ライフサイエンスコーパス: SERT

1 SERT activity is modulated by antidepressants, e.g., S-c

2 SERT binding increases correlated with treatment-induced

3 SERT crystal structures reveal two S-citalopram binding

4 SERT has garnered significant clinical attention partly

5 SERT is a target for antidepressant and psychostimulant

6 SERT is encoded by the same gene expressed in trophoblas

7 SERT knockdown in the MRN increased cocaine intake selec

8 SERT knockdown in the MRN or DRN produced anxiety-like b

9 SERT mediates the reuptake of serotonin through an alter

10 SERT nondisplaceable binding potential was quantified in

11 SERT(+) fibers were shown to distributed moderately to d

12 SERT(-/-) mice displayed higher abundances of Bacilli sp

13 SERT-mediated substrate uptake was neither affected by i

14 Here we utilize the C57BL/6J SERT Met172 model to evaluate SERT dependence for the ac

15 Consistent with its activity as a SERT substrate, 4-MEC evoked inward current in SERT-expr

16 ade (citalopram dosing) or genetic ablation (SERT(-/-)) of SERT function in vivo led to reduced serot

17 on scales down the population size of active SERT molecules and, as a consequence, lowers the effecti

18 itor binding to Asn177 mutants of ts2-active SERT.

19 In addition, SERT is a major molecular target for psychostimulants su

20 In addition, SERT Met172 mice are insensitive to chronic fluoxetine a

21 DRD2, DRD3, DAT1, COMT, DDC, GRIN2B, ADRA2C, SERT, TPH2, HTR2A, OPRK1 and OPRM1 genes.

22 facilitate rational design of high-affinity SERT allosteric inhibitors.

23 ing a protective effect of estradiol against SERT loss.

24 Although SERT(-/-) platelets displayed no difference in P-selecti

25 occupancy (<5%) was observed at 5-HT(1A) and SERT at 4 mg/day.

26 ed chimeric proteins to test whether DAT and SERT N and C termini contribute to transporter substrate

27 merous studies have investigated the DAT and SERT structural elements contributing to inhibitor and s

28 methylphenidate and desipramine for DAT and SERT, respectively, can be accounted for by their rate o

29 4-MePPP into the binding pockets for DAT and SERT.

30 urpassed pepsin for the digestion of DAT and SERT.

31 esulting mutants SERT-F604Q, SERT-I608Q, and SERT-I612Q were retained in the endoplasmic reticulum, b

32 relationship between the gut microbiome and SERT, this study assessed the fecal and cecal microbiome

33 MA analogs inhibited uptake at DAT, NET, and SERT, but lengthening the amine substituent from methyl

34 norepinephrine, and serotonin (DAT, NET, and SERT, respectively).

35 gth of 4-MA on interactions at DAT, NET, and SERT.

36 hile binding to D(3), 5-HT(1A) receptors and SERT was not detectable with the radiotracers used for t

37 T - SERT," where GoRT is the go trial RT and SERT is the stop error RT.

38 17-item Hamilton Depression Rating Scale and SERT binding as imaged by [(11)C]DASB positron emission

39 rforming reuptake of released serotonin, and SERT is the primary target for antidepressants.

40 ERT-DeltaN32 than that of wild type SERT and SERT-DeltaN22.

41 e profile of 11 to 12 week-old SERT(+/+) and SERT(-/-) mice.

42 pecies were identified between SERT(+/+) and SERT(-/-).

43 ice demonstrated decreased midbrain Tph2 and SERT expression levels and reduced Tph2 levels in the DR

44 thermore, SSRIs protected both wild-type and SERT knockout mice from behavioral despair induced by ch

45 slices reveal that alphavbeta3 receptors and SERTs are enriched in presynaptic membranes from several

46 All analogs acted as SERT substrates, though N-butyl 4-MA had very weak effec

47 t male mice expressing the autism-associated SERT Ala56 variant have altered central serotonin (5-HT)

48 aCaMKII modulation for amphetamine action at SERT in vivo as well.

49 nity interactions of many antidepressants at SERT have been ablated via knock-in substitution (SERT M

50 ion of high-affinity cocaine interactions at SERT in DAT Val559 mice, or specific inhibition of 5-HT(

51 differential effects of 4-MEC and 4-MePPP at SERT.

52 nt bacterial species were identified between SERT(+/+) and SERT(-/-).

