ライフサイエンスコーパス: MDR1

1 MDR1 methylation frequency was significantly higher in p

2 MDR1 polymorphisms are associated with both CD and UC wi

3 MDR1 promoter activity was higher in HSF-1(-/-) cardiomy

4 MDR1/ABCB1 is an interesting candidate gene for IBD.

5 MDR1/Pgp was found in 2 (12%) of 16 retinoblastomas.

6 e expression of multidrug resistance gene 1 (MDR1) protein, resulting in increased efflux and decreas

7 found that the multidrug resistance gene 1 (MDR1) transporter was responsible for the efflux of Hoec

8 owing prolonged chemotherapy, MDR protein 1 (MDR1) and CD133 increase in recurrent glioblastomas.

9 taxin-6, and multidrug resistance protein 1 (MDR1) in brain endothelial cells.

10 of IL-10 and multidrug-resistant protein 1 (MDR1) in infected macrophages (Ms) has been investigated

11 overy of the multidrug resistance protein 1 (MDR1), an ATP-binding cassette (ABC) transporter able to

12 tein (BCRP), multidrug-resistance protein 1 (MDR1), and multidrug-resistance-associated protein (MRP)

13 er proteins multi-drug resistance protein-1 (MDR1, ABCB1, P-glycoprotein) and (BCRP, ABCG2), and that

14 *6) and 2E1 (cl/c2), multidrug resistance 1 (MDR1 C3435T) P-glycoprotein, and pregnane X receptor (PX

15 he downregulation of multidrug resistance 1 (MDR1) expression and retention of drugs in cells caused

16 Multidrug resistance 1 (MDR1) gene encodes for P-glycoprotein (P-gp), a Mr 170,0

17 The multidrug resistance 1 (MDR1) gene product P-glycoprotein (P-gp) is frequently i

18 ynonymous SNP in the Multidrug Resistance 1 (MDR1) gene, part of a haplotype previously linked to alt

19 450 3A4 (CYP3A4) and multidrug resistance 1 (MDR1).

20 pression of GPX1 and multidrug resistance 1 (MDR1; ABCB1) without early treatment failures and with s

21 e product of the multidrug resistant type 1 (MDR1) gene, P-glycoprotein (Pgp), resulting in improved

22 Multidrug resistance type 1 (MDR1) protein is a member of the adenosine triphosphate

23 protein (P-gp)/multi-drug resistance type 1 (MDR1).

24 h as Cyclin D1, c-Myc, COX-2, MMP-9, ICAM-1, MDR1, Survivin, XIAP, IAP1, IAP2, FLIP, Bcl-2, Bcl-xL, a

25 ularly in many medical specialties, and ABCB/MDR1 variation appears to be a critical pharmacogenetic

26 alternative MX transporters ABCG2 and ABCB1 (MDR1, P-glycoprotein)-can significantly influence tumor

27 s) across five genes: CYP3A4, CYP3A5, ABCB1 (MDR1; encoding P-glycoprotein), NR1I2 (encoding the preg

28 c pathways that control the origin of ABCB1 (MDR1) gene activation with acquired multidrug resistance

29 ein (P-gp) 170 that is encoded by the ABCB1 (MDR1) gene.

30 In particular, ABCB1 [MDR1/P-glycoprotein (P-gp)] extrudes many types of drugs

31 ine mutation of human P-glycoprotein (ABCB1, MDR1) has been previously isolated from high colchicine

32 ole for the multidrug resistance gene (ABCB1/MDR1) and its product, P-glycoprotein 170, in the pathog

33 synthesis and drug efflux activity of ABCB1/MDR1 p-gp in murine and human CD11b(+)-myeloid cells, th

34 istration of a TLR2 ligand, preserving ABCB1/MDR1 p-gp expression.

35 dentity of germ-line variations in the ABCB1/MDR1 gene contributing to IBD susceptibility.

36 nce to support the contribution of the ABCB1/MDR1 gene in determining risk to UC but not to CD and pr

37 nting the haplotypic variations of the ABCB1/MDR1 gene were identified initially following the charac

38 defense via the multidrug transporter ABCB1/MDR1 p-gp.

39 we demonstrate that ABC transporters (ABCB1/MDR1 and ABCC2/MRP2, respectively) show dramatic overexp

40 multidrug resistant gene expression (ABCG2, MDR1).

