ライフサイエンスコーパス: drug efflux

1 iciency induced by 5-CHInd and its effect on drug efflux.

2 surface translocation and thus Pgp-mediated drug efflux.

3 actor, and increased P-glycoprotein-mediated drug efflux.

4 tance involves P-glycoprotein (Pgp)-mediated drug efflux.

5 covery of other ABC transporters involved in drug efflux.

6 plays a role in the physiological process of drug efflux.

7 d drug resistance and enhanced MRP1-mediated drug efflux.

8 ate (MTX), because of enhanced ATP-dependent drug efflux.

9 t cells exhibited increased energy-dependent drug efflux.

10 biophysical processes, among them increased drug efflux.

11 xpressing cells, an effect due to diminished drug efflux.

12 cholesterol esterification and MDR-catalyzed drug efflux.

13 l resistance of this organism through active drug efflux.

14 mediates multidrug resistance through active drug efflux.

15 d-open and outward-open states necessary for drug efflux.

16 NP was not affected by transporter-mediated drug efflux.

17 ial BLN resistance to the parasites by rapid drug efflux.

18 cross-linking inhibited ATPase activity and drug efflux.

19 intranuclear delivery, thereby circumventing drug efflux.

20 herapy by reducing ROS levels and increasing drug efflux.

21 d nontransported inhibitor of ABCG2-mediated drug efflux.

22 s a strong uncoupling of ATPase activity and drug efflux.

23 inding stimulates ATP hydrolysis followed by drug efflux.

24 administration strategies targeting reduced drug efflux.

25 BC) transporter genes, thus affecting global drug efflux.

26 eltaloop) failed to complement its defect in drug efflux.

27 d by residence in macrophages and depends on drug efflux.

28 DR1 protein expression (71%), and functional drug efflux (58%); each of these factors occurred at hig

29 ncentrations to subtoxic levels by mediating drug efflux across the cell envelope.

30 report that the conformation of P-gp and its drug efflux activity can be altered by synonymous polymo

31 y, stimulation of TLR2 induced synthesis and drug efflux activity of ABCB1/MDR1 p-gp in murine and hu

32 henotypically distinct and display increased drug efflux activity relative to daughters.

33 P-glycoprotein and drug efflux activity transfers were followed over 7 days

34 Finally, functional inhibition of ABCG2 drug efflux activity with fumitremorgin C or inhibition

35 ing a restoration of ABCG2-mediated specific drug efflux activity.

36 anslocates to the cell surface, and mediates drug efflux; alternatively, 150-kDa Pgp is cleaved to a

37 ated that these new compounds abolished P-gp drug efflux and accumulated high intracellular concentra

38 ture-activity relationships controlling both drug efflux and ATPase activity of ABCG2 and to elucidat

39 e relative roles of drug bioavailability and drug efflux and drug influx proteins in the development

40 therapy with antibiotics to prevent cellular drug efflux and has been reported to inhibit Panx1.

41 istance mediated by ABCG2 through inhibiting drug efflux and may be used potentially in humans to mod

42 ABCG2 plays a major role in anticancer-drug efflux and related tumor multidrug resistance.

43 more, this domain has activity that inhibits drug efflux and resistance function of the full-length A

44 -binding cassette (ABC) transporter-mediated drug efflux and strongly increases the apparent bioavail

45 o both CFTR channel opening and MRP-mediated drug efflux and that CFTR channels and MRP pumps utilize

46 important roles, in both the specificity of drug efflux and the sensitivity of the transporter to re

47 ich is an outer membrane protein involved in drug efflux and type I protein secretion, is required fo

48 ecule largely eludes P glycoprotein-mediated drug efflux, and an analog is currently being evaluated

49 DR1-related functions including endocytosis, drug efflux, and cell volume regulation.

50 xpression of MRP is associated with enhanced drug efflux, and that MRP transcript is widely expressed

51 i) the inhibition of P-glycoprotein mediated drug efflux; and (vii) the TAT-medicated nuclear translo

52 However, although the ability to confer drug efflux appears to have emerged on only a few occasi

53 neity of cancer cell populations in terms of drug efflux at high temporal resolution.

54 istance (MDR), which is mediated by multiple drug efflux ATP-binding cassette (ABC) transporters, is

55 (P-gp) is one of the best-known mediators of drug efflux-based multidrug resistance in many cancers.

