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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
18                            As a substrate of P-glycoprotein, a drug efflux pump associated with multi
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
23                                              P-glycoprotein (ABCB1) is expressed at the blood-retina
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 (
26 oprotein and its human counterpart, the MDR1 P-glycoprotein, ABCB1.
27 ls of TAP built on the crystal structures of P-glycoprotein, ABCB10, and Sav1866.
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
31                                          BBB P-glycoprotein activity in brain regions affected by AD
32                                  We compared P-glycoprotein activity in mild-AD patients (n = 9) and
33 tivity and protein expression; SFN increased P-glycoprotein activity in mouse spinal cord capillaries
34                                  We assessed P-glycoprotein activity in vivo in patients with tempora
35 2 are required for C1P-mediated increases in P-glycoprotein activity independent of transporter prote
36            We tested the hypothesis that BBB P-glycoprotein activity is diminished in Alzheimer disea
37 oprotein activity and suggests that impaired P-glycoprotein activity may contribute to cerebral beta-
38                                       Higher P-glycoprotein activity was associated with higher seizu
39                                          BBB P-glycoprotein activity was expressed as the (11)C-verap
40                  Compared with controls, BBB P-glycoprotein activity was significantly lower in the p
41 oliferation, hypoxic volume, and upregulated P-glycoprotein activity were identified.
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
44 ion or translation abolished upregulation of P-glycoprotein activity.
45 ncreases after tariquidar correspond to high P-glycoprotein activity.
46 of specific genes and significantly elevated p-glycoprotein activity.
47 ) blocked the effects of SFN and nutlin-3 on P-glycoprotein activity.
48 on, and the p53-activator nutlin-3 increased P-glycoprotein activity.
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
51            Structural comparison of MRP1 and P-glycoprotein advances our understanding of the common
52                    However, the silencing of P-glycoprotein, although capable of impeding drug transp
53              Herein, we report findings that P-glycoprotein, an ATP-dependent efflux drug transporter
54 transport activity and protein expression of P-glycoprotein, an ATP-driven drug efflux pump and a cri
55                                              P-glycoprotein, an ATP-driven drug efflux pump, is a maj
56                                              P-glycoprotein, an ATP-driven efflux pump, regulates per
57 multidrug efflux protein MDR1 (also known as P-glycoprotein and ABCB1).
58 MSCs overexpress efflux transporters such as P-glycoprotein and are highly drug resistant.
59 (ii) this overexpression appears specific to P-glycoprotein and does not affect other transporters; (
60                                              P-glycoprotein and drug efflux activity transfers were f
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
65  class of galloyl-based modulators targeting P-glycoprotein and MRP1.
66 esistance study in cell lines overexpressing P-glycoprotein and showed that some of these inhibitors
67 anisms of drug resistance, the expression of P-glycoprotein and the betaIII isotype of tubulin.
68 rug resistance mediated by the expression of P-glycoprotein and the betaIII isotype of tubulin.
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
71  penetration, acceptable ADME properties, no P-glycoprotein, and no hERG liability.
72 ining l-asparaginase and drugs unaffected by P-glycoprotein are most effective.
73                                    Mammalian P-glycoproteins are active drug efflux transporters loca
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
76                           Measurement of the P-glycoprotein-ATPase activity as a function of concentr
77 t unexpectedly strong down-modulation of the P-glycoprotein-ATPase by certain detergents.
78                                              P-glycoprotein-ATPase inhibition due to membrane disorde
79                                              P-glycoprotein-ATPase is an efflux transporter of broad
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
83                Interestingly, a knockdown of P-glycoprotein by RNAi was found to impede Sertoli cell
84  ATP-binding cassette transporter other than P-glycoprotein can affect in vivo tissue sensitivity tow
85           If this relation is confirmed, and P-glycoprotein can be identified as a contributor to pha
86 y the ATP-binding cassette (ABC) transporter P-glycoprotein contributes to clinical resistance to ant
87                                Inhibition of P-glycoprotein could partly resensitize sarcomatoid tumo
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
90 tine and paclitaxel through up-regulation of P-glycoprotein drug efflux pumps.
91                                          The P-glycoprotein drug pump protects us from toxins.
92 sed with drug concentration and exceeded the p-glycoprotein efflux when the latter was saturated.
