| Name | chloride channel (protein family or complex) |
|---|---|
| Synonyms | chloride channel |
| Name | diphenylamine |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 10952928 | Gong XD, Wong YL, Leung GP, Cheng CY, Silvestrini B, Wong PY: Lonidamine and analogue AF2785 block the cyclic 3', 5'-monophosphate-activated current and secretion in the rat epididymis. Biol Reprod. 2000 Sep;63(3):833-8. When added to the external solution under whole-cell patch clamp conditions, AF2785 and lonidamine inhibited the cAMP-activated current in rat epididymal cells with apparent IC (50) values of 170.6 and 631.5 microM, respectively; by comparison the IC (50) value for diphenylamine-2-carboxylate, a well-known chloride channel blocker was 1294 microM. |
33(0,1,1,3) | Details |
| 9150469 | Reeves WB: Effects of chloride channel blockers on hypoxic injury in rat proximal tubules. Kidney Int. 1997 May;51(5):1529-34. The chloride channel blocker diphenylamine-2-carboxylate (DPC) markedly reduced the degree of hypoxia-induced membrane damage as measured by the release of lactate dehydrogenase (LDH). |
32(0,1,1,2) | Details |
| 8558844 | Dray-Charier N, Paul A, Veissiere D, Mergey M, Scoazec JY, Capeau J, Brahimi-Horn C, Housset C: Expression of cystic fibrosis transmembrane conductance regulator in human gallbladder epithelial cells. Lab Invest. 1995 Dec;73(6):828-36. Stimulation of efflux by agonist of the cAMP-pathway was inhibited by diphenylamine carboxylic acid, a chloride channel blocker. |
32(0,1,1,2) | Details |
| 14715281 | Mahlangu DA, Dix JA: Halide fluxes in epithelial cells measured with an automated cell plate reader. Anal Biochem. 2004 Feb 1;325(1):28-34. Diphenylamine-2-carboxylate (a chloride channel blocker) decreased the rate by 0.12+/-0.03. |
32(0,1,1,2) | Details |
| 9575967 | O'Donnell MJ, Rheault MR, Davies SA, Rosay P, Harvey BJ, Maddrell SH, Kaiser K, Dow JA: Hormonally controlled movement across Drosophila tubules is via ion channels in stellate cells. Am J Physiol. 1998 Apr;274(4 Pt 2):R1039-49. Fluid secretion assays demonstrated sensitivity to the chloride channel blockers 5-nitro-2-(3-phenylpropylamino) diphenylamine-2-carboxylate, anthracene-9-carboxylic acid, and niflumic acid. |
32(0,1,1,2) | Details |
| 2451432 | Scheide JI, Zadunaisky JA: Effect of a chloride channel blocker on bullfrog corneal epithelium. Am J Physiol. 1988 Apr;254(4 Pt 1):C519-25. The effect of the chloride channel blocker, diphenylamine-2-carboxylate (DPC), was investigated on the bullfrog cornea epithelium using microelectrodes. |
32(0,1,1,2) | Details |
| 17074318 | Valero M, Pereboom D, Garay RP, Alda JO: Role of transport proteins in the vasorelaxant action of nitroprusside in isolated rat aorta. Eur J Pharmacol. 2006 Dec 28;553(1-3):205-8. Epub 2006 Sep 23. CPA (p-chlorophenoxy- an inhibitor of volume-sensitive channels (ClC), slightly potentiated nitroprusside vasorelaxation (by 15%), and the cystic fibrosis transmembrane conductance regulator (CFTR) chloride channel inhibitors CFTR (inh) 172 (5-[(4-Carboxyphenyl) methylene]-2-thioxo-3-[(3-trifluoromethyl) phenyl-4-th iazolidinone), DPC (diphenylamine-2,2'-dicarboxylic acid) and glibenclamide were without significant effect. |
32(0,1,1,2) | 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. 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. |
31(0,1,1,1) | Details |
