ライフサイエンスコーパス: P-gp

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

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

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

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

5 esistance-linked transporter P-glycoprotein (P-gp).

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

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

8 ernalization, and proteasomal degradation of P-gp.

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

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

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

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

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

14 maintained assembly of the drug transporter p-gp.

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

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

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

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

19 aches for identifying specific inhibitors of P-gp.

20 s in stable epithelial monolayers expressing P-gp.

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

22 to similar extents relative to inward-facing P-gp.

23 ve of 8 (compound 24) was not transported by P-gp.

24 ctionalization, can modulate the function of P-gp.

25 one of the compounds was not transported by P-gp.

26 an embryonic kidney-293 cells overexpressing P-gp.

27 elected subline KB-8-5-11 that overexpresses P-gp.

28 structure of paclitaxel (Taxol)-bound human P-gp.

29 lity or brain penetration may be affected by P-gp.

30 iation might be mediated via P-glycoprotein (P-gp), a major pathway for clarithromycin metabolism.

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

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

33 llin and in particular, the association with P-gp, a major pathway for clarithromycin metabolism.

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

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

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

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

38 e 1 (Glut-1), and permeability-glycoprotein (p-GP, ABCB1) were similarly significantly higher in the

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

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

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

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

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

44 ndividuals with genetically determined lower P-gp activity had a significantly increased risk of CV h

45 This systems pharmacology study investigated P-gp activity in mice according to organ, sex, feeding s

46 Fasting increased P-gp activity mesor and dampened its rhythm.

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

48 gle-nucleotide polymorphisms associated with P-gp activity were evaluated (rs1045642 and rs1128503 -A

49 (rhythm-adjusted mean) of ileum and hepatic P-gp activity were higher in males as compared to female

50 s1128503 -AA genotype associated with lowest P-gp activity).

51 ves can exhibit varied modulatory effects on P-gp activity, depending on structural functionalization

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

53 of intestinal P-gp, but not to assess renal P-gp activity.

54 sistent with the uptake function, the mutant P-gp also hypersensitizes HeLa cells to Rh123 by 2- to 2

55 P-glycoprotein (P-gp), also known as ABCB1, is a cell membrane transport

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

57 cPLA2 inhibition prevents overexpression of P-gp and BCRP at the blood-brain barrier in rats after s

58 Nanomolar levels of GenX inhibited P-gp and BCRP but not MRP2 transport activities in male

59 t the delivery of ispinesib is restricted by P-gp and Bcrp efflux at BBB.

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

61 We further find that elacridar-a P-gp and Bcrp inhibitor-improves brain accumulation of i

62 solic phospholipase A2 (cPLA2), resulting in P-gp and BCRP overexpression.

63 Western blotting determined P-gp and BCRP protein levels.

64 at 0.1 - 100 nM rapidly (in 1-2 h) inhibited P-gp and BCRP transport activities at the BBB through di

65 GenX reduced P-gp and BCRP transport activity in human cells.

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

67 ing in overexpression of blood-brain barrier P-gp and BCRP.

68 Biochemical assays of the ATPase activity of P-gp and by photolabeling P-gp with its transport substr

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

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

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

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

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

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

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

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

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

78 the drug efflux transporters P-glycoprotein (P-gp) and breast cancer resistance protein (BCRP).

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

80 ession, including permeability glycoprotein (P-gp) and multidrug resistance-associated protein 1 (MRP

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

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

83 Glutamate increased cPLA2, P-gp, and BCRP protein and activity levels in isolated b

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

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

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

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

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

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

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

91 efflux transporters, such as P-glycoprotein (P-gp) at the blood-brain barrier (BBB).

92 itors that specifically targets and inhibits P-gp ATP hydrolysis while not being transported by the p

93 tor and compound 8 as a partial inhibitor of P-gp ATPase activity).

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

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

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

97 jan horse approach to therapeutic evasion of P-gp based on a reversibly linked combination of HIV rev

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

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

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

101 l interactions of investigational drugs with P-gp be explored, often this information does not enter

102 P-gp belongs to the ATP-binding cassette transporter fam

103 P-gp bound to Mg(+2)-ATP, and outward-facing P-gp bound to Mg(+2)-ADP-VO(4)(-3).

104 cing apo P-gp, pre-hydrolytic (E552Q/E1197Q) P-gp bound to Mg(+2)-ATP, and outward-facing P-gp bound

105 t activity and expression of P-glycoprotein (P-gp), breast cancer resistance protein (BCRP), and mult

106 Reductions of P-gp but not BCRP transport activity were blocked by a p

107 ARgamma was required for the GenX effects on P-gp but not BCRP transport activity.

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

109 xin as a phenotyping substrate of intestinal P-gp, but not to assess renal P-gp activity.

110 ymorphisms (SNPs) of the ABCB1 gene encoding P-gp (C1236T, G2677T/A, and C3435T) on digoxin pharmacok

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

112 ansmembrane helices (TMHs) 6 and 12 of human P-gp connect the transmembrane domains with its nucleoti

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

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

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

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

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

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

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

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

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

122 Potent inhibition of P-gp efflux in cells, including human brain endothelial

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

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

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

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

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

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

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

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

131 PGES-1 inhibitor, prevented up-regulation of P-gp expression and transport activity in capillaries ex

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

133 P-gp expression may adversely affect the oral bioavailab

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

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

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

137 on, as well as miR-221-mediated reduction of P-gp expression.

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

139 -throughput screen to identify substrates of P-gp from a series of chemical libraries, testing a tota

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

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

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

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

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

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

146 measure clinically meaningful alterations in P-gp function.

