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1 dues for interaction of small molecules with P-glycoprotein.
2 d by multiple ABC transporters, particularly P-glycoprotein.
3 may be influenced by the multi-drug exporter P-glycoprotein.
4 rom the fetus toward the mother by placental P-glycoprotein.
5 and circumvented drug resistance mediated by P-glycoprotein.
6 and Messa/Dx5 cell lines, which overexpress P-glycoprotein.
7 of multidrug resistant cells overexpressing P-glycoprotein.
8 rapies with limited brain penetration due to P-glycoprotein.
9 s because of increased nuclear expression of P-glycoprotein.
10 likelihood of brain uptake being affected by P-glycoprotein.
11 t olaparib-resistant tumors that overexpress P-glycoprotein.
12 ier-related ATP-binding cassette transporter P-glycoprotein.
13 kely an efficiently transported substrate of P-glycoprotein.
14 e, which encodes the drug efflux transporter P-glycoprotein.
15 osis transmembrane conductance regulator and P-glycoprotein.
16 sm, and excretion (ADME), low propensity for p-glycoprotein 1-mediated efflux, and good passive perme
17 have cleavage activities on its target gene P-glycoprotein 11, a broad substrate efflux pump across
19 as shown in vitro to be a substrate of human P-glycoprotein, a drug-transporter involved in all steps
20 e ATP-binding cassette family like the human P-glycoprotein (ABCB1 or Pgp) are responsible for many f
21 barrier (BBB) because of efflux transport by P-glycoprotein (ABCB1) and breast cancer resistance prot
22 firmed expression and functional activity of P-glycoprotein (ABCB1) and breast cancer resistance prot
24 lux transporters at the blood-brain barrier, P-glycoprotein (ABCB1), multidrug resistance associated
25 tte (ABC) transmembrane efflux pumps such as P-glycoprotein (ABCB1), multidrug resistance protein 1 (
28 t that reduced rCBF has on assessment of BBB P-glycoprotein activity and suggests that impaired P-gly
29 20P, can rapidly and reversibly reduce basal P-glycoprotein activity and thus improve delivery of sma
30 ase activity mimicked the effects of VEGF on P-glycoprotein activity and Tyr-14 phosphorylation of ca
33 tivity and protein expression; SFN increased P-glycoprotein activity in mouse spinal cord capillaries
35 2 are required for C1P-mediated increases in P-glycoprotein activity independent of transporter prote
37 oprotein activity and suggests that impaired P-glycoprotein activity may contribute to cerebral beta-
42 for tissue hypoxia, and (11)C-verapamil for P-glycoprotein activity, in comparison with (15)O-water
43 aseline K1, corresponding to higher baseline P-glycoprotein activity, than seizure-free patients in i
49 of multiple sclerosis, also rapidly reduced P-glycoprotein activity; similar effects were found with
50 tracers to assess the transport activity of P-glycoprotein (adenosine triphosphate-binding cassette
54 transport activity and protein expression of P-glycoprotein, an ATP-driven drug efflux pump and a cri
59 (ii) this overexpression appears specific to P-glycoprotein and does not affect other transporters; (
61 be excellent substrates of the murine ABCB1A P-glycoprotein and its human counterpart, the MDR1 P-gly
62 -hydroxyeicosatetraenoic acid that regulated P-glycoprotein and junction proteins, respectively, ther
63 onfirmed their potential to inhibit the fish P-glycoprotein and modulate toxicity of other xenobiotic
64 ve, namely, 1p, was selective for ABCG2 over P-glycoprotein and MRP1, appeared not to be transported
66 esistance study in cell lines overexpressing P-glycoprotein and showed that some of these inhibitors
69 onolayer and that PHIP-M1 is a substrate for P-glycoprotein and the multiple drug resistance 2 transp
70 porters include ABCB1 (also known as MDR1 or P-glycoprotein) and ABCC1 (also known as MRP1) whose inh
74 and selective downregulation of endothelial p-glycoprotein at the blood-brain barrier that occurs in
75 rug efflux pumps at the blood-brain barrier [P-glycoprotein, ATP binding cassette b1 (Abcb1); multidr
80 2, p53, and NF-kappaB in the upregulation of P-glycoprotein, Bcrp, and Mrp2 at blood-CNS barriers.