93 properties such as permeation and especially P-glycoprotein efflux.
94 long-acting, and noncompetitive modulator of P-glycoprotein export function that may offer therapeuti
95 t to doxorubicin despite significantly lower P-glycoprotein expression in the DoxR-v cells.
96 enhanced DNA damage and obvious reduction of P-glycoprotein expression in the resistant cells treated
97                                              P-glycoprotein expression is known to be controlled by g
98 tance, and that the specific upregulation of P-glycoprotein expression is likely to be associated wit
99 ood-brain barrier permeability and increased P-glycoprotein expression.
100 )C-laniquidar is a newly developed tracer of P-glycoprotein expression.
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
103          Another SNP in CYP2B6 (983TT) and a p-glycoprotein haplotype affected AUCs without substanti
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
107 ction was not dependent on the expression of P-glycoprotein in MDR cells.
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
112  area, and concomitant use of cytochrome 3A4/P-glycoprotein inducers.
113 ostaglandin E2 receptors 1 and 2), abolished P-glycoprotein induction by C1P.
114                                              P-glycoprotein induction or activation to increase cereb
115 role for drug-drug interactions that lead to P-glycoprotein inhibition in buprenorphine-associated fa
116  associated with days of coadministration of P-glycoprotein inhibitor (r=0.35; p=0.0004).
117                                     Use of a P-glycoprotein inhibitor did not further increase the ef
118 G-829 as a novel, noncompetitive, and potent P-glycoprotein inhibitor that overcomes in vitro and in
119 olerability of NSC23925b, a novel and potent P-glycoprotein inhibitor, in rodents.
120                           PSC833, a powerful P-glycoprotein inhibitor, significantly enhanced bupreno
121                          Pretreatment with a P-glycoprotein inhibitor, which blocks blood-brain barri
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 >
127 bodyweight [</=60 kg], or concomitant use of P-glycoprotein inhibitors) were present.
128  of colchicine, but not the reference CYP3A4/P-glycoprotein inhibitors, were determined, and the phar
129 he approved on-label regimen of known CYP3A4/P-glycoprotein inhibitors.
130 ontinued during therapy with multiple CYP3A4/P-glycoprotein inhibitors.
131 dministered with most of the selected CYP3A4/P-glycoprotein inhibitors.
132  with >/= 1 combined cytochrome P450 3A4 and P-glycoprotein inhibitors.
133 hown a clear trend between lipophilicity and P-glycoprotein inhibitory activity for a class of galloy
134 onedarone increases digoxin concentration by P-glycoprotein interaction.
135  less, or concomitant medication with potent P-glycoprotein interaction.
136  psychotropic agents via cytochrome P450 and p-glycoprotein interactions.
137             It is a close homologue of human P-glycoprotein involved in multidrug resistance, and it
138                Our objectives were to assess P-glycoprotein involvement in norbuprenorphine transport
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
141                 These findings indicate that P-glycoprotein is involved in BTB restructuring during s
142                                Wild-type and P-glycoprotein knockout female Friend virus B-type mice.
143  significantly reduced in PSC833-treated and P-glycoprotein-knockout mice (p < .001), supporting P-gl
144                                           In P-glycoprotein-knockout mice, buprenorphine-related effe
145       However, lack of brain penetration and P-glycoprotein liability makes this scaffold unsuitable
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
148  cells overexpressing the efflux transporter P-glycoprotein (MDR1, P-gp, ABCB1).
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
152                              Third, to avoid P-glycoprotein-mediated drug efflux, we further designed
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
160 lls in vivo by suppressing expression of the P-glycoprotein Oca2.
161 ofound effect of the drug-transporting ABCB1 P-glycoprotein on the pharmacokinetics of drugs in human
162 entrations of HG-829 restored sensitivity to P-glycoprotein oncolytic substrates.
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
170 he occurrence of seizures appears central to P-glycoprotein overexpression.
