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1 likelihood of brain uptake being affected by P-glycoprotein.
2 t olaparib-resistant tumors that overexpress P-glycoprotein.
3 ier-related ATP-binding cassette transporter P-glycoprotein.
4 e, which encodes the drug efflux transporter P-glycoprotein.
5 osis transmembrane conductance regulator and P-glycoprotein.
6 dues for interaction of small molecules with P-glycoprotein.
7 llin was associated with an interaction with P-glycoprotein.
8 d by multiple ABC transporters, particularly P-glycoprotein.
9 rom the fetus toward the mother by placental P-glycoprotein.
10 and circumvented drug resistance mediated by P-glycoprotein.
11 and Messa/Dx5 cell lines, which overexpress P-glycoprotein.
12 did not block CYP3A4, CYP2D6 isoenzymes, or P-glycoprotein.
13 of multidrug resistant cells overexpressing P-glycoprotein.
14 rapies with limited brain penetration due to P-glycoprotein.
15 rst-pass metabolism, and efficient efflux by P-glycoprotein.
16 model of substrate and inhibitor coupling to P-glycoprotein.
17 kely an efficiently transported substrate of P-glycoprotein.
18 may be influenced by the multi-drug exporter P-glycoprotein.
19 ma serum stability and is not a substrate of P-glycoprotein 1 (permeability glycoprotein) advancing i
20 sm, and excretion (ADME), low propensity for p-glycoprotein 1-mediated efflux, and good passive perme
21 have cleavage activities on its target gene P-glycoprotein 11, a broad substrate efflux pump across
22 as shown in vitro to be a substrate of human P-glycoprotein, a drug-transporter involved in all steps
24 e ATP-binding cassette family like the human P-glycoprotein (ABCB1 or Pgp) are responsible for many f
25 e triphosphate-binding cassette transporters P-glycoprotein (ABCB1) and breast cancer resistance prot
26 barrier (BBB) because of efflux transport by P-glycoprotein (ABCB1) and breast cancer resistance prot
30 tte (ABC) transmembrane efflux pumps such as P-glycoprotein (ABCB1), multidrug resistance protein 1 (
31 itors that were high-affinity substrates for p-glycoprotein (ABCB1), the multidrug resistance protein
34 g cassette (ABC) transporters such as ABCB1 (P-glycoprotein), ABCC1 (MRP1), and ABCG2 (BCRP) are well
36 t that reduced rCBF has on assessment of BBB P-glycoprotein activity and suggests that impaired P-gly
37 20P, can rapidly and reversibly reduce basal P-glycoprotein activity and thus improve delivery of sma
40 tivity and protein expression; SFN increased P-glycoprotein activity in mouse spinal cord capillaries
42 2 are required for C1P-mediated increases in P-glycoprotein activity independent of transporter prote
44 oprotein activity and suggests that impaired P-glycoprotein activity may contribute to cerebral beta-
48 ed ABC transporter expression, and inhibited P-glycoprotein activity, suggesting direct binding and i
49 aseline K1, corresponding to higher baseline P-glycoprotein activity, than seizure-free patients in i
55 of multiple sclerosis, also rapidly reduced P-glycoprotein activity; similar effects were found with
56 scopy to uncover the basis of stimulation of P-glycoprotein adenosine 5'-triphosphate (ATP) hydrolysi
57 tracers to assess the transport activity of P-glycoprotein (adenosine triphosphate-binding cassette
61 vels of the ATP-binding cassette transporter P-glycoprotein, an efflux transporter known to detoxify
64 nNOS inhibition but also a significantly low P-glycoprotein and breast-cancer-resistant protein subst
65 (ii) this overexpression appears specific to P-glycoprotein and does not affect other transporters; (
66 be excellent substrates of the murine ABCB1A P-glycoprotein and its human counterpart, the MDR1 P-gly
67 -hydroxyeicosatetraenoic acid that regulated P-glycoprotein and junction proteins, respectively, ther
68 onfirmed their potential to inhibit the fish P-glycoprotein and modulate toxicity of other xenobiotic
69 ve, namely, 1p, was selective for ABCG2 over P-glycoprotein and MRP1, appeared not to be transported
73 onolayer and that PHIP-M1 is a substrate for P-glycoprotein and the multiple drug resistance 2 transp
74 porters include ABCB1 (also known as MDR1 or P-glycoprotein) and ABCC1 (also known as MRP1) whose inh
77 and selective downregulation of endothelial p-glycoprotein at the blood-brain barrier that occurs in
78 rug efflux pumps at the blood-brain barrier [P-glycoprotein, ATP binding cassette b1 (Abcb1); multidr
83 2, p53, and NF-kappaB in the upregulation of P-glycoprotein, Bcrp, and Mrp2 at blood-CNS barriers.