41 timulates Stat-3 transcriptional activation, MDR1 overexpression, and multidrug resistance.

42 document that although AEG-1 does not affect MDR1 gene transcription, it facilitates association of M

43 sitive feedback loop that strongly amplifies MDR1 expression and regulates drug resistance in these c

44 directly or NF-kappaB-dependently induce an MDR1/P-gp phenotype in MCF-7 cells.

45 down-regulation of BMI-1, ABCG2, ABCG5, and MDR1 expression and in a concomitant increase in E-cadhe

46 on and increased levels of ABCG2, ABCG5, and MDR1.

47 A systematic increase in both APE1 and MDR1 expression was observed in non-small-cell lung canc

48 t gefitinib inhibited the efflux of BCRP and MDR1 substrates and restored vincristine sensitivity in

49 4-AQ molecules with agents that are BCRP and MDR1 substrates.

50 rane vesicles and co-localized with BSEP and MDR1 in the apical membrane of Madin-Darby canine kidney

51 ced miR-137 expression and increased CAR and MDR1 expression in doxorubicin-resistant neuroblastoma c

52 reduced caveolae, and impaired caveolae- and MDR1-related functions including endocytosis, drug efflu

53 isms in CYP2B6, CYP2C19, CYP3A4, CYP3A5, and MDR1 were characterized.

54 Pharmacophores for cytotoxicity and MDR1 selectivity were generated to delineate the structu

55 ulators verapamil and trans-flupenthixol and MDR1-targeted siRNA increased sensitivity of multidrug-r

56 inhibitors of apoptosis proteins (IAPs) and MDR1 (multidrug-resistant protein), resulting in anti-ap

57 of PI3K or Akt, decreased Akt, NF-kappaB and MDR1 expression.

58 Both the MGC4175 and MDR1 genes are located at chromosome position 7q21.

59 CD133, DNA-PK and MDR1 were markedly elevated in these cells.

60 , DNA-dependent protein kinase (DNA-PK), and MDR1 are elevated in CD133+ GCSCs, the relationship amon

61 G islands at GSTP1, APC, RASSF1a, PTGS2, and MDR1 were hypermethylated in >85% of prostate cancers an

62 c polymorphisms of CYP 2D6 and 2E1, PXR, and MDR1 do not appear to play a role in the onset of PBC.

63 e UC in patients carrying the TLR2-R753Q and MDR1-C3435T polymorphisms was associated with increased

64 rain barrier, chemotherapeutic regimens, and MDR1 gene therapy protocols in vivo.

65 A reverse correlation between WTH3 and MDR1 gene expression was also observed in MCF7/AdrR, and

66 The anti-MDR1 HNA gapmer was substantially more potent than a pho

67 Treatment with anti-MDR1 HNA gapmer resulted in increased cellular accumulat

68 9 of Arabidopsis thaliana (formerly known as MDR1 and PGP19) belongs to the Multidrug Resistance-like

69 DR transporters include ABCB1 (also known as MDR1 or P-glycoprotein) and ABCC1 (also known as MRP1) w

70 n of drug efflux pumps, ABCB1 (also known as MDR1 or P-gp) and ABCC1 (also known as MRP1), whose inhi

71 lycoprotein (encoded by ABCB1, also known as MDR1).

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

73 We examined the relationship between MDR1/ABCB1 polymorphisms and endomyocardial biopsy-prove

74 tly, there is a significant decrease in both MDR1 and Bcl-x(L) gene expression and an enhancement in

75 BSEP, MDR1, and MDR2 ATP binding cassette transporters are tar

76 chain, MLC2, as a binding partner for BSEP, MDR1, and MDR2.

77 ntified HAX-1 as a binding partner for BSEP, MDR1, and MDR2.

78 HAX-1 was bound to BSEP, MDR1, and MDR2 in canalicular membrane vesicles and co-l

79 ls to chemotherapeutics that are effluxed by MDR1.

80 function of P-glycoprotein (P-gp) encoded by MDR1 can be influenced by genetic polymorphisms, includi

81 rate for P-glycoprotein, which is encoded by MDR1.