81 or mouse brain capillaries to SFN increased P-glycoprotein, Bcrp, and Mrp2 transport activity and pr
82 es demonstrated that effective inhibition of P-glycoprotein by DDB analogues dramatically elevated th
84 ATP-binding cassette transporter other than P-glycoprotein can affect in vivo tissue sensitivity tow
86 y the ATP-binding cassette (ABC) transporter P-glycoprotein contributes to clinical resistance to ant
88 n inhibitors of cytochrome P450 3A4 (CYP3A4)/P-glycoprotein (cyclosporine, ketoconazole, ritonavir, c
89 ral drug-resistant cell lines with activated P-glycoprotein drug efflux pumps compared to drug-sensit
92 sed with drug concentration and exceeded the p-glycoprotein efflux when the latter was saturated.
94 long-acting, and noncompetitive modulator of P-glycoprotein export function that may offer therapeuti
96 enhanced DNA damage and obvious reduction of P-glycoprotein expression in the resistant cells treated
98 tance, and that the specific upregulation of P-glycoprotein expression is likely to be associated wit
101 axel response, despite an increase in Abcb1 (P-glycoprotein) expression that was sufficient to explai
102 ineties, we generated knockouts of the three P-glycoprotein genes of mice, the Mdr1a, Mdr1b, and Mdr2
104 protein (humans, ABCG2; rodents, Abcg2) and P-glycoprotein (humans, ABCB1; rodents, Abcb1a/b) affect
105 mortem human brain tissue support a role for P-glycoprotein in clearance of cerebral beta-amyloid acr
106 ar, our findings show that the expression of P-glycoprotein in humans is compatible with the inherent
108 here is a highly localized overexpression of P-glycoprotein in the epileptogenic hippocampus of patie
109 nded-release venlafaxine (all substrates for P-glycoprotein) in a large randomized, prospective, prag
110 ionary related in full transporters, such as P-glycoprotein, in which substrates bind preferentially,
111 cells with verapamil, a general inhibitor of P-glycoprotein, increased nuclear translocation of doxor
115 role for drug-drug interactions that lead to P-glycoprotein inhibition in buprenorphine-associated fa
118 G-829 as a novel, noncompetitive, and potent P-glycoprotein inhibitor that overcomes in vitro and in
122 trols then received a 30-min infusion of the P-glycoprotein-inhibitor tariquidar followed by another
123 presence of combined cytochrome P450 3A4 and P-glycoprotein inhibitors in the Rivaroxaban Once Daily
124 ere receiving concomitant treatment with the P-glycoprotein inhibitors quinidine or verapamil) or war
125 CL) cells with romidepsin in the presence of P-glycoprotein inhibitors to prevent transporter upregul
126 ime 0 to infinity for colchicine plus CYP3A4/P-glycoprotein inhibitors versus colchicine alone were >
128 of colchicine, but not the reference CYP3A4/P-glycoprotein inhibitors, were determined, and the phar
133 hown a clear trend between lipophilicity and P-glycoprotein inhibitory activity for a class of galloy
139 f doxorubicin due to increased expression of P-glycoprotein is associated with doxorubicin resistance
140 nd does not affect other transporters; (iii) P-glycoprotein is expressed on the vascular endothelium
143 significantly reduced in PSC833-treated and P-glycoprotein-knockout mice (p < .001), supporting P-gl
146 expression of the multidrug efflux transport P-glycoprotein may play an important role in pharmacores
147 res intestinal absorption by the efflux pump P-glycoprotein MDR1 (multidrug resistant-1), encoded by
149 ced endosomal escape; (vi) the inhibition of P-glycoprotein mediated drug efflux; and (vii) the TAT-m
150 oducing fluorine on the risk of encountering P-glycoprotein mediated efflux (as measured by MDR efflu
151 nephine A (1) is a noncytotoxic inhibitor of P-glycoprotein-mediated drug efflux in multidrug-resista
