ライフサイエンスコーパス: P-gp

1 ultidrug resistance protein, P-glycoprotein (P-gp).

2 mical assays with ABCC10 and P-glycoprotein (P-gp).

3 idrug resistance transporter P-glycoprotein (P-gp).

4 also a potent stimulator of P-glycoprotein (P-gp).

5 s a linchpin for assembly and trafficking of P-gp.

6 nse via the multidrug transporter ABCB1/MDR1 p-gp.

7 s the most potent inhibitor and corrector of P-gp.

8 maintained assembly of the drug transporter p-gp.

9 sidue linker that connects the two halves of P-gp.

10 hat target the nucleotide-binding domains of P-gp.

11 domains but not the drug-binding domains of P-gp.

12 that is critical for folding and activity of P-gp.

13 ds were found that inhibit ATP hydrolysis by P-gp.

14 aches for identifying specific inhibitors of P-gp.

15 s in stable epithelial monolayers expressing P-gp.

16 r 28 within the drug-binding pocket of human P-gp.

17 d structure also reveals a unique epitope on P-gp.

18 red by either the inhibition or induction of P-gp.

19 e or presence of tariquidar, an inhibitor of P-gp.

20 was associated with increased expression of P-gp.

21 ning and closing motion of the two halves of P-gp.

22 ernalization, and proteasomal degradation of P-gp.

23 tions in the 12 TM segments (223 mutants) of P-gp.

24 t deleting NBD2 causes misprocessing of only P-gp.

25 s and functionally decreases P-glycoprotein (P-gp), a multidrug resistance transporter.

26 P-glycoprotein (P-gp), a promiscuous drug efflux pump, has been extensiv

27 NA and protein expression of p-glycoprotein (P-gp), a subfamily of ATP-binding cassette transporter i

28 st BCRP and screened against P-glycoprotein (P-gp, ABCB1) and multidrug resistance protein 1 (MRP1, A

29 tant because drug pumps like P-glycoprotein (P-gp, ABCB1) confer multidrug resistance and mutant ABC

30 P-glycoprotein (P-gp, ABCB1) is an ATP-binding cassette drug pump that p

31 The multidrug transporter P-glycoprotein (P-gp, ABCB1) is an ATP-dependent pump that mediates the

32 P-glycoprotein (P-gp, ABCB1) is an important part of the multixenobiotic

33 increased the expression of P-glycoprotein (P-gp, ABCB1), an ATP binding cassette that is usually as

34 P-Glycoprotein (P-gp, ABCB1), multidrug resistance-associated protein 1

35 unds had low affinity toward P-glycoprotein (P-gp, ABCB1).

36 -metoclopramide transport by P-glycoprotein (P-gp; ABCB1) and the breast cancer resistance protein (B

37 P-glycoprotein (P-gp; ABCB1) is an ABC drug pump that protects us from t

38 of the membrane transporter proteins ABCB1 (P-gp), ABCG2 (BCRP), and ABCC1 (MRP1), which are involve

39 Acute sertraline administration can modulate P-gp activity in the blood-brain barrier and blood-teste

40 Enhanced P-gp activity promotes the efficient removal of photosen

41 r fractions were tested on the inhibition of P-gp activity using P-gp overexpressing PLHC-1/dox cells

42 ve been tested for their ability to modulate P-gp activity.

43 ains and testes of mice due to inhibition of P-gp activity.

44 nt of CNS drug permeation is P-glycoprotein (P-gp), an endogenous blood-brain barrier (BBB) efflux tr

45 CEM/VBL cell lines, oocytes expressing human P-gp and an immortalised human brain endothelial cell li

46 unds were assessed for their potency against P-gp and another transporter (MRP1), for their apparent

47 id (poly(I:C), viral antigen) would decrease P-gp and BCRP in the human placenta.

48 using uptake assays in cells overexpressing P-gp and BCRP.

