ライフサイエンスコーパス: MDR1

1 MDR1 acted early after naive CD8+ T cell activation to s

2 MDR1 inhibition in a fusion positive ovarian cancer cell

3 MDR1 polymorphisms are associated with both CD and UC wi

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

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

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

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

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

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

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

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

12 ith ApoE and multidrug resistance protein 1 (MDR1) membrane transporter up-regulation in both the mou

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

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

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

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

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

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

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

20 450 3A4 (CYP3A4) and multidrug resistance 1 (MDR1).

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

22 Multidrug resistance-1 (MDR1) acts as a chemotherapeutic drug efflux pump in tum

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 have moderate to low efflux ratio (ER) in an MDR1-MDCK assay (19, ER = 5.2; 26, ER = 1.5).

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

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

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

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

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

50 4-AQ molecules with agents that are BCRP and MDR1 substrates.

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

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

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

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

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

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 d expression of ALDH1 in lung metastasis and MDR1/LDH-A expression in liver metastasis compared to hu

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

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

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

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 rrently approved PARP inhibitors (PARPi) are MDR1 substrates, prior chemotherapy may precondition res

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 on of Candida azole resistance genes such as MDR1, regulates other genes that are poorly characterize

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

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

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

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

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

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

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

80 ls to chemotherapeutics that are effluxed by MDR1.

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

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

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

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

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

86 ated with their recognition as substrates by MDR1.

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

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

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

90 lele (Abcb1aAME), we found that constitutive MDR1 expression among hematopoietic cells was observed i

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

92 Using a recently developed MDR1-knockin reporter allele (Abcb1aAME), we found that

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

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

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

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

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

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

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

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

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

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

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

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

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

106 1 promoter, similar to what we had shown for MDR1 promoter acetylation, and also requires NF-Y.

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

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

109 ponsible for enhanced drug resistance (e.g., MDR1).

110 role of macrophage multidrug resistance gene MDR1 on intracellular M. tuberculosis survival during an

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

112 activation of the multidrug resistance gene MDR1.

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

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

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

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

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

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

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

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

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

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

123 ABCB1 (P-glycoprotein/MDR1) is a multidrug efflux transporter that has previou

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

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

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

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

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

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

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

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

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 knockdown of MLL1 resulted in a decrease in MDR1 expression.

140 block GCS also showed a dramatic 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 ates and restored vincristine sensitivity in MDR1-expressing cells.

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

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

147 nic Mycobacterium smegmatis did not increase MDR1 expression, indicating active secretion of virulenc

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

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

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

151 se endogenous and host-derived MG can induce MDR1 and other Mrr1-regulated genes causing increased dr

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 hat ongoing efforts to intentionally inhibit MDR1 in cancer patients could be counterproductive.

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

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

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

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

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

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

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

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

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

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

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

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

170 ction increases the expression of macrophage MDR1 to extrude various chemical substances, including t

171 ed with multi-drug resistant protein 1 (MDCK-MDR1), and human U251 GBM cells.

172 wed improved permeability of DOX across MDCK-MDR1 monolayers compared to DOX alone, cytotoxicity in U

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

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

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

176 NP permeability and cytotoxicity in the MDCK-MDR1-GBM co-culture model.

177 An in vitro MDCK-MDR1-GBM co-culture model was used to assess the BBB per

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

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

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

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

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

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

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

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

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

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

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

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

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

191 ubsequent proteasome-mediated degradation of MDR1 protein.

192 ver-mimicking model showed the enrichment of MDR1+ and CPT1A+ populations, whereas the PDAC cells gro

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

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

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

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

197 on of MGD1 and MGD2 as well as expression of MDR1, which encodes an efflux pump that exports fluconaz

198 the MDR1 gene and promoted the expression of MDR1.

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

200 ighlight an important endogenous function of MDR1 in cell-mediated immune responses and suggest that

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

202 Finally, inhibition of MDR1 improves antibiotic-mediated killing of M. tubercul

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

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

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

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

207 ongly associated with the number of lines of MDR1-substrate chemotherapy given.

208 ter cell line selected for overexpression of MDR1.

209 o synonymous changes in the coding region of MDR1.

210 the role of M. tuberculosis in regulation of MDR1 and drug resistance.

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

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

213 ock factor 1, a transcriptional regulator of MDR1 through the up-regulation of miR-431.

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

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

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

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

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

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

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

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

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

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

224 ABCB1 encodes Multidrug Resistance protein (MDR1), an ATP-binding cassette member involved in the ce

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

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

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

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

229 with overexpression of the drug efflux pump MDR1.

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

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

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

233 el finding that M. tuberculosis up-regulates MDR1 during infection, which limits the exposure of M. t

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

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

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

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

238 consists of ALDH+/CD133+ and drug-resistant (MDR1+) subtypes of CSCs with specific metabolic and stem

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

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

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

242 t to inhibit WTH3 and consequently stimulate MDR1 expression.

243 6G>T, 983T>C), UGT2B7 (IVS1+985A>G, 802C>T), MDR1 3435C>T, chemokine (C-C motif) receptor 2 (CCR2) 19

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

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

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

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

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

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

250 The MDR1 exonic single nucleotide polymorphisms (SNPs) C3435

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

252 The MDR1-selective pharmacophore highlights the importance o

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

283 Of these, MDR1 promoter methylation associates with specific micro

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

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

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

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

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

289 d indirectly acts to eliminate resistance to MDR1 substrates.

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 Whereas MDR1 was dispensable for naive CD8+ T cell development,

298 50/c-Rel leading to IL-10 induction, whereas MDR1 up-regulation is mediated by PI3K/Akt and the JNK p

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

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

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