53 The interaction between SERT and alphaCaMKII was verified using biochemical assa

54 icted by the statistical interaction between SERT and DAT availability, in the amygdala, putamen, and

55 s were rescued in DAT chimeras encoding both SERT N and C termini.

56 In contrast, in Li(+) -containing buffer, SERT showed only low force interactions.

57 However, amphetamine-induced efflux by SERT-DeltaN32 or SERT-DeltaN42 (but not by SERT-DeltaN22

58 ver to support amphetamine-induced efflux by SERT.

59 y SERT-DeltaN32 or SERT-DeltaN42 (but not by SERT-DeltaN22) was markedly diminished.

60 ons is sufficient to decrease 5-HT uptake by SERT in midbrain synaptosomes.

61 substrate efflux in both cells coexpressing SERT and alphaCaMKII and brain tissue preparations.

62 Expression of the most common SERT variant (Ala56) in mice increases 5-HT clearance an

63 Consistent SERT pathology in raphe nuclei, striatum, thalamus, and

64 pared the results with those of constitutive SERT knockout.

65 To provide molecular insight, we constructed SERT homology models based on the Drosophila melanogaste

66 In contrast, SERT knockdown in the DRN increased cocaine intake selec

67 es that resulted from increased or decreased SERT activity support the idea that 5-HT signaling regul

68 ation constant (K(D)) of chemically distinct SERT and DAT inhibitors, with high temporal precision an

69 In order to distinguish SERT-dependent and -independent effects of SSRIs, we dev

70 ted RNA interference to locally downregulate SERT expression and compared the results with those of c

71 ifferent combinations of maternal and embryo SERT Ala56 genotypes to examine effects on blood, placen

72 inding of only one radioligand was enhanced; SERT radioligand binding was minimally affected.

73 e the C57BL/6J SERT Met172 model to evaluate SERT dependence for the actions of two widely prescribed

74 GI perturbations, suggesting that excessive SERT activity leads to inadequate 5-HT4-mediated neuroge

75 Using membranes from HeLa cells expressing SERT and intact rat basophilic leukemia cells, we show t

76 he bulk of the resulting mutants SERT-F604Q, SERT-I608Q, and SERT-I612Q were retained in the endoplas

77 For SERT analysis, patients on selective serotonin reuptake

78 7 for 5-HT(2A) occupancy and [(11)C]DASB for SERT occupancy; Cohort 3 underwent scanning with [(11)C]

79 state, currents was significantly lower for SERT-DeltaN32 than that of wild type SERT and SERT-Delta

80 Voxel-wise binding potentials (BP(ND)) for SERT and DAT were determined in 27 patients with SAD and

81 ent test-retest reliability was observed for SERT binding in the striatum.

82 adiol levels as a novel treatment option for SERT deficiency associated obesity and metabolic abnorma

83 perlocomotion in DAT Val559 mice arises from SERT blockade and augmented 5-HT signaling relative to c

84 Time-activity curves were derived from SERT-rich structures and fit to 2 models: a simplified r

85 nserin revealed that platelets isolated from SERT(-/-) or citalopram-treated mice have reduced activa

86 Furthermore, SERT(-/-) mice exhibited significantly lower abundances

87 beta3 and significantly contribute to global SERT function at 5-HT synapses in the midbrain.

88 between go and stop error trials or "GoRT - SERT," where GoRT is the go trial RT and SERT is the sto

89 t SFG also correlated negatively with GoRT - SERT.

90 of the 5-HT signalling system (5-HT, 5-HIAA, SERT) and TNF-alpha expression were examined in the dist

91 itter systems, SAD patients exhibited higher SERT binding in the nucleus accumbens while DAT availabi

92 However, how SERT deficiency promotes obesity is unknown.

93 -MEC and 4-MePPP with transporters for 5-HT (SERT) and dopamine (DAT) using molecular, cellular, and

94 try to study conformational changes in human SERT (hSERT) during 5-HT transport and inhibitor binding

95 Mutations in human SERT are associated with psychiatric disorders and autis

96 t X-ray crystallographic structures of human SERT at 3.15 A resolution bound to the antidepressants (

97 ling the conformational equilibrium of human SERT.

98 ard-facing conformational state of the human SERT induced by serotonin.

99 the dynamic changes that occur in the human SERT upon binding of ions, the translocation of substrat

100 ne the mechanism of antidepressant action in SERT, and provide blueprints for future drug design.