56 to the utility and overall strategy of using drug efflux blockers in patients with established Pgp ov

57 We show that E2F1 causes chemotherapeutic drug efflux both in vitro and in vivo via ABCG2.

58 locks the pump in a conformation that blocks drug efflux but activates ATPase activity.

59 ate or competitive inhibitor of Pgp-mediated drug efflux but rather acts as a noncompetitive modulato

60 We show here that SXR also regulates drug efflux by activating expression of the gene MDR1, w

61 t mitochondrial mechanism and broadly blocks drug efflux by an apparently pBR-independent, ABC transp

62 reased cell uptake and significantly reduced drug efflux by model multidrug resistant (MDR) breast ca

63 Inhibition of Pgp-mediated drug efflux by PSC-833 did not improve clinical outcomes

64 nts, but to the much broader range of cancer drugs effluxed by ABCB1.

65 The spectrum of anticancer drugs effluxed by BCRP includes mitoxantrone, camptothec

66 P-Glycoprotein-mediated drug efflux can yield a multidrug-resistance (MDR) pheno

67 Moreover, recent evidence suggests that high drug efflux cancer cells (HDECC) may be selectively enri

68 Cancer cells with active drug efflux capability are multidrug resistant and pose

69 ells can be enriched based on their inherent drug efflux capability mediated by the ABC transporter A

70 neg) cells suggesting that they possess high drug efflux capacity and intracellular drug detoxificati

71 Drug-effluxing CD4(+) T cells were characterized as CD16

72 CLL and mantle cell lymphoma, including rare drug effluxing chemotherapy resistant tumor cells that h

73 AcrA protein is a component of the multi-drug efflux complex AcrAB-TolC of Escherichia coli.

74 esistant to antifungal drugs and express the drug efflux determinants CDR1, CDR2 and MDR1.

75 problem here using the example of monitoring drug efflux from a monolayer of cancer cells with microv

76 most common cause of MDR involves increased drug efflux from cancer cells mediated by members of the

77 DR, experimental methods are needed to study drug efflux from cancer cells.

78 cancer that gives rise to passive and active drug efflux from cells.

79 ssion profiles revealed significantly higher drug efflux from leukemic SP cells than from non-SP cell

80 nto the apical membrane inner monolayer, and drug efflux from P-gp into the apical chamber, as well a

81 sical processes, one of them being increased drug efflux from resistant cells which leads to a decrea

82 nce-associated protein (MRP) responsible for drug efflux from the cancer cells (pump resistance) and

83 ancer cells through direct inhibition of the drug efflux function of ABCB1 and ABCG2.

84 The drug efflux function of P-glycoprotein (P-gp) encoded by

85 BCB1- and ABCG2-mediated MDR by blocking the drug efflux function of these transporters.

86 Consistently, a number of multi-drug efflux genes, particularly the central component To

87 er functions in tumorigenesis independent of drug efflux have not been described that might help expl

88 -binding cassette (ABC) transporter-mediated drug efflux, have been discovered.

89 orter LmrP from Lactococcus lactis catalyses drug efflux in a membrane potential and chemical proton

90 nduces chemoresistance in part by increasing drug efflux in an ABC transporter-dependent manner.

91 ional adenosine triphosphate (ATP)-dependent drug efflux in certain multidrug-resistant cancer cell l

92 (MDR1) and ATP binding cassette (ABC)-based drug efflux in human breast cancer cells.

93 Finally, the homodimers reverse Pgp-mediated drug efflux in intact cells overexpressing Pgp, and 11 A

94 totoxic inhibitor of P-glycoprotein-mediated drug efflux in multidrug-resistant human colon cancer ce

95 Drug efflux in SW626 cells is mediated by a verapamil-in

96 enhancement of nuclear accumulation and less drug efflux in the resistant cells treated by DLMC+US th

97 es avert P-gp binding, abolish P-gp-mediated drug efflux, increase intracellular drug concentration,

98 ions, the contribution of exosomes to active drug efflux increased with drug concentration and exceed

99 nterestingly, MDR1 expression and functional drug efflux increased with patient age, from a frequency

100 ATP-dependent drug efflux involves changes between the open inward-fac

101 in the subnanomolar range, resistance due to drug efflux is a common phenomenon among the antitubulin

102 P-glycoprotein (Pgp)-mediated drug efflux is a major factor contributing to the varian

103 In contrast, drug efflux is increased in cells that do not overexpres

104 cted in the efficacy with which Pgp-mediated drug efflux is reversed.

