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1 s sensitive to the specific Band 3 inhibitor 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid.
2 ylsulfonate and by the anions probenecid and 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid.
3 overy was completely abolished by 300 microM 4, 4'-diisothiocyanostilbene-2,2'-disulfonic acid.
6 K cells resulted in a Na(+)-dependent, DIDS (4,4'-diisothiocyanostilbene-2,2'-disulfonic acid)- and 5
7 which was inhibited by bicarbonate, mucosal 4,4'-diisothiocyanostilbene-2, 2'-disulfonic acid, and C
8 The anion transport inhibitor 4, 4'-diisothiocyanostilbene-2,2'-disulfonic acid comple
9 3-phenylpropylamino)-benzoic acid (NPPB) and 4, 4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS)
11 ere inhibited by apical bumetanide and basal 4,4'-diisothiocyanostilbene-2,2' disulfonic acid (DIDS).
12 ation was reversed by blocking ICl(LPA) with 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS)
14 A9C), diphenylamine-2-carboxylic acid (DPC), 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS),
15 l-isopropyl-amiloride (EIPA)-inhibitable and 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS)-
16 des) that require HCO3(-) and are blocked by 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS).
17 hibited by the bile acid transport inhibitor 4,4'-diisothiocyanostilbene-2,2'disulfonic acid (DIDS),
18 all inhibitors of anion transporters tested, 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid, diphen
19 romol/L, respectively), and (3) sensitive to 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (Ki = 0
20 by Gd3+ but not by the Cl- current blockers 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid or 5-ni
21 were abolished in the presence of ouabain or 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid or afte
22 creased with inhibition of anion exchange by 4,4*-diisothiocyanostilbene-2,2*-disulfonic acid, or by
23 Both ATP and 4, 4-diisothiocyanostilbene-2,2'-disulfonic acid produce
24 ly 20% reduction in sulfate influx of normal 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid sensiti
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