49 Here we report that the conformation of P-gp and its drug efflux activity can be altered by syno

50 mical and biophysical studies conducted with P-gp and its orthologs, or from structures of other ATP-

51 t assays were performed in Caco-2, MDCKII +/-P-gp and LLC-PK1+/-P-gp in the absence or presence of ta

52 nd restored sensitivity toward daunorubicin (P-gp and MRP1) and SN-38 (BCRP) in A2780/ADR (P-gp), H69

53 s (99m)Tc-sestamibi is a known substrate for P-gp and MRP1, which are established cellular drug efflu

54 aspects of ligand interactions with purified P-gp and other ATP-binding cassette transporters that tr

55 iles and that drug-induced overexpression of P-gp and other MDR proteins can result in acquired resis

56 g efflux pumps, ABCB1 (also known as MDR1 or P-gp) and ABCC1 (also known as MRP1), whose inhibition r

57 tein 1 (MRP1) and permeability glycoprotein (P-gp) and assess the repeatability of the inhaled (99m)T

58 f efflux transporters (e.g., P-glycoprotein (P-gp) and breast cancer resistance protein (Bcrp)) at th

59 f efflux transporters, e.g., P-glycoprotein (P-gp) and breast cancer resistance protein (BCRP), at th

60 DR, resulted in higher brain P-glycoprotein (P-gp) and lower soluble Abeta levels, effects negated wi

61 gp), LLC-MDR1-3H (expresses common haplotype P-gp), and LLC-MDR1-3HA (a mutant that carries a differe

62 nhibitor of daunorubicin (MRP1), calcein AM (P-gp), and pheophorbide A (BCRP) transport.

63 ene-silencing siRNAs (Bcl-2, P-glycoprotein [P-gp], and survivin) via encapsulation and surface coord

64 the NBD1 and NBD2 transmission interfaces in P-gp are asymmetric.

65 ection images suggest that the two halves of P-gp are separated by a central cavity that closes upon

66 NBD2 transmission interface severely reduced P-gp assembly while changes to the equivalent residues i

67 only accumulates in tumours but also reduces P-gp at a SipA dose significantly lower than free SipA.

68 e, in vivo, the role of CAR in regulation of P-gp at the BBB.

69 priori knowledge of how drugs interact with P-gp at the molecular level.

70 ld type, the linker mutant, and a methylated P-gp at up to 3.3 A resolution display significant movem

71 tidrug transporters, such as P-glycoprotein (P-gp), at the blood-brain barrier.

72 linker mimicked drug binding as it activated P-gp ATPase activity.

73 ity site, resulting in altered modulation of P-gp ATPase activity.

74 ce, which was supported by its inhibition of P-gp ATPase.

75 provides a means to predict the magnitude of P-gp-based drug interactions at the BBB and BPB when onl

76 Our data suggest that P-gp-based drug interactions at the human BBB and BPB ca

77 ivated radiotracer for functional imaging of P-gp/BCRP activity with positron emission tomography (PE

78 evelopment of prodrug tracers for imaging of P-gp/BCRP function in vivo but also highlight some chall

79 Blocking with P-gp/BCRP modulators led to increased levels of brain ra

80 DCK and LLC-PK1 cells transfected with human P-gp) but not in the remaining five.

81 ere is no high resolution structure of human P-gp, but homology models based on the crystal structure

82 nhibits the ATP hydrolysis activity of mouse P-gp by hindering the formation of a dimeric complex bet

83 e transport substrate and nucleotides, human P-gp can exist in both open [nucleotide binding domains

84 Binding Cassette transporter P-glycoprotein (P-gp), consists of two homologous halves each comprising

85 ablished based on the release and binding of P-gp-containing microparticles.

86 findings suggest that increased activity of P-gp could be responsible for increased hepatic cyclospo

87 ine deacetylation in Cyp3a and especially in P-gp/Cyp3a knockout mice but not in P-gp-deficient mice

88 ially in P-gp/Cyp3a knockout mice but not in P-gp-deficient mice was strongly up-regulated.