153 protein-knockout mice (p < .001), supporting P-glycoprotein-mediated norbuprenorphine transport at th
154 estructuring during spermatogenesis but that P-glycoprotein-mediated restructuring does not "open up"
155 L) absorption and metabolism are affected by p-glycoprotein-mediated transport and CYP3A enzyme activ
156 sporters at the blood-brain barrier, such as P-glycoprotein, might contribute to pharmacoresistance b
157 ne receptor (CAR) as a positive regulator of P-glycoprotein, multidrug resistance-associated protein
158 in genes of mice, the Mdr1a, Mdr1b, and Mdr2 P-glycoproteins, now known as Abcb1a, Abcb1b, and Abcb4,
159 genes: CYP3A4, CYP3A5, ABCB1 (MDR1; encoding P-glycoprotein), NR1I2 (encoding the pregnane X receptor
161 ofound effect of the drug-transporting ABCB1 P-glycoprotein on the pharmacokinetics of drugs in human
163 binding cassette (ABC) transporter proteins, P-glycoprotein or breast cancer resistance protein.
164 ontributor to pharmacoresistance, overcoming P-glycoprotein overactivity could be investigated as a p
165 othesis that there is an association between P-glycoprotein overactivity in some regions of the brain
166 pectrometry to identify metabolic changes in P-glycoprotein overexpressing T-cell acute lymphoblastic
167 and 44 strongly inhibited the growth of the P-glycoprotein-overexpressing multi-drug-resistant cell
168 ARAP 22 showed strong inhibition of the P-glycoprotein-overexpressing NCI-ADR-RES and Messa/Dx5M
169 r initial acute injury for the prevention of P-glycoprotein overexpression, and thus this one potenti
171 of expression of efflux transporters (e.g., P-glycoprotein (P-gp) and breast cancer resistance prote
172 eased activity of efflux transporters, e.g., P-glycoprotein (P-gp) and breast cancer resistance prote
173 tive ligand of VDR, resulted in higher brain P-glycoprotein (P-gp) and lower soluble Abeta levels, ef
174 cess limited by drug efflux proteins such as P-glycoprotein (P-gp) at the membrane of brain capillary
176 S screening hit (1) that exhibited both high p-glycoprotein (P-gp) efflux ratios in rat and human and
178 ssion and activity of the efflux transporter P-glycoprotein (P-gp) encoded by ABCB1 in human hepatoma
182 Q-starch/siRNA complexes efficiently induced P-glycoprotein (P-gp) gene silencing in the human ovaria
184 The mechanism reducing blood-brain barrier P-glycoprotein (P-gp) in Alzheimer's disease is poorly u
185 and testes are limited due to high levels of P-glycoprotein (P-gp) in the luminal membranes of brain
186 lood-brain barrier is the efflux transporter P-glycoprotein (P-gp) in the luminal plasma membrane of
195 ATP-binding cassette (ABC) drug transporter P-glycoprotein (P-gp) is often responsible for the failu
202 study, we demonstrate that the inhibition of P-glycoprotein (P-gp) significantly increases brain pene
203 cking the multidrug resistance protein Mdr1a P-glycoprotein (P-gp) was generated using a rat Mdr1a-sp
205 grows in tumours and functionally decreases P-glycoprotein (P-gp), a multidrug resistance transporte
207 increased the mRNA and protein expression of p-glycoprotein (P-gp), a subfamily of ATP-binding casset
208 ramide (dLop) images the in vivo function of P-glycoprotein (P-gp), a transporter that blocks the ent
209 rimary determinant of CNS drug permeation is P-glycoprotein (P-gp), an endogenous blood-brain barrier
211 pumps, the ATP-Binding Cassette transporter P-glycoprotein (P-gp), consists of two homologous halves
213 regulation of a multidrug resistant protein, P-glycoprotein (P-gp), suggesting an active drug efflux
214 e is connected to overexpression of membrane P-glycoprotein (P-gp), which acts as an energy dependent