| 11470857 | Gong XD, Li JC, Cheung KH, Leung GP, Chew SB, Wong PY: Expression of the cystic fibrosis transmembrane conductance regulator in rat spermatids: implication for the site of action of antispermatogenic agents. Mol Hum Reprod. 2001 Aug;7(8):705-13. The current displayed a linear I / V relationship and was inhibited by diphenylamine-2-carboxylate (DPC), a chloride channel blocker. |
31(0,1,1,1) | Details |
| 12542607 | Itoh A, Tsujikawa T, Fujiyama Y, Bamba T: Enhancement of aquaporin-3 by vasoactive intestinal polypeptide in a human colonic epithelial cell line. J Gastroenterol Hepatol. 2003 Feb;18(2):203-10. The cells were treated with protein kinase-A (PK-A) inhibitors (H-89, H-9) or chloride channel-blockers (diphenylamine-2-carboxylate (DPC), 5-nitro-2-(3-phenylpropylamino) (NPPD)). |
31(0,1,1,1) | Details |
| 2153599 | Moriarty KJ, Higgs NB, Lees M, Tonge A, Wardle TD, Warhurst G: Influence of atrial natriuretic peptide on mammalian large intestine. . Gastroenterology. 1990 Mar;98(3):647-53. The response to atrial natriuretic peptide was inhibited by (a) -free solution on the serosal surface; (b) pretreatment of the tissues with the chloride channel blocker, diphenylamine-2-carboxylate (10 (-3) M mucosally); (c) pretreatment with d,l- (10 (-4) M mucosally and serosally); (d) -free solution on the serosal surface; (e) pretreatment with tetrodotoxin (10 (-7) M to serosal surface); and (f) pretreatment with atropine (10 (-5) M serosally). |
31(0,1,1,1) | Details |
| 1297839 | Leung AY, Wong PY: Studies of transepithelial Cl- transport in cultured cauda epididymal cells of rats by the short-circuit current method. J Physiol. 1992 Nov;457:391-406. Pretreating the tissue with a chloride channel blocker diphenylamine-2-carboxylate (DPC) on the apical side significantly reduced the slope to -4.9 x 10 (-4) mu equiv h-1 cm-2 per millimolar change in [Cl-] a. 3. |
31(0,1,1,1) | Details |
| 9449327 | Tomich JM, Wallace D, Henderson K, Mitchell KE, Radke G, Brandt R, Ambler CA, Scott AJ, Grantham J, Sullivan L, Iwamoto T: Aqueous solubilization of transmembrane peptide sequences with retention of membrane insertion and function. Biophys J. 1998 Jan;74(1):256-67. As described in our previous communication, sensitivity of channel activity to diphenylamine-2-carboxylate, a chloride channel blocker, and bumetanide, an inhibitor of the Na/K/2Cl cotransporter, was used to assess changes in selectivity for the different assembled channel-forming peptides. |
31(0,1,1,1) | Details |
| 3828657 | Cox HM, Cuthbert AW, Munday KA: The effect of angiotensin II upon electrogenic ion transport in rat intestinal epithelia. Br J Pharmacol. 1987 Feb;90(2):393-401. AII responses were totally inhibited by the chloride channel blocker, diphenylamine-2-carboxylate (DPC) while cotransport inhibitors e.g. piretanide and significantly reduced the size of AII responses in colon and jejunum. |
31(0,1,1,1) | Details |
| 1647853 | Heisler S: Antagonists of epithelial channels inhibit cAMP synthesis. . Can J Physiol Pharmacol. 1991 Apr;69(4):501-6. In past studies we observed that the chloride channel blocker, diphenylamine-2-carboxylate (DPC) and chemically related drugs (Hoechst compounds 131, 143, 144) inhibited cAMP formation in mouse pituitary tumor cells. |
31(0,1,1,1) | Details |
| 3392683 | Cox HM, Cuthbert AW, Hakanson R, Wahlestedt C: The effect of neuropeptide Y and peptide YY on electrogenic ion transport in rat intestinal epithelia. J Physiol. 1988 Apr;398:65-80. Responses to both peptides were inhibited by the presence of transport inhibitors, particularly diphenylamine-2-carboxylate (DPC, a chloride channel blocker) and piretanide (Na+-K+-2Cl- co-transport inhibitor). |