89 gets within the blood-brain barrier to limit P-gp degradation in AD and improve Abeta brain clearance

90 nues within the blood-brain barrier to limit P-gp degradation in Alzheimer's disease and improve Abet

91 se inward-facing conformational snapshots of P-gp demonstrate a range of flexibility exhibited by thi

92 ation of novel drug delivery agents to evade P-gp-dependent efflux.

93 f three inward-facing conformations of mouse P-gp derived from two different crystal forms.

94 MMP9 cleavage and ubiquitinylation, mediated P-gp downmodulation.

95 The P-glycoprotein (P-gp) drug pump (ABCB1) has two transmembrane domains an

96 on about the conformational changes in human P-gp during the ATP hydrolysis cycle has not been direct

97 We also probe conformational states of human P-gp during the catalytic cycle, and demonstrate that, f

98 The homologous halves of P-gp each contain a transmembrane (TM) domain (TMD) with

99 were designed to have two functions: inhibit P-gp efflux at the BBB and revert to monomeric therapeut

100 t oxidative insults without interacting with P-gp efflux system.

101 ur findings argue that the inhibition of the P-gp efflux transporter should improve the poor pharmaco

102 onal properties such as selectivity profile, P-gp efflux, pharmacokinetic, and pharmacodynamic data.

103 (1) that exhibited both high p-glycoprotein (P-gp) efflux ratios in rat and human and poor metabolic

104 The permeability-glycoprotein (P-gp) efflux transporter is densely expressed at the blo

105 ty of the efflux transporter P-glycoprotein (P-gp) encoded by ABCB1 in human hepatoma cells (HepG2) w

106 The drug efflux function of P-glycoprotein (P-gp) encoded by MDR1 can be influenced by genetic polym

107 Ion mobility MS reveals that P-gp exists in an equilibrium between different states,

108 hotodynamic therapy (PDT) in P-glycoprotein (P-gp) expressing cells.

109 tance in cytotoxicity assay to paclitaxel in P-gp-expressing SW620/Ad300 and HEK/ABCB1 cell lines.

110 igonucleotides resulted in the inhibition of P-gp expression (a drug efflux pump to increase excretio

111 This APAP-induced increase in P-gp expression and activity was attenuated in the prese

112 We demonstrate that downmodulation of P-gp expression and function coincided with chemotherape

113 st (Lexiscan) rapidly and potently decreased P-gp expression and function in a time-dependent and rev

114 labeled with (11)C for use in PET studies of P-gp expression in humans.

115 ochemical assessment (grade 0-3) of MRP1 and P-gp expression in the lung by using parametric and nonp

116 d a vitamin D-deficient diet, lower cerebral P-gp expression was observed, but levels were restored o

117 ression was seen in 12 of 13 patients, while P-gp expression was seen in only two.

118 tion of a TLR2 ligand, preserving ABCB1/MDR1 p-gp expression.

119 /multidrug resistance (MDR)1 p-glycoprotein (p-gp) expression.

120 We find that the apparent affinities of P-gp for anticancer drugs actinomycin D and paclitaxel a

121 erties that offer reliable quantification of P-gp function at the blood-brain barrier in a pharmacolo

122 e resulted in rapid and potent inhibition of P-gp function in brain endothelial cells, as determined

123 This PET-based strategy of P-gp function investigation may provide new insight on t

124 We sought to increase the dynamic range of P-gp function measured after blockade.

125 as a model of CNS drug, we demonstrated that P-gp function not only reduces influx but also mediates

126 brain or fetal liver (reporter of placental P-gp function) activity was assessed by a 1- or 2-tissue

127 otonin reuptake inhibitors (SSRI) can affect P-gp function, in vitro and in vivo.

128 e was no significant effect of fluoxetine on P-gp function, in vitro or in vivo.

