ライフサイエンスコーパス: BCRP

1 BCRP contains one nucleotide-binding domain (NBD) follow

2 BCRP expression has also been demonstrated in pluripoten

3 BCRP expression is regulated by a number of nuclear tran

4 BCRP is a 655 amino-acid polypeptide, formally designate

5 BCRP is also expressed in the apical membrane of mammary

6 BCRP levels in cells that do not express BCR-ABL were no

7 BCRP maps to chromosome 4q22, downstream from a TATA-les

8 BCRP specifically binds heme, and cells lacking BCRP acc

9 BCRP substrates include numerous drugs (topotecan, nitro

10 BCRP-overexpressing and BCRP-negative human breast cance

11 ward daunorubicin (P-gp and MRP1) and SN-38 (BCRP) in A2780/ADR (P-gp), H69AR (MRP1), and MDCK II BCR

12 GLB was also shown to be a BCRP/Bcrp1 substrate in transwell transport experiments.

13 These results suggest that GLB is a BCRP/Bcrp1 substrate, and Bcrp1 significantly limits fet

14 study, we first determined whether GLB is a BCRP/Bcrp1 substrate.

15 e and appears to depend on the presence of a BCRP mutation at codon 482.

16 not AR protein in TRAMP are the source of a BCRP-negative and AR-negative, Foxa2- and SV40Tag-expres

17 RP1), calcein AM (P-gp), and pheophorbide A (BCRP) transport.

18 ABCG2 (BCRP/MXR/ABCP) is a half-transporter associated with mul

19 1 (P-glycoprotein), ABCC1 (MRP1), and ABCG2 (BCRP) are well known for their role in rendering cancer

20 ne transporter proteins ABCB1 (P-gp), ABCG2 (BCRP), and ABCC1 (MRP1), which are involved in the forma

21 that the major multidrug transporter ABCG2 (BCRP/MXR) is directly and specifically activated by the

22 indings highlight the need to consider ABCG2/BCRP effects during d-luciferin-based BLI and suggest no

23 cell line 22Rv1 that naturally express ABCG2/BCRP, show that ABCG2/BCRP expression and function withi

24 ow that d-luciferin is a substrate for ABCG2/BCRP but not for the MDR1 P-glycoprotein (ABCB1/Pgp), mu

25 throughput methods for identifying new ABCG2/BCRP inhibitors.

26 rs, including the potent and selective ABCG2/BCRP inhibitor fumitremorgin C.

27 aturally express ABCG2/BCRP, show that ABCG2/BCRP expression and function within regions of interest

28 rafts engineered to express transgenic ABCG2/BCRP, as well as xenografts derived from the human prost

29 ding cassette (ABC) family transporter ABCG2/BCRP affects BLI signal output from the substrate d-luci

30 17beta-estradiol and progesterone can affect BCRP expression in cancer cells.

31 sted for their inhibitory activities against BCRP and screened against P-glycoprotein (P-gp, ABCB1) a

32 unoblotting with specific antibodies against BCRP and the HA tag.

33 s may affect fetal drug exposure by altering BCRP expression in human placenta.

34 ess the efflux transporters MDR1 (KBV-1) and BCRP (KBH5.0).

35 e ABC transporters MDR-1 (Pgp-1), MRP-1, and BCRP-1.

36 owed that the expression level of Pim-1L and BCRP was up-regulated in mitoxantrone and docetaxel-resi

37 s identify the human protein, i.e., BSEP and BCRP, and lowercase letters indicate that the transporte

38 onserved the protein levels of BSEP/Bsep and BCRP/Bcrp similarly to those found in liver tissue.

39 hibition prevents overexpression of P-gp and BCRP at the blood-brain barrier in rats after status epi

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

41 I:C), viral antigen) would decrease P-gp and BCRP in the human placenta.

42 spholipase A2 (cPLA2), resulting in P-gp and BCRP overexpression.