105 aclitaxel, which suggests that P-gp-mediated drug efflux is unlikely to be the only cause of paclitax

106 and drug-susceptible isolates suggests that drug efflux may be a less significant contributor to res

107 we propose a model for the proton-dependent drug efflux mechanism of EmrE.

108 observations implicate vesicle shedding as a drug efflux mechanism potentially involved in drug resis

109 dependent, in part, upon an energy-dependent drug efflux mechanism.

110 Enhanced drug efflux mediated by ABCB1 P-glycoprotein and related

111 The accelerated drug efflux mediated by ATP-binding cassette (ABC) trans

112 oyl groups brings about high potency against drug efflux mediated by P-glycoprotein (P-gp).

113 ch resistance has been associated with rapid drug efflux mediated by the multidrug resistance gene 1

114 promoter DNA, derepression of the mexAB-oprM drug efflux operon, and increased antibiotic resistance

115 are adjacent to orthologs of the mmpS5-mmpL5 drug efflux operon.

116 Resistance is not mediated through increased drug efflux or metabolism, but is shown to emerge from l

117 of intracellular drug distribution either by drug efflux or sequestration into intracellular organell

118 ulation of glutathione, thioredoxin, and the drug efflux pathways involved in detoxification of elect

119 f the four transporter families that contain drug efflux permeases indicate that drug resistance aros

120 The drug efflux process has been proposed to entail a synchr

121 We determined whether the drug efflux protein P-glycoprotein (Pgp) could influence

122 We hypothesized that the drug efflux protein P-glycoprotein (Pgp), the product of

123 od-brain barrier (BBB), a process limited by drug efflux proteins such as P-glycoprotein (P-gp) at th

124 a new member of the family of ATP-dependent drug efflux proteins.

125 s through induction of detoxification and/or drug efflux proteins.

126 called P-glycoprotein (Pgp), which acts as a drug efflux pump actively depleting intracellular drug c

127 to that of verapamil) toward the whole-cell drug efflux pump activity of mycobacteria, thus turning

128 expression of P-glycoprotein, an ATP-driven drug efflux pump and a critical determinant of drug entr

129 P-glycoprotein (P-gp), suggesting an active drug efflux pump as a potential mechanism of drug resist

130 As a substrate of P-glycoprotein, a drug efflux pump associated with multidrug resistance, (

131 ord with the notion that MRP8 functions as a drug efflux pump for nucleotide analogs, MRP8-transfecte

132 a2 induces drug resistance by activating the drug efflux pump gene ABCC3 and anti-apoptotic Bcl-2 fam

133 The three putative drug efflux pump genes most positively affected by NorG

134 protein (Pgp) in brain capillaries that this drug efflux pump is a factor in limiting the penetration

135 fusion associated with overexpression of the drug efflux pump MDR1.

136 P-glycoprotein (P-gp, MDR1) is a promiscuous drug efflux pump of substantial pharmacological importan

137 There may exist a P-gp-mediated drug efflux pump on the apical aspect of the rabbit conj

138 MCF-7 cells and overexpression of an active drug efflux pump P-170 glycoprotein in resistant MCF-7/A

139 The drug efflux pump P-glycoprotein (P-gp) has been shown to

140 xic to a series of cell lines expressing the drug efflux pump P-glycoprotein (P-gp, ABCB1) and MRP1 (

141 tant pre-tumorigenic cells indicate that the drug efflux pump P-glycoprotein is responsible for the M

142 CYP) 3A4 and 3A5 are also transported by the drug efflux pump P-glycoprotein, we determined whether e

143 ed, but it is known to be transported by the drug efflux pump P-glycoprotein, which is expressed in e

144 s, in association with overexpression of the drug efflux pump P-glycoprotein.

145 P-Glycoprotein (Pgp), an energy-dependent drug efflux pump responsible for multidrug resistance of

146 to the presence of a novel, energy-dependent drug efflux pump similar to P-glycoprotein and multidrug

147 uman P-glycoprotein (P-gp) is a cell surface drug efflux pump that contains two nucleotide binding do

148 lted in the inhibition of P-gp expression (a drug efflux pump to increase excretion of anticancer dru

149 in (P-gp) functions as a membrane-associated drug efflux pump whose increased expression results in r

150 P-glycoprotein (Pgp) is an ATP-dependent drug efflux pump whose overexpression confers multidrug

151 ndent hydrophobic natural product anticancer drug efflux pump whose overexpression confers multidrug

152 ct point with the periplasmic component of a drug efflux pump, AcrA.