101 Bacterial community structure was altered in SERT(-/-) mice.

102 ed to determine whether there are changes in SERT availability in the early symptomatic state and if

103 Conformational changes in SERT occur upon binding of ions and substrate and are cr

104 RT substrate, 4-MEC evoked inward current in SERT-expressing Xenopus oocytes, whereas 4-MePPP was ina

105 in the midbrain, accompanied by decreases in SERT activity and reduced localization of SERTs to integ

106 e-to-female transsexuals led to decreases in SERT binding in insula, anterior, and mid-cingulate cort

107 tolerance, supporting a role for estrogen in SERT deficiency-associated obesity and glucose intoleran

108 and citalopram fail to reduce immobility in SERT Met172 mice.

109 namic across pregnancy and were increased in SERT Ala56 dams at E14.5.

110 ort that estrogen suppression is involved in SERT deficiency-induced obesity and glucose intolerance,

111 bbeta3 activation by ADP and 5-HT is lost in SERT(-/-) platelets.

112 inding site and orientation of paroxetine in SERT remain controversial.

113 iated alphaIIbbeta3 activation is reduced in SERT(-/-) platelets.

114 terations arising from genetic reductions in SERT.

115 17beta-estradiol replacement in SERT (-/-) mice reversed the obesity and glucose intoler

116 duces a dualistic conformational response in SERT.

117 tine, specifically its fluorophenyl ring, in SERT's substrate binding site directly depends on this p

118 associated with metabolic phenotype seen in SERT deficiency.

119 An opposite phenotype was seen in SERT-deficient mice and in progeny of WT dams given the

120 ce for the existence of two binding sites in SERT when accessed in a physiological context.

121 structure-based mechanisms for transport in SERT we investigated its complexes with ibogaine, a hall

122 ctures of DeltaN72/DeltaC13 and ts2-inactive SERT bound to paroxetine analogues using single-particle

123 ficant mammalian membrane proteins including SERT and DAT, neither of which tolerates complete remova

124 ent in female-to-male transsexuals increased SERT binding in amygdala, caudate, putamen, and median r

125 vels, suggesting that testosterone increases SERT expression on the cell surface.

126 ) such as fluoxetine or escitalopram inhibit SERT and are currently the principal treatment for depre

127 central nervous system, and drugs inhibiting SERT are widely used for the treatment of a variety of c

128 genetically or pharmacologically inhibiting SERT decreases LEE expression and reduces C. rodentium l

129 ility of the SERT Met172 model for isolating SERT/5-HT contributions of drug actions in vivo.

130 o conformationally dynamic transporters like SERT often require thermostabilizing mutations and antib

131 Antidepressants lock SERT in an outward-open conformation by lodging in the c

132 equence and structural homology to mammalian SERT.

133 Maternal SERT Ala56 genotype effects on forebrain 5-HT levels wer

134 Maternal SERT Ala56 genotype was associated with decreased placen

135 4.5 indicated substantial impact of maternal SERT Ala56 genotype, with alterations in immune and meta

136 ively, these findings indicate that maternal SERT function impacts offspring placental 5-HT levels, f

137 Moreover, SERT/DAT co-expression was significantly higher in SAD p

138 d TNF-alpha expression and decreased mucosal SERT expression and 5-HIAA.

139 ort activity to the folding-deficient mutant SERT-(601)PG(602)-AA.

140 Conversely, the vestibular mutant SERT-G402H merely displayed the high force population.

141 ding and flux assays on wild-type and mutant SERTs.

142 The bulk of the resulting mutants SERT-F604Q, SERT-I608Q, and SERT-I612Q were retained in

143 ere associated with increases in neocortical SERT binding in the GnRHa group relative to placebo (p =

144 SSRIs revealed that functional 5-HT2ARs, not SERTs, are necessary for the synergistic activation of a

145 Complete or cortex-specific ablation of SERT increases the number of functional PFC glutamate sy

146 n both in the presence and in the absence of SERT.

147 D2R, antagonists of 5-HT6R, and blockers of SERT.

148 of H(+) to the inward-facing conformation of SERT in (i) cancelling out the electrogenic nature of in

149 detect a more outward-facing conformation of SERT.