31(0,1,1,1) | Details |
| 1722738 | Takuma T, Ichida T: Roles of and ions in cAMP-mediated amylase exocytosis from rat parotid acini. Cell Struct Funct. 1991 Oct;16(5):405-9. The chloride channel blocker DPC (diphenylamine-2-carboxylate) also inhibited amylase release, while DIDS (4,4'-diisothiocyanostilben-2,2'-disulfonate) or bumetanide had little effect, if any, on the exocytosis. |
31(0,1,1,1) | Details |
| 1937920 | Castro GA, Harari Y: Immunoregulation of endometrial and jejunal epithelia sensitized by infection. Int Arch Allergy Appl Immunol. 1991;95(2-3):184-90. The jejunal response to antigen is inhibited by diphenylamine-2-carboxylate, a chloride channel blocker. |
31(0,1,1,1) | 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. |
31(0,1,1,1) | Details |
| 7684181 | Grotmol T, Rodnes JT, Buanes T, Christensen G, Landsverk T: Atrial natriuretic factor (ANF) does not affect ion transport in human intestine but does in porcine intestine. Acta Physiol Scand. 1993 Apr;147(4):417-29. The porcine Isc response was partly inhibited by -free solution on the serosal side, by serosal application of bumetanide (10 (-4) M) and BaCl2 (10 (-3) M), and mucosal application of the chloride-channel blocker diphenylamine-2-carboxylate (DPC) (10 (-3) M). |
31(0,1,1,1) | Details |
| 8698229 | Pang G, Buret A, O'Loughlin E, Smith A, Batey R, Clancy R: Immunologic, functional, and morphological characterization of three new human small intestinal epithelial cell lines. Gastroenterology. 1996 Jul;111(1):8-18. One monolayer (BN) consistently showed secretion in response to forskolin (10 micromol/L), which could b inhibited by -free buffer and apical addition of the chloride channel blocker diphenylamine decarboxylate. |
31(0,1,1,1) | Details |
| 2473210 | Schoppa N, Shorofsky SR, Jow F, Nelson DJ: Voltage-gated currents in cultured canine tracheal epithelial cells. J Membr Biol. 1989 Apr;108(1):73-90. The chloride channel blocker diphenylamine-2-carboxylate (DPC, 100 microM) suppressed whole-cell currents by 76.8% at 60 mV; however, currents were unaffected by the stilbenes SITS (1 mM) and DNDS (1-30 microM). |
31(0,1,1,1) | Details |
| 12654897 | Gomez T, Medina V, Ramirez CM, Dopido R, Lorenzo A, Diaz M: Regulation of transport systems A and ASC by cyclic AMP and in a reptilian duodenal model. J Exp Biol. 2003 May;206(Pt 9):1589-98. Activation of system ASC by forskolin was clearly electroneutral, as pre-incubation of the tissues with the chloride channel blocker diphenylamine-2-carboxilic acid (DPC) completely prevented forskolin-induced transepithelial electrical responses. |
31(0,1,1,1) | Details |
| 1319450 | Leung AY, Leung PY, Cheng-Chew SB, Wong PY: The role of calcitonin gene-related peptide in the regulation of anion secretion by the rat and human epididymis. J Endocrinol. 1992 May;133(2):259-68. The current could be inhibited by apical application of the chloride channel blocker, diphenylamine-2-carboxylate. |
31(0,1,1,1) | Details |
| 11023649 | Souza MM, Boyle RT, Lieberman M: Different physiological mechanisms control isovolumetric regulation and regulatory volume decrease in chick embryo cardiomyocytes. Cell Biol Int. 2000;24(10):713-21. Potassium channel blockers, quinidine and Ba (2+), and the chloride channel blocker, diphenylamine-2-carboxylate (DPC), compromise IVR in our model. |
31(0,1,1,1) | Details |