153 P-glycoprotein (P-gp), a promiscuous drug efflux pump, has been extensively studied for its a

154 P-glycoprotein (P-gp), an ATP-dependent drug efflux pump, has been implicated in multidrug resis

155 P-glycoprotein, an ATP-driven drug efflux pump, is a major obstacle to the delivery of

156 mes that neutralize oxidative stress and the drug efflux pump, P-170 glycoprotein.

157 The ATP-driven drug efflux pump, P-glycoprotein, is a critical and sele

158 sistance (MDR) phenotype, as mediated by the drug efflux pump, P-glycoprotein, is one of the most ext

159 ompounds is believed to involve blocking the drug efflux pump, P-glycoprotein.

160 brain barrier, P-glycoprotein, an ATP-driven drug efflux pump, selectively limits drug access to the

161 drug-independent assembly of the tripartite drug efflux pump, specifically in coupling the inner mem

162 in part, through regulation of transmembrane drug efflux pump.

163 nel and the adaptor protein in the assembled drug efflux pump.

164 rane-bound AcrAB proteins that function as a drug efflux pump.

165 ug resistance, functions as an ATP-dependent drug efflux pump.

166 protein and functions as an energy-dependent drug efflux pump.

167 in (P-gp), which acts as an energy dependent drug efflux pump.

168 P-glycoprotein is an ATP-dependent drug-efflux pump that can transport a diverse range of s

169 has a high self-renewal capacity, an active drug-efflux pump, and high content of anti-apoptotic pro

170 otics, resulting in stimulated expression of drug efflux pumps and induction of MDR.

171 nal profiling, that indole serves to turn on drug efflux pumps and oxidative-stress protective mechan

172 n and transport activity of three ATP-driven drug efflux pumps at the blood-brain barrier [P-glycopro

173 MDR is often caused by upregulation of drug efflux pumps by members of the fungal zinc-cluster

174 c Candida strains lacking one or more of the drug efflux pumps Cdr1p, Cdr2p, and Mdr1p to determine t

175 ant cell lines with activated P-glycoprotein drug efflux pumps compared to drug-sensitive parent cell

176 of the type I protein secretion systems and drug efflux pumps in Gram-negative bacteria.

177 our data support a model in which a role of drug efflux pumps is to mediate cell-cell communication

178 ATP)-binding cassette (ABC) transporters are drug efflux pumps responsible for the multidrug resistan

179 olC is the cell surface component of several drug efflux pumps that are responsible for bacterial res

180 Drug efflux pumps were upregulated.

181 ach family and that the diversity of current drug efflux pumps within each family arose from just one

182 AC1 (encoding a transcriptional regulator of drug efflux pumps) made independent, additive contributi

183 hemotherapy failure is the overexpression of drug efflux pumps, ABCB1 (also known as MDR1 or P-gp) an

184 radical scavenging, increased expression of drug efflux pumps, and changes in gene expression that a

185 egulation of osmoprotectant transporters and drug efflux pumps, and down-regulation of membrane porin

186 olute influx and efflux, including potential drug efflux pumps, and for products implicated in carbon

187 activation of drug efflux pumps, anti-apoptotic defense mechanisms, et

188 (MRP6, ABCC6), a member of the MRP family of drug efflux pumps, are the genetic basis of Pseudoxantho

189 oxygen species (ROS)-scavenging enzymes and drug efflux pumps, but how these genes are up-regulated

190 ven events, starting with induction of multi-drug efflux pumps, followed by the development of chromo

191 ch reduction can be effected by a variety of drug efflux pumps, of which the most widely studied is P

192 Although both can function as drug efflux pumps, only Pgp1a can act like human Pgp to

193 Immunologic detection of the drug efflux pumps, P-glycoprotein (Pgp) and multidrug re

194 overproduction of target genes that include drug efflux pumps, which in turn confer high level drug

195 axel through up-regulation of P-glycoprotein drug efflux pumps.

196 aved into Dox, thereby avoiding excretion by drug efflux pumps.

197 ly diverse lipophilic anions and function as drug efflux pumps.

198 e small multidrug resistance (SMR) family of drug efflux pumps.

199 otypes are often achieved by the activity of drug efflux pumps.

200 in the ergosterol pathway targeted by azole drugs, efflux pumps, and a transcription factor that pos

201 le isolates, with no evidence of an enhanced drug efflux rate.

