ライフサイエンスコーパス: DAT

1 DAT can be safely administered in a setting with basic c

2 DAT deficit was defined as less than 65% of putamen stri

3 DAT is the target for psychostimulants-like cocaine and

4 DAT protected the host by priming the amplification loop

5 DAT surface availability is dynamically regulated by end

6 DAT was requested by healthcare providers for 151 suspec

7 DAT-HT mice were largely resilient to these effects, how

8 DAT-Knockout (DAT-KO) mouse is currently the best animal

9 e present the first evidence linking PIP(2), DAT, DA efflux, and phosphorylation processes with AMPH

10 re activity was observed between 180 and 210 DAT.

11 l neurons in acute hippocampal slices at 270 DAT, was reduced in epileptic mice but restored to naive

12 Results: Thirty-five studies (29 DAT, 6 AADC, no vesicular monoamine type 2 studies) with

13 nine to methionine substitution at site 356 (DAT T356M) was recently identified and has been shown to

14 Among 21 participants with hyposmia and a DAT deficit (65% or less of age-expected lowest putamen

15 four (3%) GBA non-manifesting carriers had a DAT deficit.

16 res both Ack1 inactivation, which releases a DAT-specific endocytic brake, and the neuronal GTPase, R

17 nding mutation in the leucine transporter, a DAT-homologous transporter, promotes an outward-facing t

18 mpared with 2 of 22 participants (9%) with a DAT in an indeterminate range (greater than 65%-80%) and

19 13), motor symptoms (HR = 2.11), an abnormal DAT scan (HR = 1.98), colour vision abnormalities (HR =

20 ishes DAT surface expression by accelerating DAT internalization.

21 , diamino propane tetraiodothyroacetic acid (DAT), is a thyro-integrin (integrin alphavbeta3) antagon

22 Therefore, mechanisms that acutely affect DAT availability will likely exert significant impact on

23 Interactions with partner proteins alter DAT function and thereby dynamically shape dopaminergic

24 g canonical transporter activity by altering DAT's conformational equilibrium.

25 ceptor binding (R(2)=0.07, p=0.33), although DAT and D1 receptor binding was positively correlated in

26 of striatal D2/3R (VR = 1.26, p < .0001) and DAT (VR = 1.31, p = .01) availabilities and synaptic dop

27 Mean D2/3R (g = 0.17, p = .14) and DAT (g = -0.20, p = .28) availabilities did not differ b

28 features of the disorder, altered D2/3R and DAT availabilities and synaptic dopamine levels may occu

29 jective was to examine baseline clinical and DAT imaging characteristics in non-manifesting carriers

30 vealed reduced extracellular baseline DA and DAT function in Chow/Palatable rats.

31 g and related neuroadaptations in the DA and DAT systems in this model of compulsive eating.

32 both PKC-mediated DAT-Rit2 dissociation and DAT internalization.

33 The combination of hyposmia and DAT deficit was highly predictive of conversion to PD wi

34 erse events by age, duration of illness, and DAT dosage using bivariate comparisons.

35 gitudinal follow-up of clinical measures and DAT imaging occurred at specialty centers.

36 the statistical interaction between SERT and DAT availability, in the amygdala, putamen, and dorsomed

37 more lenient statistical threshold, SERT and DAT BP(ND) were also higher in other striatal and limbic

38 ise binding potentials (BP(ND)) for SERT and DAT were determined in 27 patients with SAD and 43 age-

39 Tetraiodothyroacetic acid (tetrac) and DAT as thyroid hormone derivatives influence gene expres

40 ic Rit2-KD did not affect presynaptic TH and DAT protein levels in females, nor was TH was affected i

41 ne (CAM) assay used to measure angiogenesis, DAT (500 ng/CAM) resulted in 48% inhibition of angiogene

42 oxin confirmation, and diphtheria antitoxin (DAT) is obtained from CDC for treatment.