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

44 100 nM rapidly (in 1-2 h) inhibited P-gp and BCRP transport activities at the BBB through different m

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

46 erexpression of blood-brain barrier P-gp and BCRP.

47 take assays in cells overexpressing P-gp and BCRP.

48 Glutamate increased cPLA2, P-gp, and BCRP protein and activity levels in isolated brain capil

49 G2), and that targeted knockdown of MDR1 and BCRP expression by small interfering RNA partially rever

50 (Western blots) of P-glycoprotein, Mrp2, and BCRP.

51 /kg PB increased P-glycoprotein-, Mrp2-, and BCRP-mediated transport and protein expression in brain

52 MRP4 and BCRP were not detected in any of the tumors studied.

53 BCRP-overexpressing and BCRP-negative human breast cancer cells (MCF-7) and larg

54 mitoxantrone in both BCRP-overexpressing and BCRP-negative human cell lines.

55 diotracers to study the interplay of Pgp and BCRP at the human BBB in limiting brain uptake of dual s

56 protein-1 (MDR1, ABCB1, P-glycoprotein) and (BCRP, ABCG2), and that targeted knockdown of MDR1 and BC

57 cells, indicating that these flavonoids are BCRP inhibitors.

58 or other 4-AQ molecules with agents that are BCRP and MDR1 substrates.

59 on drug resistance related proteins, such as BCRP-1, MGMT, MDR-1, MRP-1 and MRP-3, after TRP-2 transf

60 /ADR (P-gp), H69AR (MRP1), and MDCK II BCRP (BCRP) cells.

61 Blocking BCRP function in Bcrp(+/+) progenitor cells markedly red

62 ion and cytotoxicity of mitoxantrone in both BCRP-overexpressing and BCRP-negative human cell lines.

63 The spectrum of anticancer drugs effluxed by BCRP includes mitoxantrone, camptothecin-derived and ind

64 nylimidazo[4,5-b]pyridine) is transported by BCRP, MDR1, and MRP2.

65 mplexes and induces internalization of CD44, BCRP, and P-glycoprotein.

66 umulation was observed in the MCF7/MX cells (BCRP(Arg)) as compared with cells expressing the Thr and

67 ive studies are needed, preferably combining BCRP protein or mRNA quantification with functional assa

68 We demonstrate that the compromised BCRP functions during obesity are because of loss of Jan

69 istance, with no effect on the corresponding BCRP-negative cells, indicating that these flavonoids ar

70 ase (PI3K) inhibitor LY294002 also decreased BCRP levels in K562/BCRP-MX10 cells.

71 Knockdown of AhR by shRNA decreased BCRP expression, and this decrease was reversed by rescu

72 study provides the first evidence of direct BCRP regulation by PPARalpha in a human in vitro BBB mod

73 n choriocarcinoma cells with high endogenous BCRP expression (JAR and BeWo) and human cancer cells (M

74 s abolished multimer formation of endogenous BCRP and resensitized the resistant cells to chemotherap

75 ll bowel, and brain microvessel endothelium, BCRP may play a role in protecting the organism from pot

76 Using [(3)H]mitoxantrone, an established BCRP substrate, we observe a significant reduction in it

77 ssue, the rare epithelial cells that express BCRP and lack AR protein are localized in the basal cell

78 ative prostate tumor stem cells that express BCRP but not AR protein in TRAMP are the source of a BCR

79 prostate progenitor cell line that expresses BCRP and AR mRNAs, but minimal AR protein, results in st

80 FLVCR, BCRP, and PCFT/HCP-1 represent the three heme transporte

81 The expression of FLVCR, BCRP, and PCFT in mouse retina and primary mouse RPE cel

82 ariation (CV) were below 15.9% and 14.2% for BCRP/ABCG2 quantification or below 15.6% and 6.4% for BS

83 Real-time RT-PCR assays for BCRP, occludin and claudin-5 demonstrated no significant

84 the transmembrane helices are essential for BCRP function.