82 conclusion that auxin levels established by MDR1-dependent acropetal transport control lateral root

83 T ((68)Ga) radiopharmaceutical recognized by MDR1 Pgp.

84 a cytotoxic metabolite that was retained by MDR1-expressing cells better than a metabolite of simila

85 ated with their recognition as substrates by MDR1.

86 mplex was shown to be readily transported by MDR1 Pgp and, to a much lesser extent, by MRP1, but not

87 In contrast to MDR1(-) Th1 or Th17 cells, MDR1(+) Th17 cells produce both Th17 (IL-17A, IL-17F, an

88 massive mobilization and homing of ckit(+), MDR1(+), CD31(+), and CD34(+) cells into the infarcted h

89 Compound 1 demonstrated MDR1-selectivity against all P-gp-expressing cell lines

90 of ileal Crohn's disease patients displayed MDR1 loss of function.

91 nscription factor important for IL-10-driven MDR1 up-regulation is c-Fos/c-Jun and not NF-kappaB, as

92 in intact cells, disulfiram reverses either MDR1- or MRP1-mediated efflux of fluorescent drug substr

93 on of the endogenous, chromosomally embedded MDR1 gene.

94 transcription of the P-glycoprotein-encoding MDR1 gene via direct DNA binding through a novel p53 DNA

95 nto MDR cell lines, which reduced endogenous MDR1 expression.

96 ) and the coactivator p300 on the endogenous MDR1 promoter.

97 The enhanced MDR1 level due to the ectopic expression of wild-type AP

98 were markedly more effective in eradicating MDR1-expressing human xenograft tumors than SMCC-linked

99 elocytic leukemia (APL) cells do not express MDR1 and are highly sensitive to anthracyclines.

100 In vitro, cells highly expressing MDR1 had significantly decreased (64)Cu-ATSM and -PTSM r

101 Using a variety of cells stably expressing MDR1 Pgp, multidrug resistance-associated proteins (MRP1

102 ly that an IL-10 surge is a prerequisite for MDR1 up-regulation.

103 y, indicating that the Y box is required for MDR1 activation by C/EBPbeta.

104 ansferase specific for H3K4, is required for MDR1 promoter methylation, as knockdown of MLL1 resulted

105 1 promoter, similar to what we had shown for MDR1 promoter acetylation, and also requires NF-Y.

106 the 5-ethyl substituent, are substrates for MDR1.

107 Furthermore, MDR1(+) Th17 cells are refractory to several glucocortic

108 the expression of multidrug resistance gene MDR1, thereby causing drug resistance.

109 activation of the multidrug resistance gene MDR1.

110 the product of the multidrug resistance gene MDR1.

111 The multidrug resistance 1 gene (MDR1) encodes P-glycoprotein (Pgp), a member of the ATP-

112 own to induce the multidrug resistance gene (MDR1) and ATP binding cassette (ABC)-based drug efflux i

113 Variants of the multidrug resistance gene (MDR1/ABCB1) have been associated with increased suscepti

114 g the multidrug resistance transporter gene (MDR1) as a model and showing that chimeric RNA construct

115 Methylation analysis in four genes (MDR1, IL8, RARB, TGFBR2) previously linked to HNSCC or i

116 absorption by the efflux pump P-glycoprotein MDR1 (multidrug resistant-1), encoded by the ABCB1 gene.

117 inding, the investigation of P-glycoprotein (MDR1, ATP binding cassette [ABC]B1) has proceeded with g

118 ssing the efflux transporter P-glycoprotein (MDR1, P-gp, ABCB1).

119 ultidrug-resistant protein 1/P-glycoprotein (MDR1/Pgp; ABCB1), multidrug-resistant-associated protein

120 ne transporters such as ABCB1/P-glycoprotein/MDR1 and ABCC1/MRP1 causes multidrug resistance in cance

121 P-glycoprotein (P-gp, MDR1) is a promiscuous drug efflux pump of substantial p

122 ill cells that express P-glycoprotein (P-gp, MDR1), the ATPase efflux pump that confers multidrug res

123 g cassette transporters P-glycoprotein (P-gp/MDR1) and breast cancer resistance protein (BCRP).

124 x transporters such as P-glycoprotein (P-gp; MDR1, ABCB1), significantly less is known regarding its

125 l position of 1 yielded compounds of greater MDR1-selectivity.

