| Name | ATPase |
|---|---|
| Synonyms | ATP7A; MK; ATPase; Cation transporting ATPase; ATP7A protein; ATPase Cu(2+) transporting alpha polypeptide; Copper pump 1; Copper transporting ATPase 1… |
| Name | diphenylamine |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 10688613 | Masubuchi Y, Yamada S, Horie T: Possible mechanism of hepatocyte injury induced by diphenylamine and its structurally related nonsteroidal anti-inflammatory drugs. J Pharmacol Exp Ther. 2000 Mar;292(3):982-7. Further addition of oligomycin, which blocks ATPase, pronounced the protection against cell injury. |
1(0,0,0,1) | Details |
| 12769977 | O'Donnell MJ, Fletcher M, Haley CA: KCl reabsorption by the lower malpighian tubule of rhodnius prolixus: inhibition by Cl (-) channel blockers and acetazolamide. J Insect Physiol. 1997 Jul;43(7):657-665. An earlier study proposed that K (+) reabsorption involves an -sensitive apical K (+)/H (+) ATPase and Ba (2+)-sensitive basolateral K (+) channels. The results suggest that Cl (-) reabsorption is inhibited by acetazolamide and by Cl (-) channel blockers, including diphenylamine-2-carboxylate (DPC) and 5-nitro-2-(3-phenylpropylamino) (NPPB), but not by compounds that block Na (+)/K (+)/Cl (-) and K (+)/Cl (-) co-transporters. |
1(0,0,0,1) | Details |
| 148466 | Costantino-Ceccarini E, Novikoff PM, Atkinson PH, Novikoff AB: Further characterization of HeLa S3 plasma membrane ghosts. J Cell Biol. 1978 May;77(2):448-63. Ouabain-sensitive, Na+, K+- triphosphatase (ATPase) activity of the ghost fraction is purified 9.1 (+/- 2.2) times over the homogenate; recover of the activity is 12.0 (+/- 3.8%) of the homogenate. Contamination by nuclei is 0.14%, too little for DNA detection by the diphenylamine reaction. |
1(0,0,0,1) | Details |
| 1331015 | Wangemann P, Marcus DC: The membrane potential of vestibular dark cells is controlled by a large Cl- conductance. Hear Res. 1992 Oct;62(2):149-56. The PD responded to 10 (-4) mol/l ouabain with a depolarization, suggesting the presence of a (Na (+) + K+)-ATPase. |
1(0,0,0,1) | Details |
| 11875274 | Welsh MJ, Smith JJ: cAMP stimulation of HCO3- secretion across airway epithelia. JOP. 2001 Jul;2(4 Suppl):291-3. In addition, the cAMP-stimulated current was inhibited by the carbonic anhydrase inhibitor, acetazolamide, and by the apical addition of a blocker of cystic fibrosis transmembrane conductance regulator (CFTR), diphenylamine-2-carboxylate. The current was dependent on Na (+) because it was inhibited by removing Na (+) from the submucosal solution and by inhibition of the Na (+)-K (+)-ATPase with ouabain. |
1(0,0,0,1) | Details |
| 18613510 | Ren NQ, Zhang XD, Zhou GH, Chen SJ: [Induced apoptosis and mechanism of endosulfan in mouse germ cells] . Huan Jing Ke Xue. 2008 Feb;29(2):386-90. Morphology characters of spermatogenic cells observed by laser confocal scanning microscope (LCSM), DNA ladder detected by electricity swims, and increasing of DNA degeneration rate measured through diphenylamine (p < 0.01). Endosulfan might enhance concentration in the spermatogenic cells and restrained Na+ K+ -ATPase and Ca2+ Mg2+ -ATPase activities that showed endosulfan might induce spermatogenic cells in the testicle to occur apoptosis (p < 0.01), to cause the function of transporting Ca2+ to be limited, reduce the ability of excluding and send Ca2+ concentration to hoist sustainingly,i.e. overload in the cells. |
1(0,0,0,1) | Details |
| 2458457 | Bunce KT, Spraggs CF: Stimulation of electrogenic secretion by in guinea-pig isolated gastric mucosa. J Physiol. 1988 Jun;400:381-94. This interpretation was confirmed by the dependence of the basal SCC on extracellular and inhibition by the chloride channel blocker, diphenylamine-2-carboxylate. |
0(0,0,0,0) | Details |