85 Here, we provide evidence for BCRP as a MTX-transporter using an in vitro membrane ves

86 aracterization of a mouse line humanized for BCRP (hBCRP), in which the mouse coding sequence from th

87 ime, an absolution quantification method for BCRP/Bcrp and BSEP/Bsep and the differences of the prote

88 ntal evidence in support of a 6-TM model for BCRP with the amino and carboxyl termini of the MSD loca

89 as established to be 31.25 pM and 125 nM for BCRP/ABCG2 and BSEP/ABCG11, respectively.

90 ocalized beta-catenin essential not only for BCRP expression and surface localization, but also for t

91 usion, we have demonstrated a novel role for BCRP as a mediator of MTX resistance and have provided f

92 d barrier functions and establish a role for BCRP in preventing CLGI-associated obesity both in human

93 TX-Glu(2) and MTX-Glu(3) were substrates for BCRP.

94 current evidence suggesting that functional BCRP is a homodimer.

95 f the breast cancer resistance protein gene (BCRP/ABCG2), we examined the 5' untranslated region of B

96 mpared with cells expressing the Thr and Gly BCRP variants.

97 d radiotracer for functional imaging of P-gp/BCRP activity with positron emission tomography (PET).

98 pment of prodrug tracers for imaging of P-gp/BCRP function in vivo but also highlight some challenges

99 Blocking with P-gp/BCRP modulators led to increased levels of brain radioac

100 region of BCRP mRNA in cell lines with high BCRP transcriptional activity and in normal tissues.

101 ing model to study the in vivo role of human BCRP in limiting absorption and BBB penetration of subst

102 A2780/ADR (P-gp), H69AR (MRP1), and MDCK II BCRP (BCRP) cells.

103 In BCRP promoter-luciferase assays, sequential deletions of

104 croM) increased mitoxantrone accumulation in BCRP-overexpressing cells, completely reversing mitoxant

105 trate resistance to imatinib cytotoxicity in BCRP-overexpressing cells in vitro.

106 addition, we show a significant decrease in BCRP protein expression and function when PPARalpha is d

107 viding a mechanism for lack of AR protein in BCRP-expressing stem cells.

108 AhR overexpression further increased BCRP mRNA and protein expression.

109 owever, progesterone significantly increased BCRP expression and activity only in PRB-transfected cel

110 reated with clofibrate, suggesting increased BCRP efflux activity.

111 ting studies indicate that whereas increased BCRP expression is evident in cells selected for resista

112 d MET are potent AhR agonists and can induce BCRP in human placental trophoblasts by activating AhR.

113 e., clofibrate, GW7647) significantly induce BCRP mRNA and protein expression in a time- and concentr

114 plasma concentrations significantly induced BCRP mRNA up to 10-fold in human model placental JEG3 an

115 Collectively, progesterone induces BCRP expression in BeWo cells via PRB but not PRA.

116 hydroisoquinoline moiety selectively inhibit BCRP.

117 Although gefitinib inhibited BCRP more potently than MDR1 (10-fold), the inhibition o

118 bese individuals have compromised intestinal BCRP functions and that diet-induced obese mice recapitu

119 all result in significant loss of intestinal BCRP expression and compromised colonic drug efflux and

120 vestigate clinically relevant DDIs involving BCRP.

121 cells selected for resistance to irinotecan, BCRP expression is not detectable in two different cell

122 duced and selected to overexpress BCRP (K562/BCRP-MX10).

123 nib decreased the expression of BCRP in K562/BCRP-MX10 cells without affecting mRNA levels.

124 LY294002 also decreased BCRP levels in K562/BCRP-MX10 cells.

125 s greatly decreased by mitoxantrone, a known BCRP substrate, suggesting competition for transport.

126 rease in resistance to mitoxantrone, a known BCRP substrate.

127 P specifically binds heme, and cells lacking BCRP accumulate porphyrins.

128 trations in Madin-Darby canine kidney (MDCK)/BCRP cells were significantly lower than those in MDCK/v

129 concentrations approximately 2-fold in MDCK/BCRP cells, but it had no effect in MDCK/vector cells.

