ライフサイエンスコーパス: DAT

1 DAT also targeted rab7-positive endosomes with slow, lin

2 DAT is also competitively inhibited by psychostimulants

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 regulated acutely by endocyt

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

7 1) and mean total striatal (OR=0.25, p=0.04) DAT availability at any post-baseline visit.

8 p=0.01) and mean striatal (OR=6.90, p=0.04) DAT availability over the first year, and lower right pu

9 ly with age (D1 receptor: R(2)=0.12, p<0.05; DAT: R(2)=0.36, p<0.001).

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 By 35 DAT, however, broad orientation selectivity emerges in t

13 dling and open field deficits starting at 60 DAT.

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

15 Individuals with hyposmia and a DAT deficit had a 5% reduction in DAT binding annually,

16 ercentage of individuals with hyposmia and a DAT deficit that converted to PD and the change in PD cl

17 results demonstrate that PDM functions as a DAT inhibitor that may also interact with the pharmacolo

18 Incubation of the cells with noribogaine (a DAT ligand selective for the inward-facing state) and/or

19 agnosis of PD in hyposmic individuals with a DAT deficit was 17.47 (95% CI, 7.02-43.45) compared with

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

21 e-clamped (-60 mV) oocytes consistent with a DAT inhibitor profile, whereas its metabolite PM induced

22 ced an inward hDAT current consistent with a DAT substrate profile.

23 nt synucleinopathy in patients with abnormal DAT-SPECT than with normal DAT-SPECT (20% vs 6% at 3 yea

24 that were unaffected by either accelerating DAT internalization or binding a high-affinity cocaine a

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

26 After DAT-SPECT, patients were followed up during 5.7 +/- 2.2

27 These mutants did not alter DAT surface expression or surface DAT binding sites.

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

29 We found a dynamic regulation of D1 and DAT during 3 wk of abstinence.

30 ransport-associated currents through DAT and DAT-H193K, a mutant with a disrupted Zn(2+)-binding site

31 targeted to retromer-positive endosomes, and DAT/retromer colocalization was observed in male mouse d

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

33 pamine synthesis and/or release in mania and DAT blockade in bipolar depression.

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

35 Binding of D1 receptors and DAT throughout the striatum correlated negatively with a

36 nified Parkinson's Disease Rating Scale) and DAT imaging during 4-year follow-up.

37 mmalian membrane proteins including SERT and DAT, neither of which tolerates complete removal of endo

38 A specific interaction between sigma1R and DAT was detected by co-immunoprecipitation and biolumine

39 expression in VTA DA neurons in wildtype and DAT-Cnr2 cKO heterozygous but not in the homozygous DAT-

40 type in a mouse model that best approximates DAT deficiency found in DTDS.

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

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

43 At DAT, the binding of two structurally dissimilar radiolig

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

45 f VTA firing to enhanced cocaine affinity at DAT and subsequent reward processing.

46 thyl 10 (MRS7232) esters enhanced binding at DAT (EC50 approximately 35 nM) and at the norepinephrine

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

48 DAT inhibitors have similar binding poses at DAT in a conformation that differs from that of cocaine.

49 as an efficacious substrate-type releaser at DAT that evoked an inward depolarizing current and calci

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

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

52 hese results are consistent with an atypical DAT inhibitor profile and suggest that 11b may be a pote

53 of modafinil analogues that have an atypical DAT inhibitor profile.

54 study supported the hypothesis that atypical DAT inhibitors have similar binding poses at DAT in a co

55 The atypical DAT inhibitors have received attention due to their prom

56 Baseline DAT deficit was found in 51 (58.6%) patients.

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

58 For the first time, a direct link between DAT availability and reward anticipation was detected wi

59 amphetamines must be actively transported by DAT and VMAT in tandem to produce psychostimulant effect

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

61 aphy-confirmed IRBD underwent (123) I-FP-CIT DAT-SPECT.