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
175                                          The P-glycoprotein (P-gp) drug pump (ABCB1) has two transmem
176 S screening hit (1) that exhibited both high p-glycoprotein (P-gp) efflux ratios in rat and human and
177                        As a substrate of the P-glycoprotein (P-gp) efflux transporter, quinacrine is
178 ssion and activity of the efflux transporter P-glycoprotein (P-gp) encoded by ABCB1 in human hepatoma
179                  The drug efflux function of P-glycoprotein (P-gp) encoded by MDR1 can be influenced
180 ensitizers for photodynamic therapy (PDT) in P-glycoprotein (P-gp) expressing cells.
181 ecrease in ABCB1/multidrug resistance (MDR)1 p-glycoprotein (p-gp) expression.
182 Q-starch/siRNA complexes efficiently induced P-glycoprotein (P-gp) gene silencing in the human ovaria
183                         The drug efflux pump P-glycoprotein (P-gp) has been shown to promote multidru
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
187 DR) is to deliver anticancer drug along with P-glycoprotein (P-gp) inhibitor simultaneously.
188                                              P-glycoprotein (P-gp) is a multidrug transporter that us
189                                              P-glycoprotein (P-gp) is a polyspecific ATP-dependent tr
190                                              P-glycoprotein (P-gp) is a well-known membrane transport
191                                              P-glycoprotein (P-gp) is an ATP binding cassette transpo
192                                              P-glycoprotein (P-gp) is an ATP-binding cassette drug pu
193                                              P-glycoprotein (P-gp) is an ATP-binding cassette transpo
194                  The drug efflux transporter P-glycoprotein (P-gp) is highly expressed on brain endot
195  ATP-binding cassette (ABC) drug transporter P-glycoprotein (P-gp) is often responsible for the failu
196                                              P-glycoprotein (P-gp) is one of the best-known mediators
197                           The development of P-glycoprotein (P-gp) ligands remains of considerable in
198 ing hydrogen bond donors (HBDs) and reducing P-glycoprotein (P-gp) mediated efflux.
199                                              P-glycoprotein (P-gp) plays a crucial role in the develo
200                                We found that P-glycoprotein (P-gp) sequestered CA within the Golgi co
201                                              P-glycoprotein (P-gp) serves as a therapeutic target for
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
204                  Zosuquidar, which modulates P-glycoprotein (P-gp) with minimal delay of anthracyclin
205  grows in tumours and functionally decreases P-glycoprotein (P-gp), a multidrug resistance transporte
206                                              P-glycoprotein (P-gp), a promiscuous drug efflux pump, h
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
210 ractivity of multidrug transporters, such as P-glycoprotein (P-gp), at the blood-brain barrier.
211  pumps, the ATP-Binding Cassette transporter P-glycoprotein (P-gp), consists of two homologous halves
212                                        Using P-glycoprotein (P-gp), Cyp3a-, and P-gp/Cyp3a knockout m
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
218 ns such as the multidrug resistance protein, P-glycoprotein (P-gp).
219 ds 1-5 in biochemical assays with ABCC10 and P-glycoprotein (P-gp).
220 rate of the multidrug resistance transporter P-glycoprotein (P-gp).
221  of the increased nuclear expression of MDR1/P-glycoprotein (P-gp).
222 multidrug resistant cell line overexpressing P-glycoprotein (P-gp).
223 otosensitizer is also a potent stimulator of P-glycoprotein (P-gp).
224 transiently express c-Kit and stably express P-glycoprotein (P-gp)/multi-drug resistance type 1 (MDR1
225 f cell lines expressing the drug efflux pump P-glycoprotein (P-gp, ABCB1) and MRP1 (ABCC1).
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
228                                          The P-glycoprotein (P-gp, ABCB1) drug pump protects us from
229                                              P-glycoprotein (P-gp, ABCB1) is a member of the ATP-bind
230                                              P-glycoprotein (P-gp, ABCB1) is an ATP-binding cassette
231                    The multidrug transporter P-glycoprotein (P-gp, ABCB1) is an ATP-dependent pump th
232                                              P-glycoprotein (P-gp, ABCB1) is an important part of the
233 in the heart and increased the expression of P-glycoprotein (P-gp, ABCB1), an ATP binding cassette th
234                                              P-Glycoprotein (P-gp, ABCB1), multidrug resistance-assoc
235 er with mutant p53 and induces MDR1 gene and P-glycoprotein (P-gp, ABCB1), resulting in a multidrug-r
236 LP), and presence of the efflux transporter, P-glycoprotein (P-gp, ABCB1).
237 vestigated compounds had low affinity toward P-glycoprotein (P-gp, ABCB1).