130 e demonstrate robust human and loss of mouse BCRP/Bcrp mRNA and protein expression in the hBCRP mice

131 teins, including wild-type BCRP and a mutant BCRP that contains a threonine rather than an arginine a

132 rmore, overexpression of wild-type or mutant BCRP is associated with reduced intracellular accumulati

133 he transport of rhodamine 123 among nine MXR/BCRP/ABCP-overexpressing cells studied; all demonstrated

134 t not with the wild-type R482; all three MXR/BCRP/ABCP forms transported mitoxantrone.

135 Reductions of P-gp but not BCRP transport activity were blocked by a peroxisome pro

136 equired for the GenX effects on P-gp but not BCRP transport activity.

137 localization and drug-resistant activity of BCRP were compromised by T362A mutation.

138 opening the door to clinical applications of BCRP inhibition.

139 s, in order to determine the contribution of BCRP to drug resistance in human cancers.

140 The absolute differences of BCRP/Bcrp and BSEP/Bsep proteins were determined in live

141 ely little is known regarding the effects of BCRP on other CPT analogues.

142 show that gefitinib inhibited the efflux of BCRP and MDR1 substrates and restored vincristine sensit

143 o the apical membrane, and the expression of BCRP and PCFT was restricted to the basolateral membrane

144 ed that imatinib decreased the expression of BCRP in K562/BCRP-MX10 cells without affecting mRNA leve

145 wed that estrogen enhanced the expression of BCRP mRNA in the estrogen receptor (ER)-positive T47D:A1

146 High expression of BCRP was observed on the oocyte surface.

147 istent with the idea that the active form of BCRP is a homodimer or homomultimer.

148 ed in vesicles containing the mutant form of BCRP.

149 Finally, induction of BCRP expression in JEG3 and BeWo cells was accompanied b

150 Inhibition of BCRP-mediated efflux of dihydrotestosterone by novobioci

151 ted by fumitremorgin C, a known inhibitor of BCRP.

152 Potent and specific inhibitors of BCRP are now being developed, opening the door to clinic

153 Loss of BCRP expression was accompanied by imatinib-induced redu

154 ocalization, but also for the maintenance of BCRP-mediated intestinal drug efflux and barrier functio

155 Our results uncover a mechanism of BCRP-mediated intestinal drug efflux and barrier functio

156 for understanding the transport mechanism of BCRP.

157 e of amino acid 482, we analyzed a number of BCRP-overexpressing cell lines.

158 Transfection and enforced overexpression of BCRP in drug-sensitive MCF-7 or MDA-MB-231 cells recapit

159 asma membrane and induced phosphorylation of BCRP at threonine 362.

160 dicate that JAK3-mediated phosphorylation of BCRP promotes its interactions with membrane-localized b

161 (JAK3)-mediated tyrosine phosphorylation of BCRP.

162 hat tissue-specific alternative promoters of BCRP exist.

163 ), we examined the 5' untranslated region of BCRP mRNA in cell lines with high BCRP transcriptional a

164 I)-associated obesity, but the regulation of BCRP during obesity and its role in maintaining the inte

165 is study is to investigate the regulation of BCRP functional expression by peroxisome proliferator-ac

166 Studies are emerging on the role of BCRP expression in drug resistance in clinical cancers.

167 Given the critical role of BCRP in limiting fetal exposure to drugs and xenobiotics

168 nsport activity and substrate selectivity of BCRP, respectively.

169 ntial for the broad substrate specificity of BCRP.

170 udy, we determined the topology structure of BCRP by inserting hemagglutinin (HA) tags in its predict

171 f FLVCR and PCFT was upregulated and that of BCRP was downregulated.

172 In the presence of the wild-type variant of BCRP, transport of MTX into vesicles was ATP-dependent,

173 type (Arg482) or mutant (Gly482) variants of BCRP.