150 that stabilize outward-open conformations of SERT decreased phosphorylation and agents that stabilize

151 lyzed their impact on the transport cycle of SERT by biochemical approaches and by electrophysiologic

152 Mice with deletion of SERT develop metabolic syndrome as they age.

153 diction was verified by tryptic digestion of SERT-expressing membranes: in the absence of Na(+), the

154 BPND agreed with the distribution of SERT in the rat brain.

155 CVH animals showed a downregulation of SERT mRNA expression in urothelium, suggesting increased

156 The conformational dynamics of SERT transport function and inhibition is currently poor

157 demonstrate that developmental expression of SERT in this subset of PFC neurons controls synaptic mat

158 a-helix to Lys reduced surface expression of SERT-E615K.

159 llular loop 1 restored surface expression of SERT-R152E/E615K to wild type levels.

160 ormational search associated with folding of SERT.

161 (603)-Thr(613)) was important for folding of SERT.

162 humans yet they vary in their time frames of SERT disruption.

163 our results demonstrate that an increase of SERT activity is sufficient to cause the apneas in Necdi

164 -type Ca(2+) channels and was independent of SERT.

165 nnels and synaptic plasticity independent of SERT.

166 Here, we examine how sustained inhibition of SERT activity alters serotonergic signaling and influenc

167 ice with paroxetine, a chemical inhibitor of SERT, also resulted in Cyp19a1 suppression, decreased ci

168 ) to various conformational intermediates of SERT during the transport cycle.

169 determine the IR activity, surface level of SERT, and their 5-HT uptake rates.Interestingly, no sign

170 In mice, constitutive loss of SERT causes life-long increases in anxiety-related behav

171 e results are consistent with a mechanism of SERT regulation that is activated by the transport of 5-

172 Thus, the exchange mode of SERT-DeltaN32 was selectively impaired.

173 a meta-analysis to identify the patterns of SERT pathology and the relevance to symptoms.

174 The phenotype of SERT knockout rats was a summation of the phenotypes gen

175 of these mutations affect the regulation of SERT activity by cGMP-dependent phosphorylation.

176 definitive support for an essential role of SERT antagonism in the acute and chronic actions of two

177 Here, we review the role of SERT in the development of motor and nonmotor complicati

178 m dosing) or genetic ablation (SERT(-/-)) of SERT function in vivo led to reduced serotonin (5-hydrox

179 ind to the central substrate-binding site of SERT, stabilize the outward-open conformation, and inhib

180 eport cryo-electron microscopy structures of SERT-ibogaine complexes captured in outward-open, occlud

181 indicate the existence of a subpopulation of SERT responding differently to serotonin binding than hi

182 havbeta3 colocalizes with a subpopulation of SERT-containing synapses in raphe nuclei.

183 sterol plays a role in this subpopulation of SERT.

184 substituting the DAT C terminus with that of SERT affected neither substrate nor inhibitor affinities

185 Replacing the DAT N terminus with that of SERT had no effect on DA transport Vmax but significantl

186 The folding trajectory of SERT is thought to proceed through the inward facing con

187 in SERT activity and reduced localization of SERTs to integrin adhesion complexes in synapses of KI m

188 to wild-type levels, suggesting that loss of SERTs causes a deficiency in platelet activation.

189 ent with the existence of a subpopulation of SERTs that are tightly modulated by integrin alphavbeta3

190 ecal microbiome profile of 11 to 12 week-old SERT(+/+) and SERT(-/-) mice.

191 d DAT internalization, but had no effects on SERT endocytosis.

192 mouse integrin beta3 subunit gene (Itgb3) on SERT function and selective 5-hydroxytryptamine (5-HT) r

193 HT, which increases the level of inward-open SERT and may lead to unwinding of the TM5 helix to allow

194 phetamine-induced efflux by SERT-DeltaN32 or SERT-DeltaN42 (but not by SERT-DeltaN22) was markedly di

195 I-113) with greater selectivity for DAT over SERT retains locomotor activation in DAT Val559 mice.

196 PFC-SERT+ neurons establish glutamatergic synapses with subc

197 how that pharmacogenetic manipulation of PFC-SERT+ neuron activity bidirectionally modulates these sy

198 diabetes mellitus (GDM)-associated placenta, SERT is found entrapped in the cytoplasm of the GDM-trop

199 Conversely, pregnant SERT (-/-) mice displayed normalized estrogen levels, ma

200 in rats, (11)C-DASB can be used to quantify SERT density with good reproducibility.

201 he alphavbeta3-mediated mechanism of reduced SERT function indicate that decreased integrin beta3 sub

202 elated negatively with decreases in regional SERT binding, indicating a protective effect of estradio

203 els were correlated with changes in regional SERT nondisplaceable binding potential.

