of the pulvinar: Unlocking the backdoor to the limbic system. ''Biol Psychiatry''. 2007. 61: 813-8 PMID 17083920.</ref> In contrast, a 2008 meta-analysis found no significant overall association between the 5-HTTLPR polymorphism and autism.<ref name=Huang-Santangelo>{{cite journal |journal= Am J Med Genet B Neuropsychiatr Genet |date=2008 |title= Autism and serotonin transporter gene polymorphisms: a systematic review and meta-analysis |author= Huang CH, Santangelo SL |doi=10.1002/ajmg.b.30720 |pmid=18286633 |volume= 8 |pages= 828}}</ref> === rs25532 === rs25532 is a SNP (C>T) close to the site of 5-HTTLPR. It has been examined in connection with [[obsessive compulsive disorder]] (OCD).<ref>{{Cite journal | author = [[Jens R. Wendland]], [[Pablo R. Moya]], [[Matthew R. Kruse]], [[Renee F. Ren-Patterson]], [[Catherine L. Jensen]], [[Kiara R. Timpano]] & [[Dennis L. Murphy]] | title = A novel, putative gain-of-function haplotype at SLC6A4 associates with obsessive-compulsive disorder | journal = [[Human molecular genetics]] | volume = 17 | issue = 5 | pages = 717–713 | year = 2008 | month = March | doi = 10.1093/hmg/ddm343 | pmid = 18055562 | url = http://hmg.oxfordjournals.org/cgi/content/abstract/17/5/717 }}</ref> === I425V === I425V is a rare mutation on the ninth exon. Researchers have found this genetic variation in unrelated families with [[OCD]], and that it leads to faulty transporter function and regulation. A second variant in the same gene of some patients with this mutation suggests a genetic "double hit", resulting in greater biochemical effects and more severe symptoms.<ref>{{Cite journal | author = N. Ozaki, D. Goldman, W. H. Kaye, K. Plotnicov, B. D. Greenberg, J. Lappalainen, G. Rudnick and D. L. Murphy | title = Serotonin transporter missense mutation associated with a complex neuropsychiatric phenotype | journal = [[Molecular Psychiatry]] | volume = 8 | pages = 933&ndash;936 | year = [[2003]] | doi = 10.1038/sj.mp.4001365 | url = http://www.nature.com/mp/journal/v8/n11/full/4001365a.html }} News article: * {{Cite news | author = [[Reuters]] | title = Gene Found for Obsessive-Compulsive Disorder | publisher = Mental Health E-News | date = 2003-10-27 | url = http://www.nyaprs.org/Pages/View_ENews.cfm?ENewsID=2842 | accessdate = 2008-01-25 }}</ref><ref> {{Cite journal | author = R Delorme, C Betancur, M Wagner, M O Krebs, P Gorwood, P Pearl, G Nygren, C M Durand, F Buhtz, P Pickering, J Melke, S Ruhrmann, H Anckarsäter, N Chabane, A Kipman, C Reck4, B Millet, I Roy, M C Mouren-Simeoni, W Maier, M Råstam, C Gillberg, M Leboyer and T Bourgeron | title = Support for the association between the rare functional variant I425V of the serotonin transporter gene and susceptibility to obsessive compulsive disorder | journal = [[Molecular Psychiatry]] | year = [[2005]] | volume = 10 | pages = 1059–1061 | doi = 10.1038/sj.mp.4001728 | url = http://www.nature.com/mp/journal/v10/n12/full/4001728a.html }}</ref><ref>{{Cite web | author = [[Stephen Wheless]] | title = "The OCD Gene" Popular Press v. Scientific Literature: Is SERT Responsible for Obsessive-Compulsive Disorder? | publisher = [[Davidson College]] | url = http://www.bio.davidson.edu/courses/genomics/2004/Wheless/SERT.html | accessdate = 2008-06-12 }}</ref> === VNTR in STin2 === Another noncoding polymorphism is a [[VNTR]] in the second [[intron]] ([[STin2]]). It is found with three [[allele]]s: 9, 10 and 12 repeats. A [[meta-analysis]] has found that the 12 repeat allele of the STin2 VNTR polymorphism had some minor (with [[odds ratio]] 1.24) but statistical significant association with [[schizophrenia]].<ref>{{Cite journal | author = J. B. Fan & P. Sklar | title = Meta-analysis reveals association between serotonin transporter gene STin2 VNTR polymorphism and schizophrenia | journal = [[Molecular Psychiatry]] | year = 2005 | month = October | volume = 10 | issue = 10 | pages = 928&ndash;938 | pmid = 15940296 | doi = 10.1038/sj.mp.4001690 }}</ref> A 2008 meta-analysis found no significant overall association between the STin2 VNTR polymorphism and [[autism]].<ref name=Huang-Santangelo/> Furthermore a 2003 meta-analysis of [[affective disorder]]s, [[major depressive disorder]] and [[bipolar disorder]], found a little association to the intron 2 VNTR polymorphism, but the results of the meta-analysis depended on a large effect from one individual study.