174 Progesterone had little effect on BCRP expression and activity and transcriptional activit

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

176 o normal individuals whereas that of MRP4 or BCRP protein was not.

177 lesser extent, by MRP1, but not MRP2-MRP6 or BCRP/MXR.

178 ificantly lower expression for either Pgp or BCRP.

179 called breast cancer resistance protein, or BCRP).

180 ramide transport was selective for P-gp over BCRP.

181 BCR-ABL, which in turn downregulates overall BCRP levels posttranscriptionally via the PI3K-Akt pathw

182 verexpress MDR1 and KBH5.0 cells overexpress BCRP, decreased cytotoxicity in these cell lines relativ

183 cells transduced and selected to overexpress BCRP (K562/BCRP-MX10).

184 Certain tumors overexpressing BCRP were found to become resistant against various anti

185 mical staining using antibodies against Pgp, BCRP or MRP4 and von Willebrand factor.

186 acridar was consistent with that of dual Pgp/BCRP substrates.

187 ated the suitability of the radiolabeled Pgp/BCRP inhibitors (11)C-tariquidar and (11)C-elacridar to

188 Chrysin and biochanin A were the most potent BCRP inhibitors, producing significant increases in mito

189 own as the breast cancer resistance protein (BCRP or ABCG2) confers a strong survival advantage under

190 (Pgp) and breast cancer resistance protein (BCRP) are 2 major gatekeepers at the blood-brain barrier

191 Mrp2), and breast cancer resistance protein (BCRP) expression in rat and mouse brain capillaries.

192 ly induced breast cancer resistance protein (BCRP) gene transcription.

193 ibition of breast cancer resistance protein (BCRP) has little effect.

194 ransporter breast cancer resistance protein (BCRP) in MTX resistance (Volk et al., Cancer Res., 62: 5

195 Breast cancer resistance protein (BCRP) is a member of ATP-binding cassette (ABC) transpor

196 Breast cancer resistance protein (BCRP) is a newly identified ATP-binding cassette transpo

197 The breast cancer resistance protein (BCRP) is an ATP-binding cassette half transporter that c

198 Breast cancer resistance protein (BCRP) is expressed in various tissues, such as the gut,

199 Breast cancer resistance protein (BCRP) is most abundantly expressed in the apical membran

200 Breast cancer resistance protein (BCRP) plays a significant role in drug disposition and i

201 ression of breast cancer resistance protein (BCRP), a marker of pluripotent hematopoietic, muscle, an

202 in (P-gp), breast cancer resistance protein (BCRP), and multidrug resistance-associated protein 2 (MR

203 xpress the breast cancer resistance protein (BCRP), and resistance to MTX as well as to MX was revers

204 ein (MRP), breast cancer resistance protein (BCRP), and/or Pgp.

205 (P-gp) and breast cancer resistance protein (BCRP), at the blood-brain barrier is a pathological hall

206 termed the breast cancer resistance protein (BCRP), because of its identification in MCF-7 human brea

207 (MRP4) and breast cancer resistance protein (BCRP), located on endothelial cells lining brain vascula

208 ansporters breast cancer resistance protein (BCRP), multidrug-resistance protein 1 (MDR1), and multid

209 particular breast-cancer resistance protein (BCRP), to exit the BBB cells.

210 ffluxed by breast cancer resistance protein (BCRP), we assessed whether IMP3 regulates BCRP.

211 MRP1), and breast cancer resistance protein (BCRP), which may serve as novel broad-spectrum modulator

212 /MDR1) and breast cancer resistance protein (BCRP).

213 (P-gp) and breast cancer resistance protein (BCRP).

