ライフサイエンスコーパス: drug efflux

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

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

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

4 propose mechanisms for complex formation and drug efflux.

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

6 surface translocation and thus Pgp-mediated drug efflux.

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

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

9 lymerization while inhibiting P-glycoprotein drug efflux.

10 covery of other ABC transporters involved in drug efflux.

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

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

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

14 t cells exhibited increased energy-dependent drug efflux.

15 biophysical processes, among them increased drug efflux.

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

17 cholesterol esterification and MDR-catalyzed drug efflux.

18 l resistance of this organism through active drug efflux.

19 mediates multidrug resistance through active drug efflux.

20 tanding as to how acid/base chemistry drives drug efflux.

21 plication forks, reduced PARP1 trapping, and drug efflux.

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

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

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

25 cross-linking inhibited ATPase activity and drug efflux.

26 intranuclear delivery, thereby circumventing drug efflux.

27 herapy by reducing ROS levels and increasing drug efflux.

28 d nontransported inhibitor of ABCG2-mediated drug efflux.

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

30 inding stimulates ATP hydrolysis followed by drug efflux.

31 administration strategies targeting reduced drug efflux.

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

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

34 to indirectly interfere with P-glycoprotein drug efflux activity as a consequence of carbonic anhydr

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

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

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

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

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

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

41 dly restoring functional BRCA2 and promoting drug efflux activity.

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

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

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

45 over a mechanism of BCRP-mediated intestinal drug efflux and barrier functions and establish a role f

46 inal BCRP expression and compromised colonic drug efflux and barrier functions.

47 the maintenance of BCRP-mediated intestinal drug efflux and barrier functions.

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

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

50 ponent of the efflux pump, TolC, stimulating drug efflux and inducing expression of other efflux pump

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

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

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

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

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

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

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

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

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

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

61 ing cassette (ABC) transporters that mediate drug efflux, and, specifically, ABCB1, ABCG2 and ABCC1 a

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

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

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

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

66 f chemoresistance due to the presence of the drug-effluxing ATP binding cassette (ABC) transporters r

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

68 a key mediator of multidrug resistance, the drug efflux behavior of P-glycoprotein (P-gp) remains a

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

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

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

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

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

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

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

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

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

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

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

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

81 report shows a comparative response to MDR, drug efflux capability and reactive oxygen species (ROS)

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

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

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

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

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

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

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

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

90 emonstrate that KlebC binding to TolC blocks drug efflux from bacteria.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

107 Ellagic acid inhibited drug efflux in CRPC cells, but BRB extract and PCA did n

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

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

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

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

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

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

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

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

116 patients taking simvastatin, suggesting that drug-efflux interactions generate collateral toxicity th

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

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

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

120 Drug efflux is among the mechanisms leading to drug resi

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

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

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

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

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

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

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

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

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

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

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

132 In contrast to their shared roles in drug efflux, only TolC functioned in the modulation of m

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

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

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

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

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

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

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

140 d due to high expression and activity of the drug efflux protein ABCB1 (MDR1, P-glycoprotein).

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

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

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

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

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

146 The drug efflux pump ABCB1 is a key driver of chemoresistanc

147 Drug efflux pump ABCB1 is overexpressed in chemoresistan

148 pyrvinium through dysregulation of the major drug efflux pump ABCB1/MDR1.

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

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

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

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

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

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

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

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

157 sistance-1 (MDR1) acts as a chemotherapeutic drug efflux pump in tumor cells, although its physiologi

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

159 ed by greater abundance or production of the drug efflux pump MDR1.

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

161 cytosolically delivered IgGs can inhibit the drug efflux pump multidrug resistance-associated protein

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

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

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

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

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

167 and reported to be a potent inhibitor of the drug efflux pump P-glycoprotein and demonstrated the abi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

189 s" paralleled by overexpression of the ABCG2 drug efflux pump, whereas in tumors relapsing after non-

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

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

192 e FLC drug target, and AFR1, which encodes a drug efflux pump.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

209 verapamil directly inhibits M. tuberculosis drug efflux pumps through its human P-glycoprotein (PGP)

210 anscription factors, transporters, and multi-drug efflux pumps were identified from the genome.

211 Drug efflux pumps were upregulated.

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

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

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

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

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

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

218 esenchymal transition, the overexpression of drug efflux pumps, and the extracellular vesicle-mediate

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

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

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

222 Besides inducing the expression of drug efflux pumps, chemotherapy treatment alters the com

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

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

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

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

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

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

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

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

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

232 ious mechanisms, including overexpression of drug efflux pumps.

233 drug tolerance is mediated by mycobacterial drug efflux pumps.

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

235 predominantly by inducible Mef(A) and Msr(D) drug efflux pumps.

236 ce to select BBI in GIST was attributable to drug efflux pumps.

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

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

239 anisms including upregulation of C. albicans drug-efflux, regulation of oxidative stress response, an

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

241 Blocking drug efflux represents an attractive approach to combat

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

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

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

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

246 ividual genes encoding the AcrABZ-TolC multi-drug efflux system drastically reduced infection by bact

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

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

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

250 Drug efflux systems contribute to the intrinsic resistan

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

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

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

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

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

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

257 myeloid leukemia, is frequently mediated by drug efflux through P-glycoprotein (P-gp) overexpression

258 tent with a model whereby C1orf115 modulates drug efflux through regulation of the major drug exporte

259 Pdr5 and its homologues drive drug efflux through uncoupled hydrolysis of nucleotides,

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

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

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

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

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

265 d affected the function of membrane-embedded drug efflux transporter ABCB1, triggering the integrated

266 on of cancer stem cells expressing the multi-drug efflux transporter ABCB1.

267 The drug efflux transporter ABCB5 identifies cancer stem-lik

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

269 e CD44 receptor, PI3K/AKT signaling, and ABC drug efflux transporter activity.

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

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

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

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

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

275 Asia, mediated primarily by mutations in the drug efflux transporter PfCRT, we have explored whether

276 rpret data suggesting their therapeutic is a drug efflux transporter substrate?

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

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

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

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

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

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

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

284 barrier dysfunction is overexpression of the drug efflux transporters P-glycoprotein (P-gp) and breas

285 Eukaryotes use a highly conserved set of drug efflux transporters that confer pleiotropic drug re

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

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

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

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

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

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

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

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

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

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

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

297 Here, using assays to directly measure drug efflux, we find that M. tuberculosis transports the

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

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

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