126 This analysis showed that GSTP1, MDR1 and PTGS2 CGI hypermethylation as determined by COM

127 patients are 11.5 times more likely to have MDR1 methylation than BPH patients (95% confidence inter

128 High MDR1-expressing tumors showed lower tracer activity on P

129 erazine-mediated bioluminescence in a highly MDR1 Pgp-modulated manner.

130 and colorectal cancer because certain human MDR1 polymorphisms have been linked to ulcerative coliti

131 Three-dimensional modeling of human MDR1/P-gp indicates that these glycoproteins function as

132 ymphoma cell line transfected with the human MDR1 gene.

133 y canine kidney cells transfected with human MDR1 gene (MDCK/MDR1), followed by pharmacokinetics stud

134 emical protection of the Dm brain with human MDR1/Pgp.

135 psilon-Nanog signaling inhibition causes IAP/MDR1 down-regulation, apoptosis, and chemosensitivity.

136 that the loss of APE1's acetylation impaired MDR1 activation and sensitizes the cells to cisplatin or

137 A number demonstrated improved MDR1-selective activity over the lead, NSC73306 (1).

138 Using a rhodamine123 uptake assay in MDR1-MDCKII cells, we were able to identify structural m

139 block GCS also showed a dramatic decrease in MDR1 expression.

140 knockdown of MLL1 resulted in a decrease in MDR1 expression.

141 -PTSM retention and decreased the efflux in MDR1-positive cells.

142 further investigated histone methylation in MDR1 regulation and function.

143 tein (Pgp) expression, parallel reduction in MDR1 message levels, increased accumulation of the Pgp s

144 tion of C/EBPbeta plays an important role in MDR1 gene regulation.

145 ates and restored vincristine sensitivity in MDR1-expressing cells.

146 s to be also present in exporters, including MDR1.

147 CD133 and DNA-PK may increase MDR1 via the phosphatidylinositol-3-kinase (PI3K)-Akt si

148 e putative AP-1 box (-123 to -111) increased MDR1 promoter activity when stimulated by C/EBPbeta, sug

149 LL fusion protein, MLL-AF4, led to increased MDR1 expression.

150 (IBTs), to identify compounds with increased MDR1-selectivity.

151 hanced recruitment of this complex increases MDR1 promoter-dependent luciferase activity and its endo

152 tion are activated by ATRA and HDACI, induce MDR1 in APL cells, and point to the critical importance

153 In addition, ARNT-induced MDR1 expression was inhibited in Sp1-knockdown cells.

154 Both agents, ATRA or FK228, induced MDR1 mRNA.

155 ctivity together with mutant p53 and induces MDR1 gene and P-glycoprotein (P-gp, ABCB1), resulting in

156 on-dependent regulatory function in inducing MDR1-mediated drug resistance.

157 , reversed the drug resistance by inhibiting MDR1/P-gp expression in MCF-7/adr cells, and induced cel

158 rdiomyocytes, suggesting that HSF-1 inhibits MDR1 activity in the heart.

159 inked conjugates were more potent in killing MDR1-expressing cells in culture.

160 lls; after 7 days with PPMP (10 micromol/L), MDR1 expression fell by 84% and P-glycoprotein protein l

161 Mutations in Multidrug Resistance-Like1 (MDR1) reduced acropetal auxin transport in roots by 80%

162 H (expresses common haplotype P-gp), and LLC-MDR1-3HA (a mutant that carries a different valine codon

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

164 NA copy number were developed and termed LLC-MDR1-WT (expresses wild-type P-gp), LLC-MDR1-3H (express

165 ition, cytotoxicity assays show that the LLC-MDR1-3H cells are more resistant to mitoxantrone than th

166 more resistant to mitoxantrone than the LLC-MDR1-WT cells after being treated with a P-gp inhibitor.

167 vo, we used a model system composed of a low MDR1-expressing parent uterine sarcoma cell line and a d

168 inhibitor, exhibited higher WTH3, but lower MDR1, expression.

169 P-gp as it is not transported across an MDCK-MDR1 monolayer.

170 ed uptake of calcein-AM into CR1R12 and MDCK-MDR1 cells and are actively transported by Pgp in monola

171 ely transported by Pgp in monolayers of MDCK-MDR1 cells at similarly low concentrations ( approximate

172 cells transfected with human MDR1 gene (MDCK/MDR1), followed by pharmacokinetics studies in rats.