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

63 the cellular mechanisms that acutely control DAT surface expression.

64 dry matter (dm) in fruits of the cultivars 'DAT' and 'PSI', respectively.

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

66 A transport Vmax but significantly decreased DAT substrate affinities for DA and amphetamine.

67 Multiple studies have demonstrated DAT endocytic recycling and enhanced surface delivery in

68 t the bacterial metabolite desaminotyrosine (DAT) increases type I interferon expression, resulting i

69 lly associated metabolite, desaminotyrosine (DAT), protects from influenza through augmentation of ty

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

71 ERK8 activation of Rho GTPases that dictates DAT surface expression and function.SIGNIFICANCE STATEME

72 planation for previous, seemingly disparate, DAT endocytic trafficking findings.SIGNIFICANCE STATEMEN

73 nt, and suggest that compounds that disperse DAT complexes may be efficacious treatments for cocaine

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

75 are determined by the presynaptic dopamine (DAT) and serotonin (SERT) transporters, respectively.

76 biogenic amines serotonin (SERT), dopamine (DAT), and norepinephrine (NET) are targets of multiple p

77 e potential changes, which can rapidly drive DAT internalization from and insertion into the cell mem

78 , expression of hDAT-L368Q in the Drosophila DAT mutant background caused developmental lethality, in

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

80 ract with DAT to stabilize an outward-facing DAT conformation and enhance cocaine binding.

81 e, thus having an impact on the capacity for DAT to regulate extracellular DA levels.

82 Abeta peptides provides a better marker for DAT detection than a single Abeta misfold or the concent

83 setting as a valid quantification method for DAT using (18)F-FE-PE2I, because it provides differentia

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

85 9 and 10 were selective for DAT compared to A3AR in the mouse but not in humans.

86 amino-terminal substitution was specific for DAT, because replacing the SERT N and/or C termini affec

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

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

89 toward understanding mechanisms that govern DAT's plasma membrane expression and postendocytic fate.

90 reement in results for individuals with high DAT responses, who are more likely to progress to VL dis

91 2 cKO heterozygous but not in the homozygous DAT-Cnr2 cKO mice.

92 as functional recognition residues in human DAT (hDAT) for Tat-induced inhibition of DA transport an

93 sive molecular dynamics simulations of human DAT (hDAT) to explore the mechanism of this sodium relea

94 sing from folding-defective mutants of human DAT and of other related SLC6 transporters.

95 on, we identified that histidine547 on human DAT (hDAT) is critical for regulation of basal DA uptake

96 cluding serial dopamine transporter imaging (DAT-SPECT) and ICD assessment (Questionnaire for Impulsi

97 sporter kinetic properties that could impact DAT responses to amphetamines and cocaine.

98 targets on DAT for Tat binding and improving DAT-mediated dysfunction of DA transmission.

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

100 ation potentiated cocaine-induced changes in DAT conformation, which were blocked by the specific sig

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

102 urons and restored sleep to normal length in DAT-deficient (fumin) Drosophila lines expressing hDAT-V

103 smia and a DAT deficit had a 5% reduction in DAT binding annually, similar to early PD.

104 vivo that appeared to parallel reductions in DAT activity.

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

106 led receptor, the muscarinic M5R, results in DAT-mediated DA efflux through a Gbetagamma-dependent me

107 Strikingly, animals lacking Thorase in DAT(+) neurons expressed greater associative learning in

108 Genetic ablation of Thorase in DAT(+) neurons produced increased AMPAR surface expressi

109 Ribose analogues were weaker in DAT interaction than the corresponding bicyclics.

110 st this may be a viable approach to increase DAT levels in DTDS and other conditions associated with

111 wn DAT ligands for their ability to increase DAT surface expression, we found that bupropion and ibog

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

113 found that bupropion and ibogaine increased DAT surface expression, whereas others, including cocain

