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1 om a "chemical double" knockout (Oat3KO plus probenecid).
2 5-1 mg/kg per dose, every 2-3 weeks, without probenecid).
3 fibroblasts treated with the Panx1 blocker, probenecid.
4 nt, yet reversible manner in the presence of probenecid.
5 , and by pannexin blockers carbenoxolone and probenecid.
6 fects were reduced by the pannexin inhibitor probenecid.
7 exin1 (Panx1) mimetic peptide (10)Panx1, and probenecid.
8 urate-lowering drugs include allopurinol and probenecid.
9 ges pretreated with the pannexin-1 inhibitor probenecid.
10 ed with IFN-gamma that was also inhibited by probenecid.
11 by administration of non-radioactive ALA and probenecid.
12 ersed by cotreatment with the OAT6 inhibitor probenecid.
13 thiocyanatostilbene-2,2'-disulfonic acid and probenecid.
14 .v. infusion with VPA alone or with VPA plus probenecid.
15 f the efflux transporters are inhibitable by probenecid.
16 ically slowed and overshoot was abolished by probenecid.
17 nced with a 10-day course of amoxicillin and probenecid.
18 t had been preceded by prophylaxis with oral probenecid.
21 ely 0.25 muM) and pannexin channel inhibitor probenecid (10 mg/kg, IC50 approximately 11.7 muM), we s
22 or, % inhibition): 1.5 mM alphaKG, 80%; 1 mM probenecid, 100%; 1 mM piroxicam, 100%; 1 mM octanoate,
25 ansport of cGMP from colorectal epithelia by probenecid, a mechanism validated by studies in cultured
26 ockage of the tubular secretion pathway with probenecid, a necessary condition for establishment of c
27 inhibitors benzbromarone, sulfinpyrazone and probenecid all inhibit verinurad binding via a competiti
29 The cytotoxic effects were fully reversed by probenecid (an OAT1 inhibitor) and partially reversed by
30 sma concentrations of non-radioactive ALA or probenecid (an organic anion transport inhibitor) and, t
31 of this study was to examine the effects of probenecid, an inhibitor of organic anion transport, on
33 nction, or in the presence or the absence of probenecid, an organic ion transport inhibitor that appe
34 loromercuriphenylsulfonate and by the anions probenecid and 4,4'-diisothiocyanostilbene-2,2'-disulfon
36 ministered and concomitant administration of probenecid and saline hydration appeared to minimize dru
37 tly by multiple Panx inhibitors (mefloquine, probenecid, and (10)Panx1), ectonucleotidase (apyrase),
38 isothiocyanatostilbene-2,2'-disulfonic acid, probenecid, and sulfinpyrazone, inhibitors of MRP1 and M
39 of the pannexin 1 blockers carbenoxolone and probenecid, and the HlyA-induced ATP release was found t
42 for some inhibitors (up to 4-fold), such as probenecid, but not for others (an inhibitor-dependent e
46 t, inhibition of cyclic nucleotide efflux by probenecid did not affect the background Na(+) conductan
50 protein inhibitors, such as indomethacin and probenecid, effectively increased the accumulation of EG
52 observed for inhibition of PAH transport by probenecid in renal basolateral membrane vesicles (5.2-f
55 date putamen 3-5 times, and indomethacin and probenecid increased accumulation in ependyma 4-5 times.
59 apnia, we have examined the possibility that probenecid may inhibit SD through extracellular acidific
60 l-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)/probenecid mouse model was used to examine the changes i
62 blocking pannexin/gap junction channels with probenecid or carbenoxolone significantly reduced extern
64 accumulation of adenosine was not blocked by probenecid or GMP, suggesting that neither extracellular
66 ve mass treatment (SMT) with oral ampicillin-probenecid or tetracycline was then given to registered
67 cking pannexin-1 hemichannels with (10)Panx, probenecid, or carbenoxolone but not when connexin hemic
68 he selective activation of TRPV2 channels by probenecid promoted the sADP to generate a plateau poten
70 n after drug administration, confirming that probenecid readily penetrated the central nervous system
71 Inhibition of MRP4 in HTM cells by MK571 or probenecid resulted in cell shape changes and decreases
72 Depletion of PNX1 by siRNA or inhibition by probenecid resulted in significant blocking of extracell
74 t LTC4 is secreted by normal mast cells by a probenecid-sensitive mechanism that is independent of MR
76 e-fractionated poly(A)+ RNA and screened for probenecid-sensitive transport of p-aminohippurate (PAH)
78 us laevis oocytes expressing hOAT1 supported probenecid-sensitive uptake of [(3)H]p-aminohippurate (K
79 n transporter 1 (rROAT1) mediated saturable, probenecid-sensitive uptake of cidofovir, adefovir, and
81 p-aminohippurate (PAH) uptake was saturable, probenecid-sensitive, and inhibited by a wide range of o
82 hemichannels with CO(2)-saturated buffer or probenecid significantly reduced cell-cell signalling be
83 nsport inhibitors MK571, sulfinpyrazone, and probenecid, supporting a role for the MRP transporters i
84 inhibited by the pannexin 1 channel blocker probenecid, supporting a role of pannexin 1 in inflammas
85 broad-spectrum Panx1 blockers, mefloquine or probenecid, suppressed ATP release and reduced withdrawa
86 -stimulated by the organic substrates MK571, probenecid, taurocholic acid, estrone sulfate, and bromo
87 In contrast, sodium 4-phenylbutyrate and probenecid, the latter a uricosuric drug used clinically
95 tive to inhibition by bromosulfophthalein or probenecid was observed for taurocholate, estrone sulfat
98 e patient received intravenous hydration and probenecid with the infusions to reduce the nephrotoxici
99 in the US, we therefore investigated whether probenecid would have a direct effect on Chlamydia trach
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