173 In MDCKII-MDR1 cells, the tertiary thioamide-containing derivative

174 IC(50)'s of approximately 2 microM in MDCKII-MDR1 cells.

175 s, and for transport in monolayers of MDCKII-MDR1 cells.

176 tidrug-resistant, P-gp-overexpressing MDCKII-MDR1 cells, and for their colocalization with mitochondr

177 nd vinblastine in multidrug-resistant MDCKII-MDR1 cells, and for transport in monolayers of MDCKII-MD

178 rins are potent inhibitors of OATP1B1, MRP2, MDR1, and other important drug transporters.

179 HSF-1(-/-) cardiomyocytes, whereas a mutant MDR1 promoter with heat-shock element (HSE) mutation sho

180 xpression of progrowth genes, such as c-MYC, MDR1, and NF-kappaB2.

181 ging of the functional transport activity of MDR1 Pgp with ((67/68)Ga-[3-ethoxy-ENBDMPI])(+) may enab

182 This was a case-control analysis of MDR1 C3435T and G2677T SNPs in a large well-characterize

183 transcription, it facilitates association of MDR1 mRNA to polysomes, resulting in increased translati

184 earch were to investigate the association of MDR1 polymorphisms, C3435T and G2677T, and IBD.

185 posure, drug resistance, the coexpression of MDR1 and the mitochondrial localization of its protein,

186 Significant correlation of MDR1 methylation was observed with high pT category (P <

187 ubsequent proteasome-mediated degradation of MDR1 protein.

188 uptake 3-fold, and diminished expression of MDR1 by 58%, compared with untreated controls.

189 The expression of MDR1 glycoprotein (or its equivalents in mice) affects t

190 ycytidine treatment, increased expression of MDR1 mRNA transcript was found in prostate cancer cell l

191 racted with Sp1 to enhance the expression of MDR1 through Sp1-binding sites on the MDR1 promoter, res

192 CS activity down-regulates the expression of MDR1, a phenomenon that may drive the chemosensitization

193 the MDR1 gene and promoted the expression of MDR1.

194 cause of the increased nuclear expression of MDR1/P-glycoprotein (P-gp).

195 criptional activation, and the impairment of MDR1 and Bcl-x(L) gene expression.

196 RNA interference of MDR1 inhibited the rate of cell migration.

197 BCRP, ABCG2), and that targeted knockdown of MDR1 and BCRP expression by small interfering RNA partia

198 Knockdown of MDR1 expression significantly enhanced the (64)Cu-ATSM a

199 experiments were repeated after knockdown of MDR1 protein expression using MDR1-specific small interf

200 We investigated the mechanisms of MDR1 gene activation by CCAAT/enhancer binding protein b

201 ter cell line selected for overexpression of MDR1.

202 lineation of the adverse prognostic power of MDR1 in adult acute myeloid leukemia (AML) raised hopes

203 o synonymous changes in the coding region of MDR1.

204 The regulation of MDR1 by MLL1 has functional consequences in that downreg

205 Regulation of MDR1 by MLL1 was dependent on the CCAAT box within the p

206 To study the role of MDR1 expression on the accumulation of (64)Cu-diacetyl-b

207 Suppression of MDR1 by small interfering RNA or chemical reagents, or i

208 Our data suggest that upregulation of MDR1 by DeltaNp73alpha is mediated by interaction with p

209 rties of cancer cells by the upregulation of MDR1, highlighting ARNT's potential as a therapeutic tar

210 Here we sought to extend this work on MDR1-selective analogues by establishing whether 1 showe

211 cells, whereas depletion of JNK2, c-Jun, or MDR1 in CDDP-resistant cancer cells promoted apoptosis u

212 As KB/V-1 cells overexpress MDR1 and KBH5.0 cells overexpress BCRP, decreased cytoto

213 and their subcell line transfected with pHa MDR1/A retrovirus overexpressing the human ABCB1 efflux

214 (Rho), through the multidrug efflux protein MDR1 (also known as P-glycoprotein and ABCB1).