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

115 of protein-protein interactions influencing DAT cellular localization and activity, suggesting that

116 Following internalization, DAT robustly targeted to retromer-positive endosomes, an

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

118 INTERPRETATION: DAT-SPECT identifies IRBD patients at short-term risk fo

119 -016, binding affinities in the range of its DAT affinity were only observed at the serotonin transpo

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

121 After screening a set of known DAT ligands for their ability to increase DAT surface ex

122 Moreover, FoxO1 KO(DAT) mice exhibit an increased sucrose preference in con

123 xO1 specifically in the DA neurons (FoxO1 KO(DAT)) show markedly increased energy expenditure and int

124 ution was completely tolerated by the larger DAT inhibitors, which exhibited no loss in apparent affi

125 hunger' through its slow-onset long-lasting DAT inhibitor action, but also render subsequent adminis

126 Furthermore, the OB has dramatically less DAT compared with striatum, supporting the idea that COM

127 eliminary study, a greater decrease or lower DAT binding over time increases risk of incident ICD sym

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

129 Mean DAT, D2, and D1 receptor binding did not differ in suici

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

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

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

133 Further, tolerance was associated with multi-DAT complexes, which formed after cocaine exposure.

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

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

136 individuals with either indeterminate or no DAT deficit.

137 0%) and 3 of 109 participants (2.8%) with no DAT deficit (greater than 80%) at baseline.

138 nts with abnormal DAT-SPECT than with normal DAT-SPECT (20% vs 6% at 3 years, 33% vs 18% at 5 years;

139 Herein, a series of novel DAT inhibitors were synthesized, and based on its pharma

140 d the greatest potential and detected 69% of DAT-positive individuals, with rKR95 being more robust i

141 o identify genes that dictate the ability of DAT to sustain normal levels of DA clearance, we pursued

142 Allosteric activation of DAT via the Zn(2+)-binding site may be of interest to re

143 ve transition metals reduced the affinity of DAT for dopamine.

144 to be correlated with functional changes of DAT.

145 onstration of pharmacological chaperoning of DAT and suggest this may be a viable approach to increas

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 rance are unknown, and testing the impact of DAT changes on drug taking behaviors has proven difficul

149 - or BIM-induced activation or inhibition of DAT function relative to WT hDAT, indicating a change in

150 bupropion and ibogaine promote maturation of DAT by acting as pharmacological chaperones in the ER.

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 s DAergic neurotransmission, and a number of DAT coding variants have been reported in several DA-rel

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

155 inimal drug exposure, even after recovery of DAT function over prolonged abstinence periods.

156 etal ions to the outward-facing apo state of DAT and a reciprocal interaction of dopamine and transit

157 n is required for the efficient targeting of DAT to, and accumulation in, filopodia.

158 lular property, rapidly alter trafficking of DAT to and from the surface membrane.

159 Rescuing misfolded versions of DAT by pharmacochaperoning is of therapeutic interest; i

160 The mutated versions of DAT were confined to the cell bodies of the dopaminergic

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

162 ion range, they were devoid of any action on DAT-H193K.

163 euronal signaling, although their effects on DAT activity are unclear.

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

165 s indicated binding to the cocaine pocket on DAT, although molecular dynamics revealed binding differ

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

167 anistic insights into identifying targets on DAT for Tat binding and improving DAT-mediated dysfuncti

168 T, RBDSQ, CSF Abeta42, and caudate uptake on DAT imaging) allowed prediction of cognitive impairment

169 8-0.83), CSF variables (0.74, 0.68-0.81), or DAT imaging results (0.76, 0.68-0.83).

170 ition of the Gbetagamma inhibitor gallein or DAT inhibitors prevents this effect.

171 -methyl-transferase (COMT) predominates over DAT re-uptake.

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

173 for PDM therapeutic effects via initial PDM DAT inhibition followed by PM DAT substrate-induced dopa

174 ia initial PDM DAT inhibition followed by PM DAT substrate-induced dopamine release.