<ref>{{Cite journal | author = Anguelova M., Benkelfat C., Turecki G. | title = A systematic review of association studies investigating genes coding for serotonin receptors and the serotonin transporter: I. Affective disorders | journal = [[Molecular Psychiatry]] | year = 2003 | month = June | volume = 8 | issue = 6 | pages = 574&ndash;591 | pmid = 12851635 | doi = 10.1038/sj.mp.4001328 }}</ref> == Neuroimaging == The distribution of the serotonin transporter in the [[brain]] may be imaged with [[positron emission tomography]] using [[radioligand]]s called [[DASB]] and [[DAPP]], and the first studies on the human brain were reported in 2000.<ref>{{Cite journal | author = S. Houle, N. Ginovart, D. Hussey, J.H. Meyer, A.A. Wilson | title = Imaging the serotonin transporter with positron emission tomography: initial human studies with [<sup>11</sup>C]DAPP and [<sup>11</sup>C]DASB | journal = [[European Journal of Nuclear Medicine and Molecular Imaging]] | volume = 27 | issue = 11 | month = October | year = 2000 | doi = 10.1007/s002590000365 | pages = 1719 }}</ref> DASB and DAPP are not the only radioligands for the serotonin transporter. There are numerous others, with the most popular probably being the [[β-CIT]] radioligand with a [[isotopes of iodine|iodine-123]] [[isotope]] that is used for brain scanning with ''[[single photon emission computed tomography]]'' (SPECT).<ref>{{Cite journal | author = T. Brücke, J. Kornhuber, P. Angelberger, S. Asenbaum, H. Frassine, I. Podreka | title = SPECT imaging of dopamine and serotonin transporters with [<sup>123</sup>I]β-CIT. Binding kinetics in the human brain | journal = [[Journal of Neural Transmission]] | volume = 94 | issue = 2 | year = [[1993]] | month = June | pages = 137&ndash;146 | url = http://www.springerlink.com/content/q7vt554jqk32853h/ | doi = 10.1007/BF01245007 }}</ref> The radioligands have been used to examine whether variables such as age, gender or [[genotype]] are associated with differential serotonin transporter binding.<ref>{{Cite journal | author = Peter Brust, Swen Hess and Ulrich Müller and Zsolt Szabo | title = Neuroimaging of the Serotonin Transporter &mdash; Possibilities and Pitfalls | journal = [[Current Psychiatry Reviews]] | year = 2006 | month = February | volume = 2 | issue = 1 | pages = 111&ndash;149 | url = http://www-bmu.psychiatry.cam.ac.uk/publications/brust06neu.pdf | doi = 10.2174/157340006775101508 }}</ref> Healthy subjects that have a high score of [[neuroticism]] &mdash; a [[Trait theory|personality trait]] in the [[Revised NEO Personality Inventory]] &mdash; have been found to have more serotonin transporter binding in the [[thalamus]].<ref>{{Cite journal | author = [[Akihiro Takano]], Ryosuke Arakawaa, Mika Hayashia, Hidehiko Takahashia, Hiroshi Itoa & [[Tetsuya Suhara]] | title = Relationship between neuroticism personality trait and serotonin transporter binding | journal = [[Biological Psychiatry]] | volume = 62 | issue = 6 | month = September | year = [[2007]] | pages = 588&ndash;592 | doi = 10.1016/j.biopsych.2006.11.007 | pmid = 17336939 }}</ref> === Methodological issues === When the neuroimages from a DASB experiment are analyzed the kinetic models suggested by Ichise and coworkers<ref>{{Cite journal | author = Masanori Ichise, Jeih-San Liow, Jian-Qiang Lu, Akihiro Takano, Kendra Model, Hiroshi Toyama, Tetsuya Suhara, Kazutoshi Suzuki, Robert B Innis and Richard E Carson | title = Linearized Reference Tissue Parametric Imaging Methods: Application to [<sup>11</sup>C]DASB Positron Emission Tomography Studies of the Serotonin Transporter in Human Brain | journal = [[Journal of Cerebral Blood Flow & Metabolism]] | year = 2003 | volume = 23 | pages = 1096&ndash;1112 | doi = 10.1097/01.WCB.0000085441.37552.CA }}</ref> are often employed to estimate the [[binding potential]]. A [[test-retest]] [[reproducibility]] experiment has been performed to evaluate this approach for DASB.