43 stration and safety of diphtheria antitoxin (DAT), the standard treatment for diphtheria.

44 a directed against DT (diphtheria antitoxin; DAT).

45 g information on age, non-motor assessments, DAT imaging, and CSF biomarkers.

46 ansporters, eliminates substrate activity at DAT and NET, and decreases abuse liability of the compou

47 zed, and evaluated for binding affinities at DAT, as well as the serotonin transporter and sigma(1) r

48 lkyl chain length of 4-MA on interactions at DAT, NET, and SERT.

49 reveal the underlying molecular mechanism at DAT that may be leveraged to rationally optimize leads f

50 All 4-MA analogs inhibited uptake at DAT, NET, and SERT, but lengthening the amine substituen

51 directional modulation of cocaine potency at DATs in the nucleus accumbens.

52 cocaine that can lead to addiction, atypical DAT inhibitors have been developed that prevent cocaine

53 Individuals with a baseline DAT deficit experienced a 4-year decline in DAT binding

54 ockdown in DAergic neurons impacted baseline DAT surface:intracellular distribution in DAergic termin

55 ations in the functional interaction between DAT and Kv2.1 affect dopamine neuron activity.

56 physical and functional interaction between DAT and the voltage-gated K(+) channel Kv2.1 (potassium

57 , and the neuronal GTPase, Rit2, which binds DAT.

58 s model assessed AF recurrence stratified by DAT <=1 year versus >1 year.

59 ary analysis assessed outcomes stratified by DAT <=3 years versus >3 years.

60 erapies, here we examined 13 disease-causing DAT mutants that were retained in the endoplasmic reticu

61 and in vivo experiments were done to compare DAT to NDAT.

62 Compared to a competitive DAT inhibitor indatraline, both SRI-compounds displayed

63 the cellular mechanisms that acutely control DAT surface expression.

64 Treatment with amphetamine deconstructed DAT complexes, reversed tolerance, and decreased cocaine

65 dence that clustered Kv2.1 channels decrease DAT's lateral mobility and inhibit its internalization,

66 vealed that PKC activation acutely decreased DAT surface expression selectively in ventral, but not d

67 Paradoxically, despite decreased DAT levels in males, striatal DA uptake was enhanced, bu

68 onfocal, super-resolution and EM, we defined DAT localization and its membrane diffusion parameters i

69 ria and diphtheria-like illness and describe DAT use during 1996-2018 in the United States.

70 doxically, imaging studies have not detected DAT targeting to classic recycling endosomes, suggesting

71 kinase C (PKC) activation acutely diminishes DAT surface expression by accelerating DAT internalizati

72 lly, amphetamine, that is thought to disrupt DAT OF conformation, reduced the concentration of wild-t

73 c manipulations on cocaine potency at distal DATs in the nucleus accumbens as well as the behavioral

74 nt with changes in cocaine potency at distal DATs.

75 proteins for serotonin (SERT) and dopamine (DAT) in patients with social anxiety disorder (SAD).

76 ll lines revealed that PKC activation drives DAT-Rit2 surface dissociation and that the DAT N terminu

77 ke was enhanced, but was not due to enhanced DAT surface expression in either dorsal or ventral stria

78 and regulatory development to replace equine DAT.

79 In summary, TH neurons that do not express DAT or DBH are required for the autoregulation of GH sec

80 ns in the hypothalamus were found to express DAT.

81 iated viral (AAV) gene therapy by expressing DAT selectively in DA neurons and terminals, resulting i

82 ore, adult mice with reduced DAT expression (DAT-HT) were hypersensitive to short active (SA; 19:5 L:

83 High-acuity patients were eligible for DAT.

84 The outcomes for DAT-treated patients were excellent; mortality was less

85 rare in the United States, and requests for DAT have declined.

86 -terminal PDZ-binding motif was required for DAT recycling and exit from retromer.