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

176 and other conditions associated with reduced DAT function.

177 well as its human counterpart ERK8, regulate DAT surface availability via the activation of Rho prote

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

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

180 nderstanding of the mechanisms that regulate DAT function is necessary for the development of clinica

181 Importantly, both drugs rescue DAT maturation and functional activity of the DTDS-assoc

182 n of the endoplasmic reticulum (ER)-retained DAT mutant K590A.

183 st that CTDP-32476 is a potent and selective DAT inhibitor and a competitive inhibitor of cocaine bin

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

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

186 parate or combined additions of APOE status, DAT imaging, and CSF biomarkers.

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

188 e hypothesized that, in addition to striatal DAT binding, there would be differences in extrastriatal

189 h [(3)H]WIN 35,428 binding or affect surface DAT levels.

190 ly, these findings suggest that cell-surface DAT levels are sensitive to membrane potential changes,

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

192 tically to insure adequate levels of surface DAT expression and DA clearance.

193 not alter DAT surface expression or surface DAT binding sites.

194 x were elevated in phosphorylation-null T53A DAT relative to WT and charge-substituted T53D DATs, con

195 T relative to WT and charge-substituted T53D DATs, consistent with functions related to charge or pol

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

197 le in stabilizing basal DA transport and Tat-DAT interaction.

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

199 randomized trial should be performed to test DAT and DAE for metaplastic TNBC, as well as nonmetaplas

200 a that COMT enzymatic breakdown, rather than DAT recycling, is the predominant mechanism for DA clear

201 rovide compelling experimental evidence that DAT N and C termini synergistically contribute to substr

202 n RNA-mediated Vps35 knockdown revealed that DAT endocytic recycling requires intact retromer.

203 These findings underscore that DAT is critical for DA neurotransmission and homeostasis

204 In compound 3a, the DAT groups are designed to lie close to the plane of the

205 elective, but had much lower affinity at the DAT (Ki=3 muM) than JJC8-016 (Ki=116 nM).

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

207 , we demonstrate that cocaine effects at the DAT determine the reinforcing efficacy of cocaine, and p

208 as shown that reduced cocaine potency at the DAT increases cocaine taking, highlighting the key role

209 Cocaine potency at the DAT was correlated with reinforcing efficacy, but was no

210 - as well as voxel-based methods in both the DAT-rich striatum (caudate nucleus and putamen) and the

211 These results define the DAT recycling mechanism and provide a unifying explanati

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

213 Numerous studies have investigated the DAT and SERT structural elements contributing to inhibit

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

215 pounds were showing higher activities on the DAT and a higher selectivity toward DAT versus serotonin

216 Replacing the DAT N terminus with that of SERT had no effect on DA tra

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

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

219 ermanent, cocaine-induced alterations to the DAT, whereby cocaine tolerance is reinstated by minimal

220 petitive inhibitor of cocaine binding to the DAT.

221 DA signal approximately 2-fold, whereas the DAT inhibitor GBR12909 had no effect.

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

223 In compounds 3a-c, three DAT groups are attached to trigonally substituted phenyl

224 2+) on transport-associated currents through DAT and DAT-H193K, a mutant with a disrupted Zn(2+)-bind

225 strate-induced steady-state currents through DAT.

226 Gbetagamma induces the release of DA through DAT.

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

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

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

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

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

232 the Bmax values of [(3)H]WIN35428 binding to DAT in rat striatal synaptosomes and transfected cells.

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

234 ikely by interfering with cocaine binding to DAT.

235 gamma (Gbetagamma) subunits bind directly to DAT and decrease DA clearance.

236 s on the DAT and a higher selectivity toward DAT versus serotonin and norepinephrine transporters tha

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

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

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

240 The DA transporter (DAT) imposes spatial and temporal limits on DA action, a

241 LC6A3 (the gene encoding the DA transporter (DAT)) were tested.

242 is tightly regulated by the DA transporter (DAT), insuring efficient DA clearance after release.