214 Breast cancer resistance protein (BCRP)/MXR/ABCG2 is a new member of the family of ATP-dep

215 BCC1), and breast cancer resistance protein (BCRP, ABCG2) are the three major ABC transport proteins

216 The breast cancer resistance protein (BCRP, ABCG2) belongs to the superfamily of ATP binding-c

217 y of human breast cancer resistance protein (BCRP, ABCG2) in the absence of cofactors or heterologous

218 nce of the breast cancer resistance protein (BCRP, ABCG2) was confirmed by TaqMan real-time RT-PCR as

219 on against breast cancer resistance protein (BCRP, ABCG2).

220 ABCB1) and breast cancer resistance protein (BCRP, official gene symbol ABCG2) protect the conceptus

221 ) mediated breast cancer resistance protein (BCRP/ABCG2) and bile salt export pump (BSEP/ABCG11) quan

222 The human breast cancer resistance protein (BCRP/ABCG2) confers multidrug resistance and mediates th

223 ole of the breast cancer resistance protein (BCRP/ABCG2) in drug resistance in multiple myeloma (MM).

224 Breast cancer resistance protein (BCRP/ABCG2) is a molecular determinant of pharmacokineti

225 The Breast Cancer Resistance Protein (BCRP/ABCG2) is one member of ABC transporters proteins s

226 The human breast cancer resistance protein (BCRP/ABCG2) mediates efflux of drugs and organic anions

227 Breast cancer resistance protein (BCRP/ABCG2) plays an important role in determining the a

228 Breast cancer resistance protein (BCRP/ABCG2), an ATP-binding cassette (ABC) membrane-asso

229 icular for breast cancer resistance protein (BCRP/ABCG2), there is a persistent need for studies of i

230 lls by the breast cancer resistance protein (BCRP/ABCG2), yet published studies to date fail to demon

231 MDR-1) and breast cancer resistance protein (BCRP/ABCG2).

232 6), or the breast cancer resistance protein (BCRP/MXR), the (67)Ga-complex was shown to be readily tr

233 The breast cancer resistance protein (BCRP; ABCG2) is an ATP-dependent efflux multidrug transp

234 1) and the breast cancer resistance protein (BCRP; ABCG2) was tested using uptake assays in cells ove

235 nsporters: breast cancer resistance protein (BCRP; ABCG2), multidrug-resistant protein 1/P-glycoprote

236 ibition of breast cancer resistance protein (BCRP; ABCG2).

237 ein ABCG2 (breast cancer resistance protein [BCRP], mitoxantrone resistance [MXR]) is associated with

238 he multidrug resistance-associated proteins, BCRP also transported significant amounts of polyglutamy

239 in the Breakpoint Cluster Region pseudogene (BCRP) block, suggesting the existence of a possible reco

240 ings suggest that wild-type as well as R482T BCRP mediates cellular efflux of 9-AC but not 9-NC.

241 overexpression of either wild-type or R482T BCRP confers resistance to 9-AC, but not to 9-NC.

242 ted with cRNA of wild-type or mutant (R482T) BCRP.

243 Thus, PRA and PRB differentially regulate BCRP expression in BeWo cells.

244 e progesterone A and B receptors to regulate BCRP expression in a placental cell line.

245 e that IMP3 binds to BCRP mRNA and regulates BCRP expression.

246 n (BCRP), we assessed whether IMP3 regulates BCRP.

247 ach by disrupting Pim-1 signaling to reverse BCRP-mediated multidrug resistance.

248 and brain distribution studies with several BCRP probe substrates confirmed the functional activity

249 dition of 10 muM fumitremorgin C, a specific BCRP inhibitor, significantly increased the intracellula

250 nib was completely abolished by the specific BCRP inhibitor fumitremorgin C.

251 m is a valid and effective means of studying BCRP function and substrate specificity.

252 all members of the ABC G (white) subfamily, BCRP is a half transporter.