87 nalog (RTI-113) with greater selectivity for DAT over SERT retains locomotor activation in DAT Val559

88 tion of wild-type DAT and two non-functional DAT mutants, R60A and W63A, that do not accumulate in fi

89 Furthermore, DAT mRNA was increased in Chow/Palatable rats during the

90 pression is under dopamine transporter gene (DAT) promoter control to ablate Cnr2 gene in midbrain DA

91 HA-DAT was abundant in the plasma membrane of MFB axons, si

92 Intracellular HA-DAT colocalized with VPS35, a subunit of the retromer co

93 m, although the intracellular fraction of HA-DAT in MFB was more substantial.

94 Based on HA-DAT diffusion rates, plasma membrane DAT in MFB axons tu

95 286 (73%) non-manifesting carriers that had DAT imaging results, 18 (11%) LRRK2 and four (3%) GBA no

96 bility in human liver microsomes, and a hERG/DAT affinity ratio = 28.

97 It is especially unknown how DAT is transported between spatially distant midbrain so

98 , nor was TH was affected in males; however, DAT was significantly diminished in males.

99 tive phosphorylation site at Thr-48 in human DAT, a residue that has not been previously reported to

100 eported that single point mutations on human DAT (hDAT) at tyrosine88 (Y88F), lysine92 (K92M), and hi

101 Within the series, 14a showed improved DAT affinity (K(i) = 23 nM) over 3b (K(i) = 230 nM), mod

102 itogen activated protein kinase, SWIP-13, in DAT regulation.

103 AT over SERT retains locomotor activation in DAT Val559 mice.

104 ethylphenidate-induced locomotor activity in DAT Val559 mice, mimicking the effects seen with cocaine

105 e potency are associated with alterations in DAT affinity for cocaine and demonstrated that this chan

106 romotes anomalous DA efflux in vitro and, in DAT Val559 mice, leads to increased reactivity to immine

107 with DAT conformation biases and changes in DAT phosphorylation state.

108 DAT deficit experienced a 4-year decline in DAT binding of 20.23% (SD, 15.04%) compared with 3.68% (

109 e lack of cocaine-induced hyperlocomotion in DAT Val559 mice arises from SERT blockade and augmented

110 t been previously reported to be involved in DAT phosphorylation.

111 Further, when VTA DA neurons in DAT-cre mice were optically stimulated, JJC8-088 produce

112 l activation of midbrain dopamine neurons in DAT-cre mice.

113 vivo that appeared to parallel reductions in DAT activity.

114 arkably, all affinity losses were rescued in DAT chimeras encoding both SERT N and C termini.

115 igh-affinity cocaine interactions at SERT in DAT Val559 mice, or specific inhibition of 5-HT(2C) rece

116 g small molecules to block multiple sites in DAT for Tat binding.

117 ust optical intracranial self-stimulation in DAT-Cre mice, supporting an important role of DA neurons

118 However, cocaine increased DAT exit from retromer-positive endosomes significantly.

119 K2 non-manifesting carriers showed increased DAT striatal binding ratios compared with healthy contro

120 DAT N-terminus is critical for AMPH-induced DAT phosphorylation, a process required for DA efflux.

121 activation prevents methamphetamine-induced, DAT-mediated increases in firing activity of dopamine ne

122 ling endosomes, suggesting that internalized DAT targets to either degradation or an undefined recycl

123 DAT-Knockout (DAT-KO) mouse is currently the best animal model for thi

124 re ratio group exhibited significantly lower DAT availability in the posterior putamen (P = 0.024) an

125 ts in the two groups had significantly lower DAT availability on all striatal sub-regions except for

126 eat allele, previously associated with lower DAT expression and greater reward-related brain activati

127 al the intracellular mechanisms that mediate DAT endocytic recycling following constitutive and regul

128 N terminus is required for both PKC-mediated DAT-Rit2 dissociation and DAT internalization.

129 In Drosophila melanogaster, DAT deficiency results in reduced sleep.

130 d on HA-DAT diffusion rates, plasma membrane DAT in MFB axons turns over with a halftime of ~20 d, wh

131 sessed whether variations in plasma membrane DAT levels and/or phosphorylation of the threonine 53 si

132 tic factors (e.g., for WM: COMT val(158)met, DAT, BDNF val(66)met).