| 11138724 | Liu W, Sato Y, Hosoda Y, Hirasawa K, Hanai H: Effects of higenamine on regulation of ion transport in guinea pig distal colon. Jpn J Pharmacol. 2000 Nov;84(3):244-51. The initial phase with an increase in Isc was partially inhibited by serosal bumetanide and abolished by mucosal diphenylamine-2-carboxylate, a chloride channel blocker, indicating transient induction of Cl- secretion. |
31(0,1,1,1) | Details |
| 11597909 | Brady KG, Kelley TJ, Drumm ML: Examining basal transport using the nasal potential difference response in a murine model. Am J Physiol Lung Cell Mol Physiol. 2001 Nov;281(5):L1173-9. In addition, these responses were assayed in the presence of several chloride channel inhibitors, including DIDS, diphenylamine-2-carboxylate, glibenclamide, and 5-nitro-2-(3-phenylpropylamino)- and a protein kinase A inhibitor, the Rp diastereomer of 3',5'-cyclic monophosphothioate (Rp-cAMPS). |
31(0,1,1,1) | Details |
| 12183480 | Phillips JE, Hey JA, Corboz MR: Effects of ion transport inhibitors on MCh-mediated secretion from porcine airway submucosal glands. J Appl Physiol. 2002 Sep;93(3):873-81. When pretreated for 3 min with the chloride channel blocker diphenylamine-2-carboxylic acid, the methacholine (1,000 microM)-induced J (G) was inhibited to 0.20 +/- 0.06 microl. min (-1). cm (-2), and the methacholine-induced hyperpolarization was abolished. |
31(0,1,1,1) | Details |
| 8388653 | Middleton JP, Mangel AW, Basavappa S, Fitz JG: Nucleotide receptors regulate membrane ion transport in renal epithelial cells. Am J Physiol. 1993 May;264(5 Pt 2):F867-73. Diphenylamine-2-carboxylate, a chloride channel blocker, eliminated the effects of ionomycin, forskolin, and ATP on Na-K-Cl cotransport. |
31(0,1,1,1) | Details |
| 2441352 | Greger R, Schlatter E, Gogelein H: channels in the luminal membrane of the rectal gland of the dogfish (Squalus acanthias). Pflugers Arch. 1987 Jun;409(1-2):114-21. This type of chloride channel is blocked reversibly by diphenylamine-2-carboxylate (10 (-4) mol/l) and by 5-nitro-2-(3-phenylpropylamino)- (10 (-5) mol/l). |
82(1,1,1,2) | 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. Other chloride channel inhibitors, 4,4'-diisothiocyanatostilbene-2-2'-disulfonic acid and diphenylamine-2-carboxylic acid, also inhibited FITC-albumin uptake. |
35(0,1,1,5) | Details |
| 2173444 | Forsyth GW, Gabriel SE: Effects of conductance inhibitors on fluid secretion into ligated ileal and jejunal loops in pigs. Am J Vet Res. 1990 Oct;51(10):1551-5. Chloride channel blockers including diphenylamine-2-carboxylate, 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonate, 5-nitro-2-(2-phenylethylamino) and alpha-phenylcinnamic acid were tested for effects on jejunal or ileal secretion in weanling pigs. |
34(0,1,1,4) | Details |
| 11140278 | Gong XD, Wong PY: Characterization of Lonidamine and AF2785 blockade of the cyclic AMP-activated current in rat epididymal cells. J Membr Biol. 2000 Dec 1;178(3):225-33. It has been shown previously that the antifertility agents Lonidamine and its analogue AF2785, [1-(2,4-dichlorobenzyl)-indazole-3-acrylic acid] are potent inhibitors of the cAMP-activated chloride channel (CFTR) in rat epididymal cells. |
1(0,0,0,1) | Details |
| 2177182 | Sandle GI, Fraser G, Long S, Warhurst G: A cAMP-activated chloride channel in the plasma membrane of cultured human gastric cells (HGT-1). Pflugers Arch. 1990 Nov;417(3):259-63. In excised inside-out patches, channels (i) exhibited degrees of outward rectification and voltage dependence that were comparable to those seen in cell-attached patches, (ii) demonstrated a -21 mV shift of their reversal potential when bath Cl- was decreased from 149 mmol/l to 53 mmol/l (calculated Cl-:cation permeability ratio 17:1), and (iii) were highly sensitive to the Cl- channel blocker diphenylamine-2-carboxylic acid (DPC, 10 (-3) mol/l). |
