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 a xenobiotic transporter that appears to play a

6 BCRP is also expressed in the apical membrane of mammary

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

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

9 BCRP mRNA expression varied more than 1000-fold among th

10 BCRP specifically binds heme, and cells lacking BCRP acc

11 BCRP substrates include numerous drugs (topotecan, nitro

12 BCRP-overexpressing and BCRP-negative human breast cance

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

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

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

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

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

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

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

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

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

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

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

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

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

26 throughput methods for identifying new ABCG2/BCRP inhibitors.

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

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

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

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

31 17beta-estradiol and progesterone can affect BCRP expression in cancer cells.

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

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

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

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

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

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

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

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

40 MX resistance, including P-glycoprotein and BCRP/MXR (ABCG2), are not expressed in MCF7/VP cells, we

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

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

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

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

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

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

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

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

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

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

51 cells, indicating that these flavonoids are BCRP inhibitors.

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

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

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

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

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

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

58 t completely reverses resistance mediated by BCRP in vitro and is a pharmacological probe for the exp

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

74 umulation was diminished in cells expressing BCRP, suggesting that CI1033 is a substrate for this eff

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

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

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

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

79 the transmembrane helices are essential for BCRP function.

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

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

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

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

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

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

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

87 current evidence suggesting that functional BCRP is a homodimer.

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

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

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

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

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

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

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

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

96 In BCRP promoter-luciferase assays, sequential deletions of

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

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

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

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

101 AhR overexpression further increased BCRP mRNA and protein expression.

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

103 reated with clofibrate, suggesting increased BCRP efflux activity.

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

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

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

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

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

109 hydroisoquinoline moiety selectively inhibit BCRP.

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

111 vestigate clinically relevant DDIs involving BCRP.

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

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

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

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

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

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

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

119 Enforced expression of the full-length BCRP cDNA in MCF-7 breast cancer cells confers resistanc

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

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

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

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

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

125 hat amino acid 482 has a crucial role in MXR/BCRP/ABCP function and that mutation of a single amino a

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

127 When the MXR/BCRP/ABCP gene was sequenced in the cell lines studied,

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

129 equencing genomic DNA revealed wild-type MXR/BCRP/ABCP to have an arginine at position 482.

130 es suggest that, compared with wild-type MXR/BCRP/ABCP, cells having an R482T mutation have higher an

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

132 opening the door to clinical applications of BCRP inhibition.

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

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

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

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

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

138 High expression of BCRP did not correlate strongly with high expression of

139 Transfection and enforced expression of BCRP in drug-sensitive cells confer resistance to mitoxa

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

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

142 High expression of BCRP mRNA is sufficiently frequent in AML to warrant mor

143 lymphocytic leukemia) for the expression of BCRP mRNA using a quantitative reverse-transcription pol

144 ples (33%) had relatively high expression of BCRP mRNA.

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

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

147 ed in vesicles containing the mutant form of BCRP.

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

149 Inhibition of BCRP-mediated efflux of dihydrotestosterone by novobioci

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

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

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

153 for understanding the transport mechanism of BCRP.

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

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

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

157 hat tissue-specific alternative promoters of BCRP exist.

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

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

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

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

162 nsport activity and substrate selectivity of BCRP, respectively.

163 ntial for the broad substrate specificity of BCRP.

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

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

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

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

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

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

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

171 ificantly lower expression for either Pgp or BCRP.

172 called breast cancer resistance protein, or BCRP).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

189 Breast cancer resistance protein (BCRP) is a novel member of the adenosine triphosphate-bi

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

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

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

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

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

195 xpress the breast cancer resistance protein (BCRP), a recently cloned ATP binding cassette transporte

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

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

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

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

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

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

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

203 orter, the breast cancer resistance protein (BCRP), was recently found to be overexpressed in a mitox

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

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

206 d with the breast cancer resistance protein (BCRP)-the ABC transporter known to be highly overexpress

207 ently, the breast cancer resistance protein (BCRP).

208 at we term breast cancer resistance protein (BCRP).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

254 xpression of P-glycoprotein, suggesting that BCRP may cause resistance to certain antileukemic drugs

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

272 t of FTC on MCF-7 cells transfected with the BCRP gene.

273 lex nature of substrate interaction with the BCRP homodimer.

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

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

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

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

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

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

280 of disease subtype and treatment outcome to BCRP expression and function.

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

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

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

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

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

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

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

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

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

290 3, and flavopiridol (FLV), whereas wild-type BCRP transported only MX and FLV, in agreement with obse

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

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

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

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

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

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

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

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

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

300 y of SN-38 and TPT in cells transfected with BCRP but not empty vector.