238                                              P-glycoprotein (P-gp, MDR1) is a promiscuous drug efflux
239                         The ABC transporters P-glycoprotein (P-gp, official gene symbol ABCB1) and br
240            (11)C-metoclopramide transport by P-glycoprotein (P-gp; ABCB1) and the breast cancer resis
241                                              P-glycoprotein (P-gp; ABCB1) is an ABC drug pump that pr
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
244 12, or 24 mg/kg/h) of cyclosporine A (CsA, a P-glycoprotein [P-gp] inhibitor).
245 demonstrated that lenalidomide was an ABCB1 (P-glycoprotein [P-gp]) substrate.
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.
249  of vinca derivatives 16-18 able to modulate P-glycoprotein (Pgp) efflux activity is reported.
250                            Overexpression of P-glycoprotein (Pgp) increases multidrug resistance (MDR
251                                              P-glycoprotein (Pgp) is an ATP-binding cassette (ABC) tr
252                                              P-glycoprotein (Pgp) is an efflux pump important in mult
253                                              P-glycoprotein (Pgp) is one of the most biomedically rel
254                        The overexpression of P-glycoprotein (Pgp) is thought to be an important mecha
255       Multidrug resistance (MDR) mediated by P-glycoprotein (Pgp) represents a significant impediment
256 uestration of the novel anti-tumor agent and P-glycoprotein (Pgp) substrate, di-2-pyridylketone-4,4-d
257                           Saridegib, a known P-glycoprotein (Pgp) substrate, induced Pgp activity in
258         Localization of the drug transporter P-glycoprotein (Pgp) to the plasma membrane is thought t
259  resistance, are not only able to bypass the P-glycoprotein (Pgp) transporter, due to their nano-size
260  of administration and the inhibition of the P-glycoprotein (Pgp) transporter.
261                                              P-glycoprotein (Pgp), a member of the ABC transporter fa
262                                              P-glycoprotein (Pgp), a member of the ATP-binding casset
263 of human cancers express multidrug-resistant P-glycoprotein (Pgp), which correlates with a poor progn
264                                         Both P-glycoprotein (Pgp)-dependent and non-Pgp-dependent mec
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
267                                              P-glycoprotein plays a key-protective role in buprenorph
268        The multispecific efflux transporter, P-glycoprotein, plays an important role in drug disposit
269 kinase (FAK), creating the occludin/ZO-1/FAK/P-glycoprotein regulatory complex.
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
273 articipants had a baseline PET scan with the P-glycoprotein substrate (R)-[(11)C]verapamil.
274 ve, sodium channel blocker and a fluorescent p-glycoprotein substrate that was traceable.
275 d decreased by 50% brain accumulation of the P-glycoprotein substrate verapamil.
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
283                            SFN did not alter P-glycoprotein transport activity in brain and spinal co
284                        C1P treatment induced P-glycoprotein transport activity in brain capillaries r
285 naling pathway that within minutes abolishes P-glycoprotein transport activity without altering trans
286                                  C1P induced P-glycoprotein transport activity without changing trans
287 g by sphingosine 1-phosphate decreases basal P-glycoprotein transport activity.
288 rough S1PR1 to rapidly and reversibly reduce P-glycoprotein transport activity.
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
291 ed PCFT-nullizygous mice exhibited increased P-glycoprotein transport following VPA exposure.
292 c acid (VPA; 5 muM), significantly increased P-glycoprotein transport function in the wild-type anima
293 rather acts as a noncompetitive modulator of P-glycoprotein transport function.
294                However, VPA- or TCDD-induced P-glycoprotein transport was blocked in the PCFT-nullizy
295 f sterol and sphingolipid regulation of ABCB/P-glycoprotein transporters.
296 that is overexpressed in MDR cancer cells is P-glycoprotein, which actively effluxes drugs against a
297                         The second ATPase is P-glycoprotein, which confers multidrug resistance, nota
298                       The ABCB1 gene encodes P-glycoprotein, which limits brain concentrations of cer
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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