204 Remarkably, SERT inhibitor Lu AF60097, the first high-affinity S2-li

205 ition of focal adhesion kinase (FAK) rescued SERT function in synapses of KI mice, demonstrating that

206 ymporters for the biogenic amines serotonin (SERT), dopamine (DAT), and norepinephrine (NET) are targ

207 he presynaptic dopamine (DAT) and serotonin (SERT) transporters, respectively.

208 n of the transporter proteins for serotonin (SERT) and dopamine (DAT) in patients with social anxiety

209 e transporters for the monoamines serotonin (SERT) and dopamine (DAT) are prominent targets of variou

210 6A2, NET) and serotonin transporter (SLC6A4, SERT) genes and remission in depressed older adults trea

211 ly postnatal period in mice (P0-P10), Slc6a4/SERT is transiently expressed in a subset of layer 5-6 p

212 ly, coinciding with the period of PFC Slc6a4/SERT expression.

213 hat block the serotonin transporter, (Slc6a4/SERT), selective serotonin reuptake inhibitors (SSRIs) i

214 henotypes generated by MRN- and DRN-specific SERT knockdown.

215 In both acute and chronic studies, SERT Met172 mice maintained sensitivity to paroxetine, a

216 have been ablated via knock-in substitution (SERT Met172) without disrupting 5-HT recognition or upta

217 Upon rapid application of a substrate, SERT and DAT display an inwardly directed current compri

218 These data suggest SERT polymorphisms influence imatinib-induced diarrhoea

219 e Pro32Pro33 integrin alphavbeta3 suppresses SERT activity.

220 ether, these data demonstrate that sustained SERT loss of function reduces 5-HT2AR surface expression

221 The consequences of therapies targeting SERT during pregnancy warrant further evaluation.

222 Here, we demonstrated that SERT (-/-) mice display abnormal fat accumulation in bot

223 Our results show that SERT deletion is associated with dysbiosis similar to th

224 These results suggest that SERT inhibition by FLX may hinder survival in hypoxia.

225 The SERT inhibition by Lu AF60097 is demonstrated by the pot

226 5-HT uptake rates of GDM-trophoblast and the SERT expression on their surface were severalfold lower

227 riatum (caudate nucleus and putamen) and the SERT-rich extrastriatal brain regions (thalamus, hypotha

228 ent mice and in progeny of WT dams given the SERT antagonist fluoxetine.

229 Consistent with this idea, the SERT blocker fluoxetine abolished methylphenidate-induce

230 Given the central role of the SERT in the treatment of depression and anxiety disorder

231 hese tests, and reinforce the utility of the SERT Met172 model for isolating SERT/5-HT contributions

232 was specific for DAT, because replacing the SERT N and/or C termini affected neither substrate nor i

233 After fecal microbiota transplantation, the SERT expression in the colonic tissue was significantly

234 her, intestinal dysbiosis may upregulate the SERT expression and contribute to the development of chr

235 At a more lenient statistical threshold, SERT and DAT BP(ND) were also higher in other striatal a

236 impact on clearance into enterocytes through SERT.

237 methylphenidate, and desipramine binding to SERT and DAT.

238 AT and hypothalamic (123)I-FP-CIT binding to SERT are significantly lower in MSA-P and PSP than in PD

239 AT and hypothalamic (123)I-FP-CIT binding to SERT are significantly lower in MSA-P and PSP than in PD

240 extrastriatal (123)I-FP-CIT SPECT binding to SERT between MSA, PSP, and PD.

241 ion, our data suggest that Cl(-) is bound to SERT during the entire catalytic cycle.

242 cteristic binding strengths of citalopram to SERT were revealed in Na(+)-containing buffer.

243 Transfusion of wild-type platelets to SERT(-/-) mice normalized bleeding times to wild-type le

244 ose of ESC and, although somewhat similar to SERT deficiency, were not associated with changes in hip

245 ey dopaminergic (TH) and serotonergic (Tph2, SERT, and Pet-1) genes, and midbrain monoamine content i

246 there is much support for 5-HT transporter (SERT) antagonism as a basis of antidepressant efficacy,

247 tic deficiency in the host 5-HT transporter (SERT) increases the relative abundance of spore-forming

248 via its modulation of the 5-HT transporter (SERT).

249 tamine), into cells by the 5-HT transporter (SERT).