129 imately 1, indicating that in the absence of P-gp function, the distribution of (11)C-verapamil radio

130 "silent" polymorphisms significantly change P-gp function, which would be expected to affect interin

131 measure clinically meaningful alterations in P-gp function.

132 scanning is not confounded by alterations in P-gp function.

133 TPase activity at 12.5 muM without affecting P-gp function; moreover, they resensitized ABCC10-transf

134 (CAR) has been identified as a regulator of P-gp functional expression at the BBB.

135 gimen activates CAR at the BBB and increases P-gp functional expression, a clinically significant dru

136 omplexes efficiently induced P-glycoprotein (P-gp) gene silencing in the human ovarian adenocarcinoma

137 -gp and MRP1) and SN-38 (BCRP) in A2780/ADR (P-gp), H69AR (MRP1), and MDCK II BCRP (BCRP) cells.

138 The drug efflux pump P-glycoprotein (P-gp) has been shown to promote multidrug resistance (MD

139 Laniquidar, an inhibitor of P-gp, has been labeled with (11)C for use in PET studies

140 Several structural studies on purified P-gp have been reported, but only limited and sometimes

141 orated for the preparation of either MRP1 or P-gp highly selective inhibitors.

142 Expression of polymorphic P-gp, however, does not affect the host cell's morpholog

143 entrations of tariquidar did not fully block P-gp; however, higher doses of tariquidar would likely b

144 st to previous reports showing that trapping P-gp in a closed conformation highly activated ATPase ac

145 M and stimulated the basal ATP hydrolysis of P-gp in a concentration-dependent manner (EC50 ATPase =

146 e ATPase activity of purified human or mouse P-gp in a detergent micelle environment.

147 tical mechanistic steps involved in reducing P-gp in AD.

148 ulated spontaneously for the aim to suppress P-gp in advance by the earlier released TET in cancer ce

149 rigine nor carbamazepine was a substrate for P-gp in any of the model systems tested.

150 P-gp in each case is localized on the apical surface of

151 ressed at the epileptic focus with a role of P-gp in extruding AEDs from the brain.

152 hesis and drug efflux activity of ABCB1/MDR1 p-gp in murine and human CD11b(+)-myeloid cells, thus in

153 rt we compared the biochemical properties of P-gp in native membranes, detergent micelles, and when r

154 istic explanation for the polyspecificity of P-gp in substrate interactions.

155 rmed in Caco-2, MDCKII +/-P-gp and LLC-PK1+/-P-gp in the absence or presence of tariquidar, an inhibi

156 Computational models of human P-gp in the apo- and nucleotide-bound conformation show

157 g drug development for inhibiting or evading P-gp in the context of our improved understanding of the

158 reducing blood-brain barrier P-glycoprotein (P-gp) in Alzheimer's disease is poorly understood.

159 imited due to high levels of P-glycoprotein (P-gp) in the luminal membranes of brain and testes capil

160 er is the efflux transporter P-glycoprotein (P-gp) in the luminal plasma membrane of the brain capill

161 hippocampus in which the VDR is abundant and P-gp induction is greatest after 1,25(OH)2D3 treatment,

162 lopramide could be detected in the brains of P-gp-inhibited rats.

163 intravenous tariquidar, resulted in greater P-gp inhibition at the human blood-brain barrier than de

164 P-gp inhibition by tariquidar treatment increased brain

165 ed analogues were further analyzed for their P-gp inhibition constant, intrinsic toxicity, and potenc

166 In the pharmacologic situation, P-gp inhibition significantly increased metoclopramide b

167 of metoclopramide (3 mg/kg), with or without P-gp inhibition using intravenous tariquidar (8 mg/kg).