202 translocation inactivated MtrD and abolished drug efflux, rendered both MtrE and MtrE-E434K vancomyci

203 Blocking drug efflux represents an attractive approach to combat

204 ng quantitative real-time PCR and functional drug efflux studies, we observed that Tie2 activation re

205 ve, occurring in the presence and absence of drug efflux substrate.

206 about 42% of the variants lost resistance to drug efflux substrates completely or selectively.

207 MC activation, repair of DNA lesions, and/or drug efflux), support the hypothesis that a functional m

208 The promoter region of the macAB drug efflux system genes harbours a binding site for the

209 ce, which underscores the connection between drug efflux systems and virulence.

210 lation-division (RND)-type systems and/or in drug efflux systems belonging to the major facilitator (

211 Drug efflux systems contribute to the intrinsic resistan

212 Drug efflux systems play a major role in resistance to a

213 almonella virulence and a strain lacking all drug efflux systems was avirulent when mice were inocula

214 es, which results from chromosomally encoded drug-efflux systems and multiple acquired resistance mec

215 r efficacy of purine nucleosides by blocking drug efflux that may be a significant mode of resistance

216 its pKa, accounting for the pH dependency of drug efflux that we report in this work.

217 terfere with P-glycoprotein (P-gp)-dependent drug efflux, the second randomization tested the benefit

218 sis and blocks P-glycoprotein (Pgp)-mediated drug efflux to chemosensitize cancer cells at least as w

219 oth pumps must be expressed in order for the drug efflux to occur.

220 on of the MRP4 gene correlated with enhanced drug efflux; transfer of chromosome 13 containing the am

221 nstrate that genetic variation within an ABC-drug efflux transporter (Abcb5) affected susceptibility

222 cl-2), metabolic (G6PD, TKT, PPARgamma), and drug efflux transporter (ABCG2, MRP3, MRP4) genes.

223 The drug efflux transporter ABCB5 identifies cancer stem-lik

224 mmon polymorphic variant of the chemotherapy drug efflux transporter ABCG2, which contributes to norm

225 n the cytochrome P450 mono-oxygenase system, drug efflux transporter adenosine triphosphate-binding c

226 rib caused by increased P-glycoprotein (Pgp) drug efflux transporter expression.

227 P3A4 and was negated by cotreatment with the drug efflux transporter inhibitor elacridar.

228 The drug efflux transporter P-glycoprotein (P-gp) is highly

229 ession of the Abcb1b gene, which encodes the drug efflux transporter P-glycoprotein.

230 resistance-associated protein 1 (MRP1) is a drug efflux transporter that has been implicated in the

231 ic growth and differentiation, and the ABCG2 drug efflux transporter will be presented.

232 P-binding cassette (ABC) membrane-associated drug efflux transporter, is known to localize at the blo

233 expression and transport activity of the key drug efflux transporter, P-glycoprotein (6 h EC(50) was

234 , and they were not substrates for the ABCB1 drug efflux transporter.

235 ions of the anticancer drug vinorelbine with drug efflux transporters and cytochrome P450 3A drug-met

236 Mammalian P-glycoproteins are active drug efflux transporters located in the plasma membrane.

237 ced cellular drug concentrations mediated by drug efflux transporters, and permeability barriers asso

238 ession of several cytochromes P450 (CYP) and drug efflux transporters.

239 -gp and MRP1, which are established cellular drug efflux transporters.

240 , mediated by the ATP-binding cassette (ABC) drug efflux transporters.

241 the founding member of a family of bacterial drug efflux transporters.

242 of resistance must be nonspecific, involving drug-efflux transporters such as ATP-binding cassette su

243 MDR) mediated by the ABCB1, ABCC1, and ABCG2 drug-efflux transporters.

244 resistance glycoprotein MDR1 and functional drug efflux using sensitive flow cytometric techniques.

245 Stimulation of drug efflux was detectable in the cells expressing P-gly

246 Mean multidrug resistance-protein-mediated drug efflux was significantly lower in the leukemic blas

247 Given the role of AcrAB-TolC in multi-drug efflux we suggest that CsrA is a potential drug tar

248 Third, to avoid P-glycoprotein-mediated drug efflux, we further designed another delivery vehicl

249 Stability and drug efflux were identified as two factors limiting rust

250 Reversal of resistance by blocking drug efflux with fumitremorgin C should allow for functi