1(0,0,0,1) | Details |
| 8989410 | Picaud SA, Larsson HP, Grant GB, Lecar H, Werblin FS: -gated chloride channel with -transporter-like properties in cone photoreceptors of the tiger salamander. J Neurophysiol. 1995 Oct;74(4):1760-71. The current reversed near the equilibrium potential for Cl-, was decreased by three Cl- channel blockers, 5-nitro-2-(3-phenyl-propylamino) 4,4'-diisothiocyanostilbene-2,2'-disulfonate, and diphenylamine 2,2'-dicarboxylic acid, and was eliminated when was substituted for both internal and external Cl-, features consistent with the current being mediated by a Cl- channel. 3. |
1(0,0,0,1) | Details |
| 2456807 | Wong PY: Inhibition by chloride channel blockers of anion secretion in cultured epididymal epithelium and intact epididymis of rats. Br J Pharmacol. 1988 May;94(1):155-63. Addition of diphenylamine-2-carboxylate (DPC) and 5-nitro-2-(3-phenylpropylamino)- (NPPB) caused an inhibition of the SCC when added to the apical or basolateral side. 5. |
1(0,0,0,1) | Details |
| 8745282 | Fritsch J, Edelman A: Modulation of the hyperpolarization-activated Cl- current in human intestinal T84 epithelial cells by phosphorylation. J Physiol. 1996 Jan 1;490 ( Pt 1):115-28. ICl,hyp was partially inhibited by 1 mM diphenylamine-2-carboxylic acid or 0.1 mM 5-nitro-2-(3-phenylpropylamino)- and was completely blocked by Cd2+ (> 300 microM). We conclude that hyperpolarization-activated Cl- channels similar to those of ClC-2 channels (mammalian homologue of Torpedo chloride channel ClC-0) are present in T84 cells, and that their gating properties are modulated by phosphorylation. |
1(0,0,0,1) | Details |
| 8889957 | Brzuszczak IM, Zhao J, Bell C, Stiel D, Fielding I, Percy J, Smith R, O'Loughlin EV: Cyclic AMP-dependent anion secretion in human small and large intestine. . J Gastroenterol Hepatol. 1996 Sep;11(9):804-10. The chloride channel blocker DPC inhibits secretion in both areas. The Isc was inhibited by diphenylamine decarboxylate (DPC; Cl- channel blocker), bumetanide (basolateral Na+/K+/2Cl- cotransporter), BaCl2 (basolateral K+ channel) and Cl- free buffer in both segments and indomethacin (cyclo-oxygenase inhibitor) in colon alone. |
1(0,0,0,1) | Details |
| 10866956 | Zhang ZR, McDonough SI, McCarty NA: Interaction between permeation and gating in a putative pore domain mutant in the cystic fibrosis transmembrane conductance regulator. Biophys J. 2000 Jul;79(1):298-313. The cystic fibrosis transmembrane conductance regulator (CFTR) is a chloride channel with distinctive kinetics. S1118F-CFTR currents are blocked in a voltage-dependent manner by diphenylamine-2-carboxylate (DPC); the affinity of S1118F-CFTR for DPC is similar to that of the wild-type channel, but blockade exhibits moderately reduced voltage dependence. |
1(0,0,0,1) | Details |
| 7519611 | Reisin IL, Prat AG, Abraham EH, Amara JF, Gregory RJ, Ausiello DA, Cantiello HF: The cystic fibrosis transmembrane conductance regulator is a dual ATP and chloride channel. J Biol Chem. 1994 Aug 12;269(32):20584-91. The stable transfection of mouse mammary carcinoma cells, C127i, with the cDNA for human CFTR resulted in the appearance of a diphenylamine-2-carboxylate-inhibitable Cl- channel, which was activated by cAMP under whole-cell and cell-attached conditions and by protein kinase A plus ATP under excised, inside-out conditions. |
1(0,0,0,1) | Details |