| 8766016 | Poulsen JH, Machen TE: HCO3-dependent pHi regulation in tracheal epithelial cells. . Pflugers Arch. 1996 Jul;432(3):546-54. Cl-free solution and 500 microM H2DIDS (dihydro-4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid, blocks anion exchange and the outwardly rectifying Cl channel, ORCC), both blocked apparent anion exchange activity, but had no effect on the recovery; 100 microM DNDS (4-4''-dinitro-2-2'-stilbenedisulfonate blocks the ORCC but not the cystic fibrosis transmembrane conductance regulator, CFTR) had no effect on pHi recovery; DPC (diphenylamine carboxylate, blocks the CFTR and the ORCC) caused a complete and reversible inhibition of the recovery. |
0(0,0,0,0) | Details |
| 11124965 | Kogan I, Ramjeesingh M, Huan LJ, Wang Y, Bear CE: Perturbation of the pore of the cystic fibrosis transmembrane conductance regulator (CFTR) inhibits its atpase activity. J Biol Chem. 2001 Apr 13;276(15):11575-81. Epub 2000 Dec 21. However, in the present study we show that the R347D mutation and diphenylamine-2-carboxylate (an open pore inhibitor) also inhibit CFTR ATPase activity, revealing a novel mechanism for cross-talk from the pore to the catalytic domains. |
84(1,1,1,4) | Details |
| 9840102 | Scheurlen C, Allgayer H, Hardt M, Kruis W: Effect of short-term topical corticosteroid treatment on mucosal enzyme systems in patients with distal inflammatory bowel disease. Hepatogastroenterology. 1998 Sep-Oct;45(23):1539-45. Prior to and after topical steroid treatment, basolateral (Na++K+)-ATPase activity (coupled optical assay), specific 3H ouabain binding (rapid filtration method), 5'-nucleotidase (microdetection method of and mucosal DNA levels (diphenylamine reaction) were determined from biopsy homogenates. |
33(0,1,1,3) | Details |
| 1387229 | Ruiz OS, Arruda JA: ATP-dependent renal H+ translocation: regional localization, kinetic characteristics, and dependence. Proc Soc Exp Biol Med. 1992 Sep;200(4):562-70. The effect of on H+ translocation was blocked by the chloride channel inhibitor, diphenylamine-2 carboxylic acid. We characterized Mg (2+)-dependent ATPase activity in membranes from the renal cortex, the outer and inner stripes of the outer medulla, and papillary vesicles. |
8(0,0,0,8) | Details |
| 1336307 | Pappas CA, Koeppen BM: Electrophysiological properties of cultured outer medullary collecting duct cells. Am J Physiol. 1992 Dec;263(6 Pt 2):F1004-10. The Cl- conductance was also found to have a significant permeability to HCO3- and was inhibited by the Cl (-)-channel blockers diphenylamine carboxylic acid and 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid. Current generated by the H (+)-adenosinetriphosphatase (H (+)-ATPase) was quantitated. |
3(0,0,0,3) | Details |
| 2531144 | Petretski JH, Wolosker H, de Meis L: Activation of Ca2+ uptake and inhibition of reversal of the sarcoplasmic reticulum Ca2+ pump by aromatic compounds. J Biol Chem. 1989 Dec 5;264(34):20339-43. The effects of aromatic compounds in sarcoplasmic reticulum Ca2+-ATPase were investigated. The order found was triphenylphosphine greater than diphenylamine greater than 3-nitrophenol greater than greater than 1,3- |
3(0,0,0,3) | Details |
| 9662559 | Cheng HS, Leung PY, Cheng Chew SB, Leung PS, Lam SY, Wong WS, Wang ZD, Chan HC: Concurrent and independent HCO3- and Cl- secretion in a human pancreatic duct cell line (CAPAN-1). J Membr Biol. 1998 Jul 15;164(2):155-67. However, an inhibitor of H+-ATPase, N-ethylmaleimide did suppress the Isc (IC50 = 22 microM). Apical addition of Cl- channel blocker, diphenylamine-2,2'-dicarboxylic acid (DPC, 1 mm), but not disulfonic acids, DIDS (100 microM) or SITS (100 microM), exerted an inhibitory effect on both Cl- and HCO-3-dependent forskolin-induced Isc responses. |
2(0,0,0,2) | Details |