84 or mouse brain capillaries to SFN increased P-glycoprotein, Bcrp, and Mrp2 transport activity and pr
86 y the ATP-binding cassette (ABC) transporter P-glycoprotein contributes to clinical resistance to ant
89 lpighamoeba infection on fluid secretion and P-glycoprotein-dependent detoxification by desert locust
92 s novel, acting to indirectly interfere with P-glycoprotein drug efflux activity as a consequence of
93 ral drug-resistant cell lines with activated P-glycoprotein drug efflux pumps compared to drug-sensit
96 um infection, we characterized the effect of P-glycoprotein efflux on bumped kinase inhibitor pharmac
97 sed with drug concentration and exceeded the p-glycoprotein efflux when the latter was saturated.
99 long-acting, and noncompetitive modulator of P-glycoprotein export function that may offer therapeuti
100 thase-1 reduces seizure-induced increases of P-glycoprotein expression and activity at the blood-brai
102 enhanced DNA damage and obvious reduction of P-glycoprotein expression in the resistant cells treated
104 tance, and that the specific upregulation of P-glycoprotein expression is likely to be associated wit
108 axel response, despite an increase in Abcb1 (P-glycoprotein) expression that was sufficient to explai
109 ineties, we generated knockouts of the three P-glycoprotein genes of mice, the Mdr1a, Mdr1b, and Mdr2
111 protein (humans, ABCG2; rodents, Abcg2) and P-glycoprotein (humans, ABCB1; rodents, Abcb1a/b) affect
112 mortem human brain tissue support a role for P-glycoprotein in clearance of cerebral beta-amyloid acr
113 ar, our findings show that the expression of P-glycoprotein in humans is compatible with the inherent
115 here is a highly localized overexpression of P-glycoprotein in the epileptogenic hippocampus of patie
116 nded-release venlafaxine (all substrates for P-glycoprotein) in a large randomized, prospective, prag
117 ionary related in full transporters, such as P-glycoprotein, in which substrates bind preferentially,
121 role for drug-drug interactions that lead to P-glycoprotein inhibition in buprenorphine-associated fa
125 G-829 as a novel, noncompetitive, and potent P-glycoprotein inhibitor that overcomes in vitro and in
129 trols then received a 30-min infusion of the P-glycoprotein-inhibitor tariquidar followed by another
130 presence of combined cytochrome P450 3A4 and P-glycoprotein inhibitors in the Rivaroxaban Once Daily
131 ere receiving concomitant treatment with the P-glycoprotein inhibitors quinidine or verapamil) or war
132 CL) cells with romidepsin in the presence of P-glycoprotein inhibitors to prevent transporter upregul
135 hown a clear trend between lipophilicity and P-glycoprotein inhibitory activity for a class of galloy
142 nd does not affect other transporters; (iii) P-glycoprotein is expressed on the vascular endothelium
146 ons to increase brain exposure by decreasing P-glycoprotein liability while maintaining potency and s
147 expression of the multidrug efflux transport P-glycoprotein may play an important role in pharmacores
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 sporters at the blood-brain barrier, such as P-glycoprotein, might contribute to pharmacoresistance b
153 in genes of mice, the Mdr1a, Mdr1b, and Mdr2 P-glycoproteins, now known as Abcb1a, Abcb1b, and Abcb4,
154 genes: CYP3A4, CYP3A5, ABCB1 (MDR1; encoding P-glycoprotein), NR1I2 (encoding the pregnane X receptor
157 ofound effect of the drug-transporting ABCB1 P-glycoprotein on the pharmacokinetics of drugs in human
159 binding cassette (ABC) transporter proteins, P-glycoprotein or breast cancer resistance protein.
160 ontributor to pharmacoresistance, overcoming P-glycoprotein overactivity could be investigated as a p
161 othesis that there is an association between P-glycoprotein overactivity in some regions of the brain
162 pectrometry to identify metabolic changes in P-glycoprotein overexpressing T-cell acute lymphoblastic
163 and 44 strongly inhibited the growth of the P-glycoprotein-overexpressing multi-drug-resistant cell
164 ARAP 22 showed strong inhibition of the P-glycoprotein-overexpressing NCI-ADR-RES and Messa/Dx5M
165 r initial acute injury for the prevention of P-glycoprotein overexpression, and thus this one potenti
167 eased activity of efflux transporters, e.g., P-glycoprotein (P-gp) and breast cancer resistance prote
168 erexpression of the drug efflux transporters P-glycoprotein (P-gp) and breast cancer resistance prote
169 of expression of efflux transporters (e.g., P-glycoprotein (P-gp) and breast cancer resistance prote
170 tive ligand of VDR, resulted in higher brain P-glycoprotein (P-gp) and lower soluble Abeta levels, ef
171 om treatment by efflux transporters, such as P-glycoprotein (P-gp) at the blood-brain barrier (BBB).