| 10368184 | Leonhardt N, Vavasseur A, Forestier C: ATP binding cassette modulators control abscisic acid-regulated slow anion channels in guard cells . Plant Cell. 1999 Jun;11(6):1141-52. Because the CFTR, a chloride channel, is sensitive to glibenclamide and able to interact with K+ channels, we investigated its presence in guard cells. Potent CFTR inhibitors, such as glibenclamide and diphenylamine-2-carboxylic acid, triggered stomatal opening in darkness. |
1(0,0,0,1) | Details |
| 9078271 | Mohamed A, Ferguson D, Seibert FS, Cai HM, Kartner N, Grinstein S, Riordan JR, Lukacs GL: Functional expression and apical localization of the cystic fibrosis transmembrane conductance regulator in MDCK I cells. Biochem J. 1997 Feb 15;322 ( Pt 1):259-65. The cAMP-stimulated iodide release is sensitive to glybenclamide, diphenylamine carboxylic acid and 5-nitro-2-(3-phenylpropylamino) but not to 4,4'-di-isothiocyanostilbene-2,2'-disulphonic acid, an inhibitor profile characteristic of the CFTR chloride channel. |
0(0,0,0,0) | Details |
| 11850506 | Piper AS, Greenwood IA, Large WA: Dual effect of blocking agents on Ca2+-activated Cl (-) currents in rabbit pulmonary artery smooth muscle cells. J Physiol. 2002 Feb 15;539(Pt 1):119-31. The effects of the Cl- channel antagonists, niflumic acid (NFA), dichloro-diphenylamine 2-carboxylic acid (DCDPC) and diisothiocyanato-stilbene-2,2'-disulphonic acid (DIDS) on Ca2+-activated Cl- current (I (Cl (Ca))) evoked by adding fixed intracellular concentrations ([Ca2+] i) to the pipette solution were studied in rabbit pulmonary artery myocytes. |
0(0,0,0,0) | Details |
| 2434915 | Wangemann P, Wittner M, Di Stefano A, Englert HC, Lang HJ, Schlatter E, Greger R: Cl (-)-channel blockers in the thick ascending limb of the loop of Henle. Pflugers Arch. 1986;407 Suppl 2:S128-41. On the basis of our findings with diphenylamine-2-carboxylate we have searched for compounds which possess an even higher affinity for the Cl (-)-channels in the basolateral membrane of the thick ascending limb of the loop of Henle. |
0(0,0,0,0) | Details |
| 9815050 | Goyal RK, He XD: Evidence for NO. redox form of as nitrergic inhibitory neurotransmitter in gut. Am J Physiol. 1998 Nov;275(5 Pt 1):G1185-92. We examined the effects of soluble guanylate cyclase inhibitors LY-83583 and 1H-[1,2,4] oxadiazolo [4,3-a] quinoxalin-1-one (ODQ), potassium-channel blockers and putative chloride-channel blockers diphenylamine-2-carboxylate (DPC) and niflumic acid (NFA) on the hyperpolarization elicited by an NO. donor, diethylenetriamine/NO adduct (DNO), NO in solution, and an NO+ donor, sodium nitroprusside (SNP), in the guinea pig ileal circular muscle. |
0(0,0,0,0) | Details |
| 1337946 | Pahlavan P, Mejicano G, Ruiz OS, Arruda JA: Anion channel in basolateral cortical membranes of the rabbit kidney. . Miner Electrolyte Metab. 1992;18(6):386-91. The chloride channel inhibitor diphenylamine-2-carboxylic acid inhibited 36Cl uptake in a dose-dependent fashion. 36Cl uptake was inhibited equally by unlabeled iodide and but not by or indicating that the basolateral anion conductance is relatively selective. 36Cl uptake was pH independent but was dependent. |
0(0,0,0,0) | Details |
| 3380641 | Stutts MJ, Gatzy JT, Boucher RC: Activation of conductance induced by in tracheal epithelium. Pflugers Arch. 1988 Mar;411(3):252-8. The increased unidirectional Cl- flux induced by high K+ exposure was inhibited by luminal exposure to diphenylamine-2-carboxylic acid (DPC) or other chloride channel blockers, but was not inhibited by loop diuretics. |