215 mulate the ATPase activity of purified human P-glycoprotein (P-gp)-His(10), and their ability to prom
216 epsy and subsequently to study if changes in P-glycoprotein (P-gp)-mediated efflux of flumazenil at t
217 es at the blood-brain barrier (BBB), such as P-glycoprotein (P-gp)-mediated efflux, can limit brain u
224 transiently express c-Kit and stably express P-glycoprotein (P-gp)/multi-drug resistance type 1 (MDR1
226 activities against BCRP and screened against P-glycoprotein (P-gp, ABCB1) and multidrug resistance pr
227 clinically important because drug pumps like P-glycoprotein (P-gp, ABCB1) confer multidrug resistance
233 in the heart and increased the expression of P-glycoprotein (P-gp, ABCB1), an ATP binding cassette th
235 er with mutant p53 and induces MDR1 gene and P-glycoprotein (P-gp, ABCB1), resulting in a multidrug-r
242 uman ATP-binding cassette (ABC) transporter, P-glycoprotein (P-gp; ABCB1), mediates the ATP-dependent
243 wn substrate for efflux transporters such as P-glycoprotein (P-gp; MDR1, ABCB1), significantly less i
246 rodrug and MDR gene-silencing siRNAs (Bcl-2, P-glycoprotein [P-gp], and survivin) via encapsulation a
247 e triphosphate-binding cassette transporters P-glycoprotein (Pgp) and breast cancer resistance protei
248 c resistance to olaparib caused by increased P-glycoprotein (Pgp) drug efflux transporter expression.
256 uestration of the novel anti-tumor agent and P-glycoprotein (Pgp) substrate, di-2-pyridylketone-4,4-d
259 resistance, are not only able to bypass the P-glycoprotein (Pgp) transporter, due to their nano-size
263 of human cancers express multidrug-resistant P-glycoprotein (Pgp), which correlates with a poor progn
265 acyclines and other chemotherapeutics due to P-glycoprotein (pgp)-mediated export is a frequent probl
266 al cycle of the mouse ABC efflux transporter P-glycoprotein (Pgp; also known as ABCB1), which has a c
270 s were studied using plethysmography and the P-glycoprotein role at the blood-brain barrier using in
271 PSC833-treated mice (p < .001), supporting a P-glycoprotein role in norbuprenorphine pharmacokinetics
272 nce predominantly involves overexpression of P-glycoprotein, so AZD2461 was developed as a poor subst
276 ed controls (n = 9) using PET with a labeled P-glycoprotein substrate, (11)C-verapamil, and (15)O-wat
277 tion of VEGF increased brain distribution of P-glycoprotein substrates morphine and verapamil, but no
278 increased brain uptake of three radiolabeled P-glycoprotein substrates, (3)H-verapamil (threefold inc
279 selected analogues into a homology model of P-glycoprotein suggest that benzophenones show an intera
280 interfere with the cellular defense protein P-glycoprotein, termed transporter interfering compounds
281 ications that markedly reduce recognition by P-glycoprotein, the key efflux transporter at the blood-
282 we have employed purified and reconstituted P-glycoprotein to study its interaction with ivacaftor a
285 naling pathway that within minutes abolishes P-glycoprotein transport activity without altering trans
289 a signaling cascade to dynamically regulate P-glycoprotein transport at the BBB and offers potential
290 The quiescent, nucleotide-free state in the P-glycoprotein transport cycle appears to bind ivacaftor
292 c acid (VPA; 5 muM), significantly increased P-glycoprotein transport function in the wild-type anima
296 that is overexpressed in MDR cancer cells is P-glycoprotein, which actively effluxes drugs against a
299 ytochrome P450 3A, and the drug transporter, P-glycoprotein, which predisposes these agents to many d
300 oxin (TCDD), produced a similar induction of P-glycoprotein, which tightened the BBB, thereby increas
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