<ref>{{Cite journal | author = Jae Seung Kim, Masanori Ichise, Janet Sangare, and Robert B. Innis | title = PET Imaging of Serotonin Transporters with [<sup>11</sup>C]DASB: Test–Retest Reproducibility Using a Multilinear Reference Tissue Parametric Imaging Method | journal = [[Journal of Nuclear Medicine]] | volume = 47 | issue = 2 | pages = 208–214 | year = 2006 }}</ref> == Neuroimaging and genetics== Studies on the serotonin transporter have combined neuroimaging and genetics methods, e.g., a [[voxel-based morphometry]] study found less [[grey matter]] in perigenual [[anterior cingulate cortex]] and [[amygdala]] for short allele carriers of the [[5-HTTLPR]] polymorphism compared to subjects with the long/long genotype.<ref>{{Cite journal | author = Lukas Pezawas, [[Andreas Meyer-Lindenberg]], Emily M. Drabant, Beth A. Verchinski, Karen E. Munoz, Bhaskar S. Kolachana, Michael F. Egan, Venkata S. Mattay, Ahmaad R. Hariri & [[Daniel R. Weinberger]] | title = 5-HTTLPR polymorphism impacts human cingulate-amygdala interactions: a genetic susceptibility mechanism for depression | journal = [[Nature Neuroscience]] | volume = 8 | issue = 6 | month = June | year = [[2005]] | doi = 10.1038/nn1463 | pages = 828 }}</ref> ==References== {{reflist|2}} ==Further reading== {{refbegin | 2}} * NIH press release: [http://www.nih.gov/news/pr/aug2003/niaaa-18.htm Serotonin Transporter Gene Shown to Influence College Drinking Habits] * {{Cite journal | author = J.P. Roiser, L.J. Cook, J.D. Cooper, D.C. Rubinsztein, B.J. Sahakian | url = http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=pubmed&list_uids=15741482&dopt=Abstract | title = Association of a Functional Polymorphism in the Serotonin Transporter Gene With Abnormal Emotional Processing in Ecstasy Users | journal = [[American Journal of Psychiatry]] | year = 2005 | month = March | volume = 162 | issue = 3 | pages = 609–612 | doi = 10.1176/appi.ajp.162.3.609 | pmid = 15741482 }} {{PBB_Further_reading | citations = *{{cite journal | author=Ueno S |title=Genetic polymorphisms of serotonin and dopamine transporters in mental disorders |journal=J. Med. Invest. |volume=50 |issue= 1-2 |pages= 25–31 |year= 2003 |pmid= 12630565 |doi= }} *{{cite journal | author=Anguelova M, Benkelfat C, Turecki G |title=A systematic review of association studies investigating genes coding for serotonin receptors and the serotonin transporter: II. Suicidal behavior |journal=Mol. Psychiatry |volume=8 |issue= 7 |pages= 646–53 |year= 2004 |pmid= 12874600 |doi= 10.1038/sj.mp.4001336 }} *{{cite journal | author=Holmes A, Hariri AR |title=The serotonin transporter gene-linked polymorphism and negative emotionality: placing single gene effects in the context of genetic background and environment |journal=Genes Brain Behav. |volume=2 |issue= 6 |pages= 332–5 |year= 2004 |pmid= 14653304 |doi= }} *{{cite journal | author=Smits KM, Smits LJ, Schouten JS, ''et al.'' |title=Influence of SERTPR and STin2 in the serotonin transporter gene on the effect of selective serotonin reuptake inhibitors in depression: a systematic review |journal=Mol. Psychiatry |volume=9 |issue= 5 |pages= 433–41 |year= 2004 |pmid= 15037864 |doi= 10.1038/sj.mp.4001488 }} *{{cite journal | author=Cho HJ, Meira-Lima I, Cordeiro Q, ''et al.'' |title=Population-based and family-based studies on the serotonin transporter gene polymorphisms and bipolar disorder: a systematic review and meta-analysis |journal=Mol. Psychiatry |volume=10 |issue= 8 |pages= 771–81 |year= 2005 |pmid= 15824745 |doi= 10.1038/sj.mp.4001663 }} *{{cite journal | author=Serretti A, Benedetti F, Zanardi R, Smeraldi E |title=The influence of Serotonin Transporter Promoter Polymorphism (SERTPR) and other polymorphisms of the serotonin pathway on the efficacy of antidepressant treatments |journal=Prog. Neuropsychopharmacol. Biol. Psychiatry |volume=29 |issue= 6 |pages= 1074–84 |year= 2005 |pmid= 15939518 |doi= 10.1016/j.pnpbp.2005.03.013 }} *{{cite journal | author=Craig IW |title=The importance of stress and genetic variation in human aggression |journal=Bioessays |volume=29 |issue= 3 |pages= 227–36 |year= 2007 |pmid= 17295220 |doi= 10.1002/bies.20538 }} }} {{refend}} {{Membrane transport proteins}} {{Neurotransmitter transporters}} [[Category:Membrane biology]] [[Category:Neurotransmitter transporters]] [[Category:Solute carrier family]] [[ja:セロトニントランスポーター遺伝子]] <!-- The PBB_Controls template provides controls for Protein Box Bot, please see Template:PBB_Controls for details. --> {{PBB_Controls | update_page = yes | require_manual_inspection = no | update_protein_box = yes | update_summary = yes | update_citations = yes }}