0(0,0,0,0) | Details |
| 10381142 | Panesar NS: Role of and inhibitory action of inorganic on gonadotropin-stimulated steroidogenesis in mouse Leydig tumor cells. Metabolism. 1999 Jun;48(6):693-700. A chloride-channel inhibitor, diphenylamine-2-carboxylate (DPC), at concentrations up to 0.6 mmol/L stimulated basal steroid secretion and hCG 10 IU/L stimulated cAMP production, but higher concentrations had an inhibitory effect. |
31(0,1,1,1) | 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. |
31(0,1,1,1) | Details |
| 9784583 | Abdulnour-Nakhoul S, Boulpaep EL: Transcellular pathways in ambystoma proximal tubule. J Membr Biol. 1998 Nov 1;166(1):15-35. Addition of the chloride-channel blocker diphenylamine-2-carboxylate to the lumen or bath, increases the aiCl by 2.4 +/- 0.6 mm or 2.9 +/- 1.0 mm respectively. |
31(0,1,1,1) | Details |
| 8762062 | Brown CD, Dudley AJ: Chloride channel blockers decrease intracellular pH in cultured renal epithelial LLC-PK1 cells. Br J Pharmacol. 1996 Jun;118(3):443-4. A significant intracellular acidification was found with addition of 100 microM 5-nitro-2-(3-phenylpropylamino)- (NPPB), niflumic acid, flufenamate and diphenylamine-2-carboxylate (DPC) but not with 4,4'-diisothiocyanatostilbene-2-2'disulphonic acid (DIDS). |
3(0,0,0,3) | Details |
| 7980604 | Gerard C, Rigot V, Penel C: Chloride channel blockers inhibit the Na+/I- symporter in thyroid follicles in culture. Biochem Biophys Res Commun. 1994 Nov 15;204(3):1265-71. |
2(0,0,0,2) | Details |
| 11781380 | Kulka M, Gilchrist M, Duszyk M, Befus AD: Expression and functional characterization of CFTR in mast cells. . J Leukoc Biol. 2002 Jan;71(1):54-64. However, chloride channel expression in mast cells has been poorly understood. An inhibitor of CFTR-dependent Cl (-) flux, diphenylamine-2-carboxylate down-regulates mast cell mediator release. |
2(0,0,0,2) | Details |
| 16859673 | Valero MS, Garay RP, Gros P, Alda JO: Cystic fibrosis transmembrane conductance regulator (CFTR) chloride channel and Na-K-Cl cotransporter NKCC1 isoform mediate the vasorelaxant action of in isolated rat aorta. Eur J Pharmacol. 2006 Aug 21;544(1-3):126-31. Epub 2006 Jun 28. Isolated, endothelium-denuded rat aorta was contracted with 1 microM, and the vasorelaxant responses to were investigated under conditions where CFTR was inhibited by DPC (diphenylamine-2-carboxylic acid) or glibenclamide (n=6 for compound). |
2(0,0,0,2) | Details |
| 20049895 | Silva HB, Medei E, Rodrigues DC, Rondinelli E, Almeida NA, Goldenberg RC, de Carvalho AC, Nascimento JH: Voltage-dependent and currents in S17 bone marrow stromal cell line. J Cell Physiol. 2010 Apr;223(1):244-51. This current was abolished either by 500 microM SITS (4,4'-diisothiocyanatostilbene-2-2'-disulfonic acid) or 500 microM DPC (diphenylamine-2-carboxylic acid) a cystic fibrosis transmembrane conductance regulator (CFTR) chloride channel blocker, identifying it as a Cl (-) current. |
6(0,0,1,1) | Details |
| 1708205 | Heisler S: Chloride channel blockers inhibit ACTH secretion from mouse pituitary tumor cells. Am J Physiol. 1991 Apr;260(4 Pt 1):E505-12. When cells were simultaneously exposed to diphenylamine-2-carboxylate (DPC) or related substances (Hoechst compounds 131, 143, and 144) and the adenylate cyclase activator forskolin, ACTH secretion was inhibited by 76-95% [half-maximal inhibitory concentration (IC50) 450, 15, 84, and 32 microM, respectively]. |
2(0,0,0,2) | Details |