253 HA-tagged BCRP mutants were expressed in HEK cells and tested for

254 Together, these data demonstrate that BCRP is a MTX and MTX-polyglutamate transporter and reve

255 In summary, we find that BCRP overexpression in the drug-selected cells is accomp

256 These data indicated that BCRP causes the multidrug-resistance phenotype.

257 These studies show that BCRP causes measurable imatinib resistance, but this eff

258 ls to chemotherapeutic drugs suggesting that BCRP phosphorylation induced by Pim-1L was essential for

259 Hydropathy analysis suggests that BCRP consists of a nucleotide-binding domain (residues a

260 o MTX as well as to MX was reversible by the BCRP inhibitor, GF120918.

261 h BCRP expression, and was reversible by the BCRP inhibitors fumitremorgin C and GF120918.

262 ovide evidence herein for a novel ERE in the BCRP promoter.

263 duced reduction of phosphorylated Akt in the BCRP-expressing K562 cells.

264 he sequence of the 5'-flanking region of the BCRP gene and found a putative estrogen response element

265 e suggests that alternative promoters of the BCRP gene exist.

266 activity and transcriptional activity of the BCRP promoter in PRA-transfected cells; however, cotrans

267 E) identified between -243 to -115 bp of the BCRP promoter region significantly attenuated the proges

268 Initial characterization of the BCRP promoter revealed that it is TATA-less with 5 putat

269 ciferase assays, sequential deletions of the BCRP promoter showed that the region between -243 and -1

270 onsistently, transcriptional activity of the BCRP promoter was induced 2- to 6-fold by 10(-8) to 10(-

271 Flavonoid glycosides had no effects on the BCRP-mediated transport of mitoxantrone.

272 cytotoxicity and the ability to reverse the BCRP-mediated SN-38 resistance.

273 revealed specific binding of ERalpha to the BCRP promoter through the identified ERE.

274 Specific binding of both PRA and PRB to the BCRP promoter through the identified PRE was confirmed u

275 lex nature of substrate interaction with the BCRP homodimer.

276 recombination breakpoint near or within the BCRP block, providing a starting point for future breakp

277 were most likely located near or within the BCRP module.

278 an cancer cells (MCF-7 and Igrov1) and their BCRP-overexpressing, drug-selected, multidrug-resistant

279 Thereby BCRP acts as an efflux pump, mediating the elimination o

280 Therefore, BCRP expression isolates prostate stem/tumor stem cells

281 data obtained demonstrate that IMP3 binds to BCRP mRNA and regulates BCRP expression.

282 uction in drug accumulation was sensitive to BCRP inhibition by GF120918.

283 e most potent compounds are selective toward BCRP and 2-fold more potent than the reference Ko143.

284 P1, ABCC1) to confirm the selectivity toward BCRP.

285 ith Pim-1L, and we found the ABC transporter BCRP/ABCG2 as one of the potential interacting partners

286 forms complexes with multidrug transporters, BCRP (ABCG2) and P-glycoprotein (ABCB1), in the plasma m

287 iety of efflux proteins, including wild-type BCRP and a mutant BCRP that contains a threonine rather

288 ls at levels comparable to that of wild-type BCRP and predominantly localized on the plasma membrane

289 Wild-type BCRP appeared to have low affinity, but high capacity, f

290 expressed at levels comparable to wild-type BCRP as revealed by immunoblotting with specific antibod

291 3, and flavopiridol (FLV), whereas wild-type BCRP transported only MX and FLV, in agreement with obse

292 onformation-sensitive antibody, to wild-type BCRP, P392A, or P485A in a concentration-dependent manne

293 P392A or P485A compared to that of wild-type BCRP.

294 est that cells can, upon hypoxic demand, use BCRP to reduce heme or porphyrin accumulation, which can

295 nvestigated the molecular mechanism by which BCRP expression in human placental choriocarcinoma BeWo

296 MTX resistance correlated with BCRP expression in all of the cell lines expressing the

297 to this antifolate directly correlated with BCRP expression, and was reversible by the BCRP inhibito

298 f the CPT A ring facilitate interaction with BCRP and have implications for the clinical development

299 en reported; however, their interaction with BCRP is unknown.

300 Pim-1L was co-localized with BCRP on the plasma membrane and induced phosphorylation