168 lchicine indicated that most of the observed P-gp inhibition was due to the presence of noncompetitiv

169 ibution of the drug (i.e., in the absence of P-gp inhibition) across these barriers is available thro

170 d tumors based on the synergistic effects of P-gp inhibition, enhanced endocytosis and intracellular

171 : injected under baseline conditions without P-gp inhibition, injected 1 h after intravenous tariquid

172 We propose that on deliberate or inadvertent P-gp inhibition, the upper boundary of increase in human

173 Tariquidar is a unique P-gp inhibitor because it locks the pump in a conformati

174 , expressed in toxicity equivalents of model P-gp inhibitor cyclosporine A) revealed high inhibitory

175 sized 21 derivatives of the third-generation P-gp inhibitor HM30181, which is structurally related to

176 LLC-MDR1-WT cells after being treated with a P-gp inhibitor.

177 egated with coadministration of elacridar, a P-gp inhibitor.

178 ituted furazan rings with MC70, a well-known P-gp inhibitor.

179 r anticancer drug along with P-glycoprotein (P-gp) inhibitor simultaneously.

180 h) of cyclosporine A (CsA, a P-glycoprotein [P-gp] inhibitor).

181 This study, conducted in humans, examined 2 P-gp inhibitors (tariquidar, a known inhibitor, and disu

182 , interactions between novel drugs and known P-gp inhibitors are now being systematically evaluated d

183 morphine brain accumulation was enhanced by P-gp inhibitors in APAP-treated animals, suggesting P-gp

184 ain goal of this study was identification of P-gp inhibitors in contaminated sediments using the effe

185 Several P-gp inhibitors or modulators have been investigated in

186 pe and haplotype P-gp respond differently to P-gp inhibitors that block efflux of rhodamine 123 or mi

187 ough lipophilicity plays a dominant role for P-gp inhibitors, all compounds investigated showed LipE

188 ncentrations when coadministered with potent P-gp inhibitors, thus increasing the risk for drug toxic

189 the three AEDs in the absence or presence of P-gp inhibitors.

190 ydrogen bond (IMHB) which allows reaching of P-gp inhibitory activity at the submicromolar IC50 level

191 presence of IMHB as a key element for a high P-gp inhibitory activity.

192 No P-gp interaction was observed for lamotrigine or carbama

193 P-gp is different from CFTR (ABCC7) in that deleting NBD

194 P-gp is expressed in the plasma membrane of many cell ty

195 thesis for refractory epilepsy proposes that P-gp is over expressed at the epileptic focus with a rol

196 P-gp is reduced at the blood-brain barrier in AD, which

197 The function of rescued cell surface mutant P-gp is similar to that of wild-type protein.

198 Our data suggest that P-gp is unlikely to contribute to the pathogenesis of re

199 P-glycoprotein (P-gp) is a multidrug transporter that uses energy from A

200 P-glycoprotein (P-gp) is a polyspecific ATP-dependent transporter linked

201 P-glycoprotein (P-gp) is a well-known membrane transporter expressed in

202 P-glycoprotein (P-gp) is an ATP binding cassette transporter that efflux

203 P-glycoprotein (P-gp) is an ATP-binding cassette drug pump that protects

204 P-glycoprotein (P-gp) is an ATP-binding cassette transporter that confer

205 The drug efflux transporter P-glycoprotein (P-gp) is highly expressed on brain endothelial cells and

206 sette (ABC) drug transporter P-glycoprotein (P-gp) is often responsible for the failure of chemothera

207 P-glycoprotein (P-gp) is one of the best-known mediators of drug efflux-

208 roximately 13,000 compounds against cellular P-gp levels.

209 ties predictive of good permeability and low P-gp liability.

210 aspects for developing potent and selective P-gp ligands have been highlighted, providing a solid st

211 ives in order to design potent and selective P-gp ligands.

212 The development of P-glycoprotein (P-gp) ligands remains of considerable interest, mostly f

213 and termed LLC-MDR1-WT (expresses wild-type P-gp), LLC-MDR1-3H (expresses common haplotype P-gp), an

214 These results suggest that P-gp may act as a stereoselective barrier to prevent pio

215 P-glycoprotein (P-gp, MDR1) is a promiscuous drug efflux pump of substan

216 efflux transporters such as P-glycoprotein (P-gp; MDR1, ABCB1), significantly less is known regardin

217 uorine atoms does not lead to higher risk of P-gp mediated efflux.