133 ostimulants inhibit DA reuptake and multiple DAT coding variants have been reported in patients with

134 or participants with an indeterminate and no DAT deficit, respectively (P = .002).

135 0%) and 3 of 109 participants (2.8%) with no DAT deficit (greater than 80%) at baseline.

136 To restrict the action of DAT to the integrin alphavbeta3 receptors on the cell su

137 robes of the DAT, biochemical assessments of DAT membrane availability and phosphorylation, and cocai

138 analyses, we demonstrate the association of DAT with PP1 and PP2A in the mouse brain and heterologou

139 to be correlated with functional changes of DAT.

140 8 binds in an outward facing conformation of DAT, similar to cocaine.

141 at biosynthesis and lysosomal degradation of DAT are confined to soma.

142 Unexpectedly, the mean diameter of DAT-labeled MFB axons was observed to be twice larger th

143 teases surpassed pepsin for the digestion of DAT and SERT.

144 Intracellular uptake and distribution of DAT and NDAT in U87 glioblastoma cells were evaluated us

145 an be understood through the distribution of DAT in the brain.

146 taining the Gbetagamma-interacting domain of DAT blocked the ability of mSIRK to induce DA efflux, co

147 olerance is associated with the formation of DAT-DAT complexes, and that amphetamine disperses these

148 ed baseline extracellular DA and function of DAT in vivo using quantitative "no-net-flux" microdialys

149 l dopamine uptake, Tat-induced inhibition of DAT function, and dynamic transport process.

150 However, trafficking itineraries of DAT, which determine its cell-surface concentration near

151 To examine the mechanisms of DAT filopodial targeting, we used quantitative live-cell

152 o ablate Cnr2 gene in midbrain DA neurons of DAT-Cnr2 conditional knockout (cKO) mice.

153 We determined the outcomes of DAT-treated patients and describe the occurrence and ris

154 rosophila and people, pharmacochaperoning of DAT in D. melanogaster may allow us to bridge that gap.

155 sing DA availability through the reversal of DAT function (DA efflux).

156 (4363 ng/mL) was 8-fold greater than that of DAT (548 ng/mL).

157 ime, mechanisms of the long-range traffic of DAT in intact brain and acute brain slices from the knoc

158 hich explains the extremely slow turnover of DAT protein in the brain.

159 tion to extending our basic understanding of DATs and their role in cocaine reinforcement, we serendi

160 that Rit2 and Ack1 independently converge on DAT to facilitate PKC-stimulated DAT endocytosis.

161 examine the impact of transporter ligands on DAT residue Thr-53, a proline-directed phosphorylation s

162 ly discrete homeostatic braking mechanism on DAT by inducing a relative increase in inward-facing tra

163 le, seemingly disparate, previous reports on DAT's postendocytic fate.

164 rted the highest activity and selectivity on DAT.

165 Across all the participants, DAT availability in the midbrain correlated positively w

166 The third pattern (TH-positive, DAT-negative, ZsGreen-negative) was found in A12-A13.

167 The second pattern (TH-positive, DAT-negative, ZsGreen-positive) was found in A11.

168 The first pattern (TH-positive, DAT-positive, ZsGreen-positive) was found in A8-A10.

169 pared with healthy controls that can precede DAT deficit.

170 Conclusion: Striatal presynaptic DAT function is clearly lower in PSP patients than in PD

171 microbe, Clostridium orbiscindens, produced DAT and rescued antibiotic-treated influenza-infected mi

172 Caudate nucleus and putamen DAT function was clearly lower in PSP than in PD (caudat

173 ane diffusion is the main mode of long-range DAT transport through MFB, although the contribution of

174 kinson's disease that correlate with reduced DAT binding.