| 2439981 | Bijman J, Englert HC, Lang HJ, Greger R, Fromter E: Characterization of human sweat duct conductance by chloride channel blockers. Pflugers Arch. 1987 May;408(5):511-4. To characterize the conductance of human sweat duct the effect of various analogues of diphenylamine-2-carboxylate was investigated on the transepithelial potential difference (PDT) and resistance (RT) of isolated microperfused sweat ducts. |
1(0,0,0,1) | Details |
| 11159013 | Fortner CN, Lorenz JN, Paul RJ: Chloride channel function is linked to epithelium-dependent airway relaxation. Am J Physiol Lung Cell Mol Physiol. 2001 Feb;280(2):L334-41. In perfused mouse tracheas, the responses to SP and ATP were both inhibited by the Cl- channel inhibitors diphenylamine-2-carboxylate and 5-nitro-2-(3-phenylpropylamino) |
1(0,0,0,1) | Details |
| 10644658 | Meng X, Reeves WB: Effects of chloride channel inhibitors on H (2) O (2)-induced renal epithelial cell injury. Am J Physiol Renal Physiol. 2000 Jan;278(1):F83-90. Substitution of Cl (-) by or the inclusion of certain Cl (-) channel blockers, e.g., diphenylamine-2-carboxylate (DPC), 5-nitro-2-(3-phenylpropylamino). (NPPB), and niflumic acid, prevented the H (2) O (2)-induced loss of membrane integrity to LDH. |
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| 16081479 | Robert R, Norez C, Becq F: Disruption of CFTR chloride channel alters mechanical properties and cAMP-dependent Cl- transport of mouse aortic smooth muscle cells. J Physiol. 2005 Oct 15;568(Pt 2):483-95. Epub 2005 Aug 4. |
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| 19168702 | Noe J, Petrusca D, Rush N, Deng P, VanDemark M, Berdyshev E, Gu Y, Smith P, Schweitzer K, Pilewsky J, Natarajan V, Xu Z, Obukhov AG, Petrache I: CFTR regulation of intracellular pH and ceramides is required for lung endothelial cell apoptosis. Am J Respir Cell Mol Biol. 2009 Sep;41(3):314-23. Epub 2009 Jan 23. CFTR was detected as a functional chloride channel in primary lung endothelial cells isolated from both pulmonary arteries (human or mouse) and bronchial arteries (sheep). Both specific CFTR inhibition with 2-(phenylamino) diphenylamine-2-carboxylic acid, 5-[(4-carboxyphenyl) methylene]-2-thioxo-3-[(3-trifluoromethyl) phenyl-4-thi azolidinone (CFTR (inh)-172), or 5-nitro-2-(3-phenylpropylamino) and CFTR knockdown significantly attenuated endothelial cell apoptosis induced by staurosporine or H (2) O (2). |
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| 8796127 | Walsh KB, Wang C: Effect of chloride channel blockers on the cardiac CFTR and L-type currents. Cardiovasc Res. 1996 Aug;32(2):391-9. RESULTS: The inhibitory effects of clofibric acid, p-chlorophenoxy gemfibrozil, diphenylamine-2-carboxylate (DPC), anthracene-9-carboxylate, 4,4'dinitrostilbene-2,2'-disulfonic acid and indanyloxyacetic acid 94 were examined on the two currents. |
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| 2463365 | Schmid A, Gogelein H, Kemmer TP, Schulz I: Anion channels in giant liposomes made of endoplasmic reticulum vesicles from rat exocrine pancreas. J Membr Biol. 1988 Sep;104(3):275-82. The channel activity is not influenced by changing the free Ca2+ concentration from 1 mmol/liter to less than 10 (-9) mol/liter on either side, and is also not affected by typical Cl- -channel blockers like diphenylamine-2-carboxylate (DPC, 1 mmol/liter) or 4-acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic acid (SITS, 1 mmol/liter). Another chloride channel with a single-channel conductance of 79 +/- 6 pS (n = 4) was less frequently observed. |
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