218 eve robust aqueous solubility while avoiding P-gp mediated efflux.

219 otential of these analogues as modulators of P-gp mediated MDR in cancer cells.

220 ently to study if changes in P-glycoprotein (P-gp)-mediated efflux of flumazenil at the blood-brain b

221 ary was evaluated for its ability to inhibit P-gp-mediated daunomycin efflux in MDR cells.

222 tive agents should be considered when strong P-gp-mediated drug-drug interactions are present.

223 ing of the structural basis and mechanism of P-gp-mediated MDR.

224 he potency of progesterone as a modulator of P-gp-mediated multidrug resistance was established by es

225 st stimulating effects of hydroxyl groups on P-gp-mediated transport.

226 hibitors in APAP-treated animals, suggesting P-gp-mediated transport.

227 Permeability glycoprotein (P-gp) mediates the export of drugs from cells located in

228 secretion effector, SipA, is responsible for P-gp modulation through a pathway involving caspase-3.

229 compound 1 and verapamil, a first-generation P-gp modulator.

230 Nonetheless, P-gp, Mrp2, Cyp3a, and Ces2a clearly restricted vinorelb

231 ess c-Kit and stably express P-glycoprotein (P-gp)/multi-drug resistance type 1 (MDR1).

232 te leukemia, with permeability glycoprotein (P-gp), multidrug resistance-associated protein 1, and br

233 ug) for targeting permeability glycoprotein (P-gp), multidrug resistant protein 1 (MRP-1), B-cell lym

234 The in vitro modulation of P-gp of compounds 1-14 was evaluated through a combinati

235 The ABC transporters P-glycoprotein (P-gp, official gene symbol ABCB1) and breast cancer resi

236 C-metoclopramide transport was selective for P-gp over BCRP.

237 ement with an orthogonal criterion involving P-gp overexpressing ADR-RES cells.

238 Biological experiments on an independent P-gp overexpressing cell line, the vincristine-resistant

239 ted on the inhibition of P-gp activity using P-gp overexpressing PLHC-1/dox cells and calcein-AM as m

240 nsport in monolayers of multidrug-resistant, P-gp-overexpressing MDCKII-MDR1 cells, and for their col

241 ancer cell lines including KBV200 cells with P-gp overexpression.

242 rly for those P-gp substrate drugs for which P-gp plays a significant role in excluding the drug from

243 P-glycoprotein (P-gp) plays a crucial role in the development of multidr

244 in-AM transport, the linker-shortened mutant P-gp possesses basal ATPase activity and binds ATP only

245 d proteasome-dependent degradation, reducing P-gp protein expression and transport activity in isolat

246 ved that only Abeta40 triggered reduction of P-gp protein expression and transport activity levels; t

247 Following APAP treatment, P-gp protein expression was increased up to 1.4-1.6-fold

248 e ubiquitin-proteasome system, and monitored P-gp protein expression, transport activity, and P-gp-ub

249 From a clinical perspective, P-gp rapidly extrudes lipophilic therapeutic agents, whi

250 e large, polyspecific drug-binding pocket of P-gp recognizes a variety of structurally unrelated comp

251 However, the mechanism responsible for P-gp reduction in AD is not well understood.

252 dentify the steps involved in Abeta-mediated P-gp reduction, we inhibited protein ubiquitination, pro

253 iptional inhibitor actinomycin D, suggesting P-gp regulation is CAR-dependent.

254 ort assays show that wild-type and haplotype P-gp respond differently to P-gp inhibitors that block e

255 ntribute to the development of new selective P-gp reversal agents.