250 expression and activity of 5-HT Transporter (SERT/Slc6a4) in 5-HT neurons leading to an increase of 5

251 tions with the serotonin (5-HT) transporter (SERT), we hypothesized that the lack of cocaine-induced

252 ariants of the serotonin (5-HT) transporter (SERT, encoded by SLC6A4) have been identified in ASD.

253 eceptor subtypes, the serotonin transporter (SERT) and 5-HT-producing enzymes was determined in the u

254 The serotonin transporter (SERT) and other monoamine transporters operate in either

255 on forces between the serotonin transporter (SERT) and the S- and R-enantiomers of citalopram on the

256 th change in cerebral serotonin transporter (SERT) binding following intervention.

257 epressants target the serotonin transporter (SERT) by inhibiting serotonin reuptake.

258 for quantification of serotonin transporter (SERT) density and affinity in vivo in rats and mice.

259 C-HOMADAM) imaging of serotonin transporter (SERT) density in healthy control subjects.

260 -binding to the human serotonin transporter (SERT) expressed in HEK-293 cells.

261 In addition, serotonin transporter (SERT) expression was upregulated in both DRN projection

262 tributed to a reduced serotonin transporter (SERT) function.

263 eractions between the serotonin transporter (SERT) gene and ITGB3, which encodes the beta3 subunit th

264 T studies imaging the serotonin transporter (SERT) have been used and provided evidence for the key r

265 indings implicate the serotonin transporter (SERT) in autism spectrum disorder (ASD).

266 Serotonin transporter (SERT) is a transmembrane transport protein which re-upta

267 The serotonin transporter (SERT) is an integral membrane protein that exploits pree

268 Serotonin transporter (SERT) is responsible for reuptake and recycling of 5-hyd

269 om wild-type rats and serotonin transporter (SERT) knockout mice.

270 -HT(1A), 5-HT(2A) and serotonin transporter (SERT) occupancies of brexpiprazole in adult subjects wit

271 ot potentiated by the serotonin transporter (SERT) or the noradrenaline transporter (NET) inhibitors

272 Serotonin transporter (SERT) plays a critical role in regulating extracellular

273 ced expression of the serotonin transporter (SERT) promotes anxiety and cocaine intake in both humans

274 The serotonin transporter (SERT) regulates neurotransmission by the biogenic monoam

275 The serotonin transporter (SERT) regulates neurotransmitter homeostasis through the

276 The serotonin transporter (SERT) terminates serotonergic neurotransmission by perfo

277 The serotonin transporter (SERT) terminates serotonergic signalling through the sod

278 The serotonin transporter (SERT) terminates serotonin signaling by rapid presynapti

279 only observed at the serotonin transporter (SERT), dopamine D2-like, and sigma1 receptors.

280 t the plasma membrane serotonin transporter (SERT), modulate hemostasis.

281 dest affinity for the serotonin transporter (SERT), predominantly represented in extrastriatal bindin

282 ransporter (DAT), and serotonin transporter (SERT)-by the use of porcine pepsin and three alternative

283 Rodents exposed to serotonin transporter (SERT)-inhibiting antidepressants during development show

284 mpairment/loss in the serotonin transporter (SERT).

285 by the high-affinity serotonin transporter (SERT).

286 the membrane-embedded serotonin transporter (SERT).

287 The serotonin transporter (SERT/SLC6A4) has a rich pharmacology including inhibitor

288 orting folding of the serotonin transporter (SERT; SLC6A4).

289 tion in the serotonin re-uptake transporter (SERT) gene.

290 anslocation of serotonin (5-HT) transporter, SERT to the plasma membrane of the trophoblast in placen

291 mmunostaining for the serotonin transporter, SERT, we describe the complete pattern of distribution o

292 uently removed by the serotonin transporter, SERT.

293 t uptake by serotonin reuptake transporters (SERTs) prevented the pooling of serotonin from prolongin

294 ects were not observed in paroxetine-treated SERT (-/-) mice.

295 ity markedly decreased amphetamine-triggered SERT-mediated substrate efflux in both cells coexpressin

296 wer for SERT-DeltaN32 than that of wild type SERT and SERT-DeltaN22.

297 patients with constipation also upregulated SERT in Caco-2 cells.

298 ments that govern drug selectivity at DAT vs SERT.

299 voltage-independent rate-limiting step where SERT may return to the outward-facing state in a KCl- or

300 nd noradrenaline transporters, together with SERT, are members of the neurotransmitter sodium symport