| Name | CFTR |
|---|---|
| Synonyms | ABC35; ABCC 7; ABCC7; ATP binding cassette transporter sub family C member 7; CF; CFTR; CFTR/MRP; MRP 7… |
| Name | diphenylamine |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 8737083 | Cantiello HF: Role of the actin cytoskeleton in the regulation of the cystic fibrosis transmembrane conductance regulator. Exp Physiol. 1996 May;81(3):505-14. A functional characterization of CFTR in either cell type included cAMP-induced, linear whole-cell and single-channel currents in symmetrical Cl-, permeability to ATP, and inhibition by either diphenylamine-carboxylate (DPC) or a monoclonal antibody raised against CFTR. |
89(1,1,1,9) | Details |
| 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. 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). |
88(1,1,1,8) | Details |
| 14668136 | Scott-Ward TS, Li H, Schmidt A, Cai Z, Sheppard DN: Direct block of the cystic fibrosis transmembrane conductance regulator Cl (-) channel by niflumic acid. Mol Membr Biol. 2004 Jan-Feb;21(1):27-38. However, the chemical structure of niflumic acid resembles that of diphenylamine-2-carboxylate, a drug that inhibits the cystic fibrosis transmembrane conductance regulator (CFTR) Cl (-) channel. |
86(1,1,1,6) | Details |
| 7541942 | Prat AG, Xiao YF, Ausiello DA, Cantiello HF: cAMP-independent regulation of CFTR by the actin cytoskeleton. . Am J Physiol. 1995 Jun;268(6 Pt 1):C1552-61. The actin-activated Cl- channels (symmetrical Cl-) had a linear conductance of 9.3 pS and were inhibited by diphenylamine-2-carboxylate and monoclonal antibodies raised against CFTR. |
86(1,1,1,6) | Details |
| 10666040 | Lader AS, Wang Y, Jackson GR Jr, Borkan SC, Cantiello HF: cAMP-activated anion conductance is associated with expression of CFTR in neonatal mouse cardiac myocytes. Am J Physiol Cell Physiol. 2000 Feb;278(2):C436-50. The cAMP-activated currents were inhibited by diphenylamine-2-carboxylate, glibenclamide, and an anti-cystic fibrosis transmembrane conductance regulator (CFTR) monoclonal antibody. |
86(1,1,1,6) | Details |
| 9530112 | Cantiello HF, Jackson GR Jr, Grosman CF, Prat AG, Borkan SC, Wang Y, Reisin IL, O'Riordan CR, Ausiello DA: Electrodiffusional ATP movement through the cystic fibrosis transmembrane conductance regulator. Am J Physiol. 1998 Mar;274(3 Pt 1):C799-809. Purified CFTR-mediated ATP currents were activated by protein kinase A and ATP (1 mM) from the "intracellular" side of the molecule and were inhibited by diphenylamine-2-carboxylate, glibenclamide, and anti-CFTR antibodies. |
86(1,1,1,6) | Details |
| 8622979 | Gottlieb RA, Dosanjh A: Mutant cystic fibrosis transmembrane conductance regulator inhibits acidification and apoptosis in C127 cells: possible relevance to cystic fibrosis. Proc Natl Acad Sci U S A. 1996 Apr 16;93(8):3587-91. That this resistance to the induction of apoptosis depended upon the loss of CFTR activity is shown by the finding that inhibition of the CFTR with diphenylamine carboxylate in C127/wt cells conferred similar protection. |
85(1,1,1,5) | 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. 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. |
85(1,1,1,5) | Details |
| 8397274 | McCarty NA, McDonough S, Cohen BN, Riordan JR, Davidson N, Lester HA: Voltage-dependent block of the cystic fibrosis transmembrane conductance regulator Cl- channel by two closely related arylaminobenzoates. J Gen Physiol. 1993 Jul;102(1):1-23. CFTR is blocked by diphenylamine-2-carboxylate (DPC) when applied extracellularly at millimolar concentrations. |
84(1,1,1,4) | Details |
| 7515570 | Schwiebert EM, Flotte T, Cutting GR, Guggino WB: Both CFTR and outwardly rectifying channels contribute to cAMP-stimulated whole cell currents. Am J Physiol. 1994 May;266(5 Pt 1):C1464-77. These results were obtained by exploiting dissimilar biophysical properties of CFTR and ORCC currents such as the degree of rectification of the current-voltage relationship, the difference in sensitivity to Cl- channel-blocking drugs such as 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), calixarenes, and diphenylamine carboxylic acid (DPC), and the opposing Cl- relative to I- permeabilities of the two channels. |
34(0,1,1,4) | 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). |
84(1,1,1,4) | Details |
| 12181292 | Cowley EA, Linsdell P: Oxidant stress stimulates anion secretion from the human airway epithelial cell line Calu-3: implications for cystic fibrosis lung disease. J Physiol. 2002 Aug 15;543(Pt 1):201-9. This increase was almost entirely abolished by the addition of diphenylamine-2-carboxylate (DPC), implicating the cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channel in the response. |
83(1,1,1,3) | Details |
| 7539784 | Ohrui T, Shen BQ, Mrsny RJ, Widdicombe JH: A method for measuring Cl efflux from dispersed cells of airway epithelium. J Appl Physiol. 1995 Mar;78(3):1197-202. Increases in efflux in response to either temperature or cAMP-elevating agents were inhibited by diphenylamine-2-carboxylate, a blocker of CFTR. |
83(1,1,1,3) | Details |
| 17699556 | Soodvilai S, Jia Z, Yang T: peroxide stimulates secretion in primary inner medullary collecting duct cells via mPGES-1-derived Am J Physiol Renal Physiol. 2007 Nov;293(5):F1571-6. Epub 2007 Aug 15. This increase was almost abolished by the cystic fibrosis transmembrane conductance regulator (CFTR) Cl (-) channel inhibitors diphenylamine-2-carboxylic acid (DPC) and CFTR inhibitor-172. |
81(1,1,1