172 cess limited by drug efflux proteins such as P-glycoprotein (P-gp) at the membrane of brain capillary
174 S screening hit (1) that exhibited both high p-glycoprotein (P-gp) efflux ratios in rat and human and
176 ssion and activity of the efflux transporter P-glycoprotein (P-gp) encoded by ABCB1 in human hepatoma
180 Q-starch/siRNA complexes efficiently induced P-glycoprotein (P-gp) gene silencing in the human ovaria
181 Overexpression of ABC transporters like P-glycoprotein (P-gp) has been correlated with resistanc
183 The mechanism reducing blood-brain barrier P-glycoprotein (P-gp) in Alzheimer's disease is poorly u
184 d cross-talk between the miR-221 network and P-glycoprotein (P-gp) in doxorubicin-induced drug resist
186 and testes are limited due to high levels of P-glycoprotein (P-gp) in the luminal membranes of brain
187 lood-brain barrier is the efflux transporter P-glycoprotein (P-gp) in the luminal plasma membrane of
188 throughout the multidrug efflux transporter P-glycoprotein (P-gp) in three distinct conformational s
200 ATP-binding cassette (ABC) drug transporter P-glycoprotein (P-gp) is often responsible for the failu
205 drug resistance, the drug efflux behavior of P-glycoprotein (P-gp) remains a prominent challenge in c
207 study, we demonstrate that the inhibition of P-glycoprotein (P-gp) significantly increases brain pene
209 cking the multidrug resistance protein Mdr1a P-glycoprotein (P-gp) was generated using a rat Mdr1a-sp
211 ether this association might be mediated via P-glycoprotein (P-gp), a major pathway for clarithromyci
212 grows in tumours and functionally decreases P-glycoprotein (P-gp), a multidrug resistance transporte
214 increased the mRNA and protein expression of p-glycoprotein (P-gp), a subfamily of ATP-binding casset
216 rimary determinant of CNS drug permeation is P-glycoprotein (P-gp), an endogenous blood-brain barrier
218 on the transport activity and expression of P-glycoprotein (P-gp), breast cancer resistance protein
219 pumps, the ATP-Binding Cassette transporter P-glycoprotein (P-gp), consists of two homologous halves
221 regulation of a multidrug resistant protein, P-glycoprotein (P-gp), suggesting an active drug efflux
222 e is connected to overexpression of membrane P-glycoprotein (P-gp), which acts as an energy dependent
223 epsy and subsequently to study if changes in P-glycoprotein (P-gp)-mediated efflux of flumazenil at t
230 transiently express c-Kit and stably express P-glycoprotein (P-gp)/multi-drug resistance type 1 (MDR1
231 activities against BCRP and screened against P-glycoprotein (P-gp, ABCB1) and multidrug resistance pr
232 clinically important because drug pumps like P-glycoprotein (P-gp, ABCB1) confer multidrug resistance
237 in the heart and increased the expression of P-glycoprotein (P-gp, ABCB1), an ATP binding cassette th
245 wn substrate for efflux transporters such as P-glycoprotein (P-gp; MDR1, ABCB1), significantly less i
247 rodrug and MDR gene-silencing siRNAs (Bcl-2, P-glycoprotein [P-gp], and survivin) via encapsulation a
248 e triphosphate-binding cassette transporters P-glycoprotein (Pgp) and breast cancer resistance protei
249 c resistance to olaparib caused by increased P-glycoprotein (Pgp) drug efflux transporter expression.
258 uestration of the novel anti-tumor agent and P-glycoprotein (Pgp) substrate, di-2-pyridylketone-4,4-d
261 resistance, are not only able to bypass the P-glycoprotein (Pgp) transporter, due to their nano-size
265 sed rather than decreased by the activity of P-glycoprotein (Pgp), a transporter conferring multidrug
266 of human cancers express multidrug-resistant P-glycoprotein (Pgp), which correlates with a poor progn
268 acyclines and other chemotherapeutics due to P-glycoprotein (pgp)-mediated export is a frequent probl
269 al cycle of the mouse ABC efflux transporter P-glycoprotein (Pgp; also known as ABCB1), which has a c
271 ily B member 1 (ABCB1) multidrug transporter P-glycoprotein plays a central role in clearance of xeno
273 ilic drug doxorubicin hydrochloride and anti-P-glycoprotein siRNA, synergistic therapeutic activity i
274 nce predominantly involves overexpression of P-glycoprotein, so AZD2461 was developed as a poor subst
275 inhibitor of the ABC-B/multidrug resistance/P-glycoprotein subfamily of transporters in land plants,
279 ed controls (n = 9) using PET with a labeled P-glycoprotein substrate, (11)C-verapamil, and (15)O-wat
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
288 a signaling cascade to dynamically regulate P-glycoprotein transport at the BBB and offers potential
289 The quiescent, nucleotide-free state in the P-glycoprotein transport cycle appears to bind ivacaftor
291 c acid (VPA; 5 muM), significantly increased P-glycoprotein transport function in the wild-type anima
294 luxed out of normal proximal tubules through P-glycoprotein transporter while being retained in cance
296 ssette subfamily (ABC-B/multidrug resistance/P-glycoprotein) transporters from land plants have homol
297 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