215 reatment of cells expressing the MDR protein MDR1 (ABCB1B) showed no cross-resistance to hSGZ.

216 -glycoprotein [multidrug resistance protein (MDR1); ABCB1], the in vivo effect on this and other tran

217 is of a functional green fluorescent protein-MDR1 translational fusion showed the protein to be auxin

218 the expression of drug transporter proteins MDR1, MRP1, and ABCG2.

219 pendent on the CCAAT box within the proximal MDR1 promoter, similar to what we had shown for MDR1 pro

220 with overexpression of the drug efflux pump MDR1.

221 e STS to chemotherapeutic agents by reducing MDR1 phosphorylation via transcriptional repression of P

222 ults indicate that CD133 and DNA-PK regulate MDR1 through the PI3K- or Akt-NF-kappaB signal pathway.

223 th recombinant IL-10 and Sb(R)LD up-regulate MDR1 in M with different time kinetics, where phosphoryl

224 ting that the AP-1 site negatively regulates MDR1 activation by C/EBPbeta.

225 hat p63 and p73 activate rather than repress MDR1 transcription, and they do so through an upstream p

226 unds transported by the multidrug resistance MDR1 P-glycoprotein (Pgp).

227 activity levels of the multidrug-resistance MDR1/ABCB1 encoded P- glycoprotein (P-gp) have an impact

228 ession of genes involved in drug resistance (MDR1) and stem cell markers (CD133, CD34, KIT).

229 Overexpression of multidrug resistance (MDR1) P-glycoprotein (Pgp) remains an important barrier

230 APE1 downregulation sensitizes MDR1-overexpressing tumor cells to cisplatin or doxorubi

231 ived from IL-10(-/-) mice are unable to show MDR1 up-regulation on infection with Sb(R)LD.

232 Several cell lines with similar MDR1 DNA copy number were developed and termed LLC-MDR1-

233 t to inhibit WTH3 and consequently stimulate MDR1 expression.

234 2 to -73) abolished the C/EBPbeta-stimulated MDR1 promoter activity, indicating that the Y box is req

235 6G>T, 983T>C), UGT2B7 (IVS1+985A>G, 802C>T), MDR1 3435C>T, chemokine (C-C motif) receptor 2 (CCR2) 19

236 sed on the alternative strategy of targeting MDR1 promoter activation to knockdown P-gp expression in

237 gefitinib inhibited BCRP more potently than MDR1 (10-fold), the inhibition of both transporters occu

238 (95% confidence interval 4.87-27.0) and that MDR1 methylation is independent of the age.

239 Additionally, we report that MDR1 methylation correlates with regional nodal metastas

240 It has also been shown that MDR1 activation is accompanied by increased methylation

241 We had previously shown that MDR1 transcription is regulated by epigenetic events suc

242 The MDR1 3435 TT genotype (34.6% vs 26.5%; P = .04; odds rat

243 The MDR1 exonic single nucleotide polymorphisms (SNPs) C3435

244 The MDR1 gene encodes P-glycoprotein 170, an efflux transpor

245 The MDR1-selective pharmacophore highlights the importance o

246 Liver expression of Abcb1a and Abcb1b, the MDR1 proteins in mouse liver, was determined by real-tim

247 we also demonstrated that RHA activated the MDR1 promoter in the MDR variant cells but not in the dr

248 e show that DNA-PKcs resides with RHA at the MDR1 promoter in a multiprotein complex.

249 a is mediated by interaction with p53 at the MDR1 promoter.

250 NA-anchoring functions, respectively, at the MDR1 promoter.

251 enomenon of drug resistance, mediated by the MDR1/ABCB1 gene and seen in tumor cells to chemotherapeu

252 -glycoprotein and its human counterpart, the MDR1 P-glycoprotein, ABCB1.

253 For patients receiving platinum drugs, the MDR1 C3435T variant allele was associated with significa

254 nscription complex containing C/EBPbeta, the MDR1 promoter sequences (-250 to +54), and the hBrm prot

255 To evade the MDR1-mediated resistance, we conjugated the highly cytot

256 s a substrate for ABCG2/BCRP but not for the MDR1 P-glycoprotein (ABCB1/Pgp), multidrug resistance pr

257 n reducing expression of P-glycoprotein, the MDR1 gene product.