243 tion of the D1 receptor- and DA transporter (DAT)-binding sites, but D2-like receptor binding was una

244 argeted to VTA DA neurons in DA transporter (DAT)-cre mice (ChR2+ group; n = 6).

245 t least in part, by reducing DA transporter (DAT)-dependent uptake.

246 ally at the human dopamine (DA) transporter (DAT) and inhibit DA uptake.

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

248 MENT The neuronal dopamine (DA) transporter (DAT) recaptures released DA and modulates DAergic neurot

249 , mediated by the dopamine (DA) transporter (DAT), terminates DAergic neurotransmission and constrain

250 Dopamine transporter (DAT) availability was assessed with PET and [(11)C]PE2I

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

252 and quantify striatal dopamine transporter (DAT) binding in vivo.

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

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

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

256 The human dopamine transporter (DAT) has a tetrahedral Zn(2+)-binding site.

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

258 on testing followed by dopamine transporter (DAT) imaging can accurately and efficiently identify ind

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

260 The dopamine transporter (DAT) is an important regulator of brain dopamine (DA) ho

261 Although the dopamine transporter (DAT) is the primary site of action for cocaine, and the

262 Dopamine transporter (DAT) is the target of cocaine and HIV-1 transactivator o

263 lst increased striatal dopamine transporter (DAT) levels would lead to reduced dopaminergic function

264 ) is a newly developed dopamine transporter (DAT) PET radioligand.

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

266 The dopamine transporter (DAT) regulates dopamine (DA) neurotransmission by recapt

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

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

269 It is targeting the dopamine transporter (DAT) with moderate selectivity, thereby leading to reupt

270 slower, independent of dopamine transporter (DAT), increasing the lifetime of extracellular dopamine.

271 evel regulation by the dopamine transporter (DAT), the membrane expression and trafficking of which a

272 ction mutations in the dopamine transporter (DAT), which often affects transporter trafficking and fo

273 aine inhibition of the dopamine transporter (DAT), which results in tolerance.

274 ine uptake through the dopamine transporter (DAT).

275 e, a substrate for the dopamine transporter (DAT).

276 in site of action, the dopamine transporter (DAT).

277 c targets, such as the dopamine transporter (DAT).

278 radiographic survey of dopamine transporter (DAT; [(3)H]mazindol), D1 receptor ([(3)H]SCH23390), and

279 nd biomarkers (CSF and dopamine transporter [DAT] imaging results).

280 2,4-Diamino-1,3,5-triazinyl (DAT) groups are known to form N-H...N hydrogen bonds acc

281 Bupropion and ibogaine increased wild type DAT protein levels and also promoted maturation of the e

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

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

284 ) modulated the transport cycle of wild-type DAT with affinities in the low micromolar range.

285 h less efficiently compared to the wild-type DAT.

286 f Abeta peptides in Dementia Alzheimer type (DAT) patients, which indicated an overall shift to beta-

287 0 matched controls without RBD who underwent DAT-SPECT.

288 e findings suggest that JJC8-016 is a unique DAT inhibitor that has no cocaine-like abuse potential b

289 findings suggest that CTDP-32476 is a unique DAT inhibitor that not only could satisfy 'drug hunger'

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

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

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

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

294 mers into monomers, which then interact with DAT to stabilize an outward-facing DAT conformation and

295 Through interactions with DAT, methamphetamine increases extracellular dopamine le

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

297 our data show that Gbetagamma interacts with DAT to promote DA efflux.

298 factory testing assessed longitudinally with DAT imaging 2 and 4 years after baseline and by annual c

299 developed synucleinopathy from patients with DAT deficit that remained disease free after 3 years of

300 greater than 25% discriminated patients with DAT deficit who developed synucleinopathy from patients