| 1699427 | Malinowska DH: Cl- channel blockers inhibit acid secretion in rabbit parietal cells. Am J Physiol. 1990 Oct;259(4 Pt 1):G536-43. Mechanisms of gastric parietal cell secretory membrane Cl- transport and the role of this Cl- transport in acid secretion were investigated by examining the effects of two Cl- channel blockers, diphenylamine-2-carboxylate (DPC) and 9-anthracene carboxylate (9-AC) on acid secretion using isolated, enriched rabbit parietal cells. H (+)-K (+)-ATPase activity in situ in permeable parietal cells, measured as 2-methyl-8-(phenylmethoxy) imidazo (1,2) -3-acetonitrile (SCH28080)-inhibitable ATP hydrolysis, was higher in stimulated compared with resting cells. |
2(0,0,0,2) | Details |
| 11263994 | Sasaki Y, Nagai J, Kitahara Y, Takai N, Murakami T, Takano M: Expression of chloride channel, ClC-5, and its role in receptor-mediated endocytosis of albumin in OK cells. Biochem Biophys Res Commun. 2001 Mar 23;282(1):212-8. The effect of chloride channel inhibitors on receptor-mediated endocytosis of albumin was examined in OK cells and compared to that of vacuolar H (+)-ATPase inhibitors. Other chloride channel inhibitors, 4,4'-diisothiocyanatostilbene-2-2'-disulfonic acid and diphenylamine-2-carboxylic acid, also inhibited FITC-albumin uptake. |
2(0,0,0,2) | Details |
| 9019717 | Brodin B, Rytved KA, Nielsen R: An increase in [Ca2+] i activates basolateral channels and inhibits apical channels in frog skin epithelium. Pflugers Arch. 1996 Nov-Dec;433(1-2):16-25. The endoplasmic reticulum -ATPase inhibitor thapsigargin (0.4 microM) increased [Ca2+] i from 66 +/- 9 to 137 +/- 19 nM (n = 13, P = 0.002). Serosal addition of the chloride channel inhibitors 4, 4'-diisothiocyanatostilbene-2,2'-disulphonic acid (DIDS), diphenylamine-2-carboxylate (DPC), indanyloxyacetic acid 94 (IAA-94) and reversed the depolarization induced by thapsigargin, indicating that channels were activated by the increase in [Ca2+] i. |
1(0,0,0,1) | Details |
| 1700627 | Reenstra WW, Forte JG: Characterization of K+ and Cl- conductances in apical membrane vesicles from stimulated rabbit oxyntic cells. Am J Physiol. 1990 Nov;259(5 Pt 1):G850-8. At 75 mM K+ the Cl- channel blocker diphenylamine-2-carboxylate inhibited ATP-dependent pH gradient formation when the Cl- concentration was 1 mM; however, when the Cl- concentration was greater than 5 mM no inhibition was observed. Conductive K+ and Cl- fluxes were assayed by several methods: by their effects on pH gradient formation by endogenous H (+)-K (+)-ATPase, by the protonophore-induced dissipation of preformed pH gradients, and by the effects of channel blockers. pH gradient formation by H (+)-K (+)-ATPase required K+ and was greatly reduced when the permeant anion was replaced by or |
1(0,0,0,1) | Details |
| 14647974 | Kim HJ, Yum KS, Sung JH, Rhie DJ, Kim MJ, Min DS, Hahn SJ, Kim MS, Jo YH, Yoon SH: increases intracellular [Ca2+] in U87 cells mainly by influx of extracellular Ca2+ and partly by release of intracellular stores. Naunyn Schmiedebergs Arch Pharmacol. 2004 Feb;369(2):260-7. Epub 2003 Nov 28. Treatment for 10 min with mefenamic acid (100 micro M) and flufenamic acid (100 micro M), derivatives of diphenylamine-2-carboxylate, blocked the -induced [Ca2+] i increase in non-treated and thapsigargin-treated cells but indomethacin (100 micro M) did not affect the increases. Treatment with the inhibitor of endoplasmic reticulum Ca2+-ATPase thapsigargin (1 micro M) also significantly inhibited the -induced [Ca2+] i increases. |
1(0,0,0,1) | Details |
| 9755067 | Breton S, Hammar K, Smith PJ, Brown D: secretion in the male reproductive tract: involvement of Cl--independent HCO-3 transport. Am J Physiol. 1998 Oct;275(4 Pt 1):C1134-42. We have previously demonstrated that a vacuolar H+-ATPase [proton pump (PP)] is present in the apical pole of apical and narrow cells in the caput epididymis and of clear cells in the corpus and cauda epididymis and that this PP is responsible for the majority of secretion in the proximal vas deferens. In the presence of Cl-, diphenylamine-2-carboxylate (DPC) had no effect, whereas SITS inhibited secretion by 63.7 +/- 11.3% when applied together with DPC. |
1(0,0,0,1) | Details |