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

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

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

150 ion of ABC transporters like P-glycoprotein (P-gp) has been correlated with resistances in cancer che

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

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

153 anocarba nucleosides inhibit the activity of P-gp; however, a fluorescent derivative of one of the co

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

155 ODIPY)-verapamil transport mediated by human P-gp (IC(50) 2.4 +/- 0.6 uM); however, the BODIPY-conjug

156 Sex-specific circadian changes were found in P-gp ileum mRNA and protein levels, circadian amplitudes

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

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

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

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

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

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

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

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

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

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

167 was then evaluated for its interactions with P-gp in vitro.

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

169 ween the miR-221 network and P-glycoprotein (P-gp) in doxorubicin-induced drug resistance of leukemia

170 activity of the transporter P-glycoprotein (P-gp) in humans.

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

172 multidrug efflux transporter P-glycoprotein (P-gp) in three distinct conformational states: predomina

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

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

175 ates to reverse multidrug resistance through P-gp inhibition and to mitigate the off-target pharmacol

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

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

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

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

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

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

182 cells were also tested in the presence of a P-gp inhibitor (tariquidar) to assess reversibility of t

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

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

185 d design to improve the characteristics of a P-gp inhibitor previously identified by us.

186 nidine to a polymer will permit its use as a P-gp inhibitor through mitigation of its distribution in

187 which hinders its clinical application as a P-gp inhibitor.

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

189 explore the FDA-approved drug quinidine as a P-gp inhibitor.

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

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

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

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

194 Intensive efforts to identify P-gp inhibitors for use in combination therapy have not

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

196 association at 0-14 days modified by use of P-gp inhibitors or substrates (interaction p-value: 0.02

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

198 his hit compound represents a novel class of P-gp inhibitors that specifically targets and inhibits P

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

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

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

202 Here we tested the P-gp interaction of some A(3) adenosine receptor agonist

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

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

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

206 P-glycoprotein (P-gp) is a multidrug transporter that is expressed on th

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

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

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

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

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

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

213 binding cassette transporter P-glycoprotein (P-gp) is known to be expressed at barrier sites, where i

214 binding cassette transporter P-glycoprotein (P-gp) is known to limit both brain penetration and oral

215 P-glycoprotein (P-gp) largely influences the pharmacokinetics (PK) and t

216 llaries from humanized mPGES-1 mice to study P-gp levels.

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

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

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

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

221 ained its ability to inhibit the function of P-gp (log IC(50) of 4.20 nM for quinidine and 4.61 nM fo

222 eterozygotes or those homozygous for the non-P-gp-lowering allele (rs1045642 AA: HR 1.39, 95% CI 1.20

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

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

225 ing potency and selectivity while minimizing P-gp mediated efflux was fine-tuning of hydrogen bond ac

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

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

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

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

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

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

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

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

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

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

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

237 h NBDs, and they suggest that pre-hydrolytic P-gp occupies an occluded conformation.

238 s regard, understanding the interaction with P-gp of drug entities in development is important and hi

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

240 Transforming P-gp or an ABC drug exporter from an efflux transporter

241 GenX did not reduce P-gp- or BCRP-associated ATPase activity in an in vitro

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

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

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

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

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

247 onal states: predominantly inward-facing apo P-gp, pre-hydrolytic (E552Q/E1197Q) P-gp bound to Mg(+2)

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

249 ospholipase A2, COX-2, and mPGES-1 increases P-gp protein expression and transport activity levels.

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

251 ice revealed endogenous circadian rhythms of P-gp protein expression with a shorter period, larger am

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

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

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

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

256 the drug efflux behavior of P-glycoprotein (P-gp) remains a prominent challenge in cancer treatment.

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

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

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

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

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

262 ther PARP inhibitors, but pamiparib is not a P-gp substrate and shows excellent drug metabolism and p

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

264 rameter estimates to refine PK models of any P-gp substrate to account for sex, feeding and circadian

265 nd liver concentrations of talinolol, a pure P-gp substrate, significantly differed according to sex,

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

267 meability, and is not an efflux transporter (P-gp) substrate.

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

269 Combinations of P-gp substrates and inhibitors were assessed to demonstr

270 Of the tested compounds, a total of 90 P-gp substrates were identified, including 55 newly iden

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

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

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

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

275 we focus on the transporter P-glycoprotein (P-gp) that is partly responsible for limited ASD brain u

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

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

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

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

280 P-gp transport activity returned to control levels after

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

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

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

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

285 enerating PGE2, prevents blood-brain barrier P-gp up-regulation after status epilepticus (SE).

286 y signaling steps underlying seizure-induced P-gp up-regulation and suggest that mPGES-1 inhibitors c

287 mPGES-1 inhibitors could potentially prevent P-gp up-regulation in epilepsy.

288 subtype 1, are involved in seizure-mediated P-gp up-regulation.

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

290 P-glycoprotein (P-gp) was identified as the main efflux transporter acro

291 tify novel compounds that are transported by P-gp, we developed a high-throughput screen using the KB

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

293 Similar to the efflux function of wild-type P-gp, we found that uptake by the 14A mutant is ATP hydr

294 f these helices in the transport function of P-gp, we substituted a group of 14 conserved residues (s

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

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

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

298 ATPase activity of P-gp and by photolabeling P-gp with its transport substrate [(125)I]-iodoarylazido

299 multiforme, blocking the efflux function of P-gp with verapamil enhanced the therapeutic efficiency

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