175 Furthermore, adult mice with reduced DAT expression (DAT-HT) were hypersensitive to short act

176 Protein phosphatases (PPs) also regulate DAT activity, but the specific residues associated with

177 Molecular networks that regulate DAT are poorly understood, particularly in vivo Using a

178 Molecular mechanisms that regulate DAT expression, trafficking, and function, particularly

179 t into mechanisms that mediate PKC-regulated DAT internalization and reveal unexpected region-specifi

180 orting a role for this residue in regulating DAT activity.

181 cells enhances the activity of inner retinal DAT (also known as SLC6A3; a dopamine reuptake transport

182 We reviewed DAT requests from 1997-2018.

183 lds, which resulted in several new selective DAT inhibitors and gave valuable insights into the struc

184 for dopamine, norepinephrine, and serotonin (DAT, NET, and SERT, respectively).

185 Moreover, SERT/DAT co-expression was significantly higher in SAD patien

186 A shorter DAT <=1 year was associated with a lower relative risk o

187 in uptake inhibition were observed for small DAT inhibitors, whereas substituting the DAT C terminus

188 Conversely, JJC8-091 steers DAT towards a more occluded conformation.

189 anisms by which Rit2 controls PKC-stimulated DAT endocytosis are unknown.

190 whether Rit2 is required for PKC-stimulated DAT endocytosis in DAergic terminals or whether there ar

191 ine studies demonstrated that PKC-stimulated DAT endocytosis requires both Ack1 inactivation, which r

192 converge on DAT to facilitate PKC-stimulated DAT endocytosis.

193 urther, Rit2 was required for PKC-stimulated DAT internalization in both male and female ventral stri

194 egion-specific differences in PKC-stimulated DAT trafficking in bona fide DAergic terminals.

195 sex-dependent differences in PKC-stimulated DAT trafficking.

196 A, there was no correlation between striatal DAT and D1 receptor binding (R(2)=0.07, p=0.33), althoug

197 diated by Enzyme) labeling to couple surface DAT directly to fluorophore, and tracked DAT's postendoc

198 Moreover, T48A-DAT displayed increased palmitoylation, suggesting that

199 and membrane diffusion of HA-epitope tagged DAT in the medial forebrain bundle (MFB) of a knock-in m

200 the knock-in mouse expressing epitope-tagged DAT.

201 ously identified a novel therapeutic target: DAT oligomer complexes.

202 stabilizing basal dopamine transport and Tat-DAT integration.

203 doxorubicin, bevacizumab, and temsirolimus (DAT) (N = 39) or liposomal doxorubicin, bevacizumab, and

204 ter had a positive direct antiglobulin test (DAT).

205 We then tested DAT-HT mice and WT littermates in psychiatry-relevant be

206 the concentrations of NDAT were higher than DAT/Cremophor EL micelles in heart, lung, liver, spleen,

207 We previously demonstrated that DAT uptake regulates fluctuations in extracellular dopam

208 ed using confocal microscopy and showed that DAT reached the nucleus, but NDAT was restricted from th

209 e axonal transport, our studies suggest that DAT traffics between midbrain and striatum, mainly by la

210 cedure, and find that cocaine potency at the DAT also tracks differences in perseverative responding.

211 nd sensitization of cocaine's actions at the DAT was reversed.

212 on-related changes in cocaine potency at the DAT, consistent with an incentive-sensitization view of

213 ces cocaine use and cocaine's potency at the DAT.

214 e, and it increased cocaine's potency at the DAT.

215 that MPH-induced regional variations in the DAT and NET-enriched FC maps were significantly correlat

216 Residues 582 to 596 in the DAT carboxy terminus were identified as the primary bind

217 icant serotonergic plasticity arising in the DAT Val559 model that involves enhanced 5-HT(2C) signali

218 ree the effects of cocaine at inhibiting the DAT vary across sleep/wake state.