256 P-glycoprotein (P-gp) serves as a therapeutic target for the development

257 trate that the inhibition of P-glycoprotein (P-gp) significantly increases brain penetration of piogl

258 e mass spectrometry (MS) to probe the intact P-gp small molecule-bound complex in a detergent micelle

259 P-gp specific ATPase assay and the cytotoxicity modulati

260 rease brain uptake of the avid and selective P-gp substrate (11)C-N-desmethyl-loperamide (dLop) while

261 ed oxidative stress with poor interaction as P-gp substrate and very low cytotoxicity.

262 inically significant, particularly for those P-gp substrate drugs for which P-gp plays a significant

263 mmended guidelines for the administration of P-gp substrate drugs will be expanded.

264 ynamic biodistribution of (11)C-verapamil, a P-gp substrate, in the nonhuman primate Macaca nemestrin

265 of IS needed higher doses of cyclosporin, a P-gp substrate, to obtain the cyclosporin target blood c

266 The P-gp substrate, tritiated digoxin ([(3)H] digoxin), was

267 Understanding the structural basis of P-gp, substrate polyspecificity has been hampered by its

268 nly prescribed cardiovascular drugs that are P-gp substrates and observe interactions involving P-gp

269 as anticancer agents and steroids, are known P-gp substrates and/or inhibitors, and many cardiovascul

270 biliary excretion, and urinary excretion of P-gp substrates can therefore be altered by either the i

271 Pharmacokinetic studies with the Mdr1a P-gp substrates loperamide, indinavir, and talinolol ind

272 e (SVM) was 86.7% accurate in discriminating P-gp substrates on independent test data, exceeding prev

273 e created a large set of 934 high-confidence P-gp substrates or nonsubstrates by enforcing agreement

274 res had an overarching influence: nearly all P-gp substrates were large (>35 atoms including H) and d

275 r the ability of therapeutic agents that are P-gp substrates, to enter the brain when co-administered

276 nd elongated derivative 6g behaved as strong P-gp substrates.

277 actinomycin-D, and rapamycin, which are also P-gp substrates.

278 multidrug resistant protein, P-glycoprotein (P-gp), suggesting an active drug efflux pump as a potent

279 Owing to the enhanced cellular uptake and P-gp suppression mediated by TET, significantly more PTX

280 ubstrates and observe interactions involving P-gp that may be relevant to clinical practice.

281 We used a structural model of human P-gp that we obtained from molecular dynamics experiment

282 interaction between the hybrid compounds and P-gp, the main excretory transporter of the BBB, was fou

283 cs often selects for cells which overexpress P-gp, thereby creating populations of cancer cells resis

284 osporine A reduces the association of mutant P-gp, thus allowing it to be trafficked to the cell surf

285 y provide new insight on the contribution of P-gp to the variability of response to CNS drugs between

286 demonstrate that, following ATP hydrolysis, P-gp transitions through a complete closed conformation

287 Additionally, APAP increased P-gp transport of BODIPY-verapamil in freshly isolated r

288 The increase in P-gp transporter by OPN was mediated by binding to alpha

289 protein expression, transport activity, and P-gp-ubiquitin levels.

290 We demonstrate that Abeta40 drives P-gp ubiquitination, internalization, and proteasome-dep

291 hanism of action and high selectivity toward P-gp, unlike the lead compound.

292 P-gp uses ATP hydrolysis to catalyze the transport of a

293 When P-gp was completely inhibited, the brain and fetal liver

294 The potency of CsA to inhibit P-gp was tissue-independent (maternal BBB half-maximal i

295 r is fundamental for functionally decreasing P-gp, we engineered a nanoparticle mimic that both overc

296 umour growth with a concomitant reduction in P-gp when used with an existing chemotherapeutic drug (t

297 essed in HeLa cells, led to misprocessing of P-gp, which thus failed to transport the drug substrates

298 Compound 28 inhibited the photolabeling of P-gp with [(125)I]-iodoarylazidoprazosin with IC50 = 0.7

299 Here we constructed a mutant murine P-gp with a shortened linker to facilitate structural de

300 -close motion alters the surface topology of P-gp within the drug-binding pocket, providing a mechani