258 ymous single-nucleotide polymorphisms in the MDR1 (multidrug resistance 1 or ABCB1) gene involving fr

259 showed excellent membrane permeation in the MDR1-MDCKII model and encouraging oral pharmacokinetic p

260 ative and alternate states may be minor, the MDR1 case illustrates that the barriers may nevertheless

261 ese changes then cause the expression of the MDR1 (P-glycoprotein/P-gp) gene and the anti-apoptotic g

262 RscA is a member of the MDR1 family of ABC transporters, and we found that it is

263 d c-Jun bound to the promoter regions of the MDR1 gene and promoted the expression of MDR1.

264 petal auxin transport due to mutation of the MDR1 gene caused 21% of nascent lateral roots to arrest

265 Allelic variations of the MDR1 gene determine disease extent as well as susceptibi

266 er frequently involves overexpression of the MDR1 gene product P-glycoprotein (P-gp), a drug transpor

267 previously linked to altered function of the MDR1 gene product P-glycoprotein (P-gp), nonetheless res

268 biquitination regulates the stability of the MDR1 gene product, P-glycoprotein, thereby affecting the

269 We hypothesize that inactivation of the MDR1 gene through CpG methylation contributes to the pat

270 is hypothesis, CpG methylation status of the MDR1 promoter and its correlation with clinicopathologic

271 increased H4 and H3-Lys9 acetylation of the MDR1 promoter and recruitment of the nuclear transcripti

272 C3435T and G2677 polymorphisms of the MDR1/ABCB1 gene correlate with cellular expression level

273 ion of MDR1 through Sp1-binding sites on the MDR1 promoter, resulting in a reversal of the effect of

274 lated APE1 (AcAPE1)-YB-1-p300 complex on the MDR1 promoter.

275 e against MM cell lines that overexpress the MDR1/P-glycoprotein multidrug efflux pump.

276 Among efavirenz recipients, the MDR1 position 3435 TT genotype was associated with decre

277 eport that ANA-modified siRNAs targeting the MDR1 gene can exhibit improved efficacy as compared to u

278 designed transcription factors targeting the MDR1 promoter.

279 on experiment, miR-298 directly bound to the MDR1 3' untranslated region and regulated the expression

280 factor (NF)-kappaB, which interacts with the MDR1 promoter, were also elevated in these cells.

281 Of these, MDR1 promoter methylation associates with specific micro

282 Thus, MDR1(+) Th17 cells may be important mediators of chronic

283 nd we believe that this may be attributed to MDR1/ABCB1 encoded P-gp mediating the efflux of immunosu

284 ankyrin (a cytoskeletal protein) binding to MDR1 resulting in the efflux of chemotherapeutic drugs (

285 In contrast to MDR1(-) Th1 or Th17 cells, MDR1(+) Th17 cells produce bo

286 d control oligonucleotides were delivered to MDR1-expressing cells using transfection with the cation

287 , suggesting that cytotoxicity was linked to MDR1 function, not to other, nonspecific factors arising

288 d indirectly acts to eliminate resistance to MDR1 substrates.

289 protein, we propose to name this transcript MDR1 and Mitochondrial Taxol Resistance Associated Gene

290 are substrates for the multidrug transporter MDR1.

291 tional activation and multidrug transporter, MDR1 (P-glycoprotein) gene expression.

292 ate expression of the multidrug transporter, MDR1 (P-glycoprotein), in an interdependent, but Akt-ind

293 nes that overexpress the efflux transporters MDR1 (KBV-1) and BCRP (KBH5.0).

294 We found that DeltaNp73alpha upregulates MDR1 mRNA and p-glycoprotein (p-gp), which is involved i

295 r knockdown of MDR1 protein expression using MDR1-specific small interfering RNAs.

296 In vivo, MDR1(+) Th17 cells are enriched and activated in the gut

297 50/c-Rel leading to IL-10 induction, whereas MDR1 up-regulation is mediated by PI3K/Akt and the JNK p

298 Treatment of drug resistant cells with MDR1-targeted siRNAs resulted in reduction of P-glycopro

299 OATP1A2, either alone or in combination with MDR1, significantly transported doxorubicin.

300 ve approaches for predicting structures with MDR1-selective activity and aid in directing the search