219 microscopy, and compared the effects of the DAT inhibitor cocaine and its fluorescent analog JHC1-64

220 ases being linked to distinct regions of the DAT N terminus.

221 ptake rate, increased phosphorylation of the DAT, and enhanced cocaine potency observed after periods

222 c voltammetry, pharmacological probes of the DAT, biochemical assessments of DAT membrane availabilit

223 sphorylation of the threonine 53 site on the DAT accounts for fluctuations in DA neurotransmission.

224 data, aromatic l-AADC results paralleled the DAT findings.

225 all DAT inhibitors, whereas substituting the DAT C terminus with that of SERT affected neither substr

226 Finally, we found that the DAT carboxy-terminal PDZ-binding motif was required for

227 s DAT-Rit2 surface dissociation and that the DAT N terminus is required for both PKC-mediated DAT-Rit

228 rate that the interaction of PIP(2) with the DAT N-terminus is critical for AMPH-induced DAT phosphor

229 sphate (PIP(2)), directly interacts with the DAT N-terminus to support DA efflux in response to AMPH.

230 ts increase DA through interactions with the DAT, we also examined to what degree the effects of coca

231 The 'DAT' cultivar was interesting for its high palmitoleic a

232 Five patients died during their DAT infusion or soon afterwards, but no deaths were attr

233 ligand binding and substrate uptake by these DAT mutants were restored.

234 Gbetagamma induces the release of DA through DAT.

235 peptide, mSIRK, increases DA efflux through DAT in heterologous cells and primary dopaminergic neuro

236 and ablation, or diagnosis-to-ablation time (DAT), on AF recurrence following catheter ablation.

237 ic TNBC as a surrogate for mesenchymal TNBC, DAT and DAE had notable activity in mesenchymal TNBC.

238 afterwards, but no deaths were attributed to DAT.

239 Striatal (123)I-FP-CIT binding to DAT and hypothalamic (123)I-FP-CIT binding to SERT are s

240 al attenuation of cocaine and Tat binding to DAT are of great scientific and clinical interest.

241 veloped that prevent cocaine from binding to DAT, but they themselves are not cocaine-like.

242 ikely by interfering with cocaine binding to DAT.

243 factors associated with adverse reactions to DAT.

244 ace DAT directly to fluorophore, and tracked DAT's postendocytic itinerary in immortalized mesencepha

245 Surprisingly, 25 d after transplantation (DAT) and >2 weeks after vision onset, we found that tPV

246 tained up to 270 days after transplantation (DAT).

247 brain dopamine (DA) release, DA transporter (DAT) availability, and reward responses.

248 The rare DA transporter (DAT) coding substitution Ala559Val found in subjects wit

249 DANs), binds directly to the DA transporter (DAT), and is implicated in several DA-related neuropsych

250 ted by the cocaine-sensitive DA transporter (DAT).

251 here an atypical dopamine (DA) transporter (DAT) inhibitor, CTDP-32476, that may have translational

252 H), which binds to the dopamine transporter (DAT) and the norepinephrine transporter (NET), to unrave

253 cing expression of the dopamine transporter (DAT) are associated with some conditions.

254 3) receptor (D2/3R) or dopamine transporter (DAT) availabilities, or synaptic dopamine levels in 983

255 alysis of the striatal dopamine transporter (DAT) availability between the two groups.

256 The dopamine transporter (DAT) belongs to the neurotransmitter:sodium symporter (N

257 nuclein A53T mutant or dopamine transporter (DAT) blockers also differentially affects the dopamine o

258 Dopamine transporter (DAT) controls dopamine neurotransmission by clearing syn

259 The dopamine transporter (DAT) controls the spatial and temporal dynamics of dopam

260 retrograde labeling in dopamine transporter (DAT) Cre mice revealed that a large majority of BA proje

261 ne (DA) content by the dopamine transporter (DAT) ensures the phasic nature of the DA signal, which u

262 s in the regulation of dopamine transporter (DAT) functions.

263 -function mutations in dopamine transporter (DAT) gene, leading to severe neurological disabilities i

264 rect inhibition of the dopamine transporter (DAT) has been implicated as a mediating factor of HIV-1

265 The dopamine transporter (DAT) has been implicated in a variety of arousal-related

266 Dopamine transporter (DAT) has been shown to accumulate in filopodia in neuron

267 selectivity toward the dopamine transporter (DAT) has previously led to the promising thiazole-contai

268 mine the usefulness of dopamine transporter (DAT) imaging to identify idiopathic rapid eye movement s

269 cales, 123-I Ioflupane dopamine transporter (DAT) imaging, and biological variables.

270 Atypical dopamine transporter (DAT) inhibitors have shown therapeutic potential in prec

271 IFICANCE STATEMENT The dopamine transporter (DAT) is a key regulator of dopamine neurotransmission an

272 e hydroxylase (TH) and dopamine transporter (DAT) mRNA using quantitative polymerase chain reaction (

273 cells that express the dopamine transporter (DAT) or dopamine beta-hydroxylase (DBH; marker of noradr

274 As the dopamine transporter (DAT) plays a prominent role in the reinforcing effects o

275 The dopamine transporter (DAT) regulates dopamine neurotransmission via reuptake o

276 l modifications at the dopamine transporter (DAT) to increase the ability of cocaine to inhibit its f

277 cocaine effects at the dopamine transporter (DAT) with aberrant cocaine-taking behaviors.

278 apacity to inhibit the dopamine transporter (DAT), and emerging evidence suggests that differences in

279 ne transporter (LeuT), dopamine transporter (DAT), and serotonin transporter (SERT)-by the use of por

280 , DRD4, and DRD5), the dopamine transporter (DAT), and vesicular transporters (VMAT1 and VMAT2).

281 Tracers for dopamine transporter (DAT), aromatic amino acid decarboxylase (AADC), or vesic

282 In dopamine transporter (DAT)-Cre mice, overexpression of COMT, specifically in d

283 caine's effects at the dopamine transporter (DAT).

284 el binding mode at the dopamine transporter (DAT).

285 ne hydroxylase (TH) or dopamine transporter (DAT).

286 he plasma membrane distribution of wild-type DAT and two non-functional DAT mutants, R60A and W63A, t

287 tion, reduced the concentration of wild-type DAT in filopodia.

288 At 5-year follow-up, DAT-SPECT had 75% sensitivity, 51% specificity, 44% posi

289 beta3 receptors on the cell surface, we used DAT-conjugated PLGA nanoparticles (NDAT) in an active ta

290 We used DAT-KO mouse as model for DTDS to explore the potential

291 VTA DA neurons were identified using DAT-Cre male mice that carried an optrode with minimal i

292 from other patients with COVID-19 that were DAT negative.

293 However, how and whether DAT function and regulation directly participate in rewa

294 e, we used chimeric proteins to test whether DAT and SERT N and C termini contribute to transporter s

295 SERT binding in the nucleus accumbens while DAT availability in the amygdala, hippocampus, and putam

296 as in the functional circuit associated with DAT.

297 that this change in affinity coincides with DAT conformation biases and changes in DAT phosphorylati

298 relative risk of AF recurrence compared with DAT >1 year (relative risk, 0.73 [95% CI, 0.65-0.82]; P<

299 fold at a dose of 3 mg/kg when compared with DAT, and C(max) of NDAT (4363 ng/mL) was 8-fold greater

300 ated Cnr2-floxed mice that were crossed with DAT-Cre mice, in which Cre- recombinase expression is un

301 we revealed that the sigma1R interacts with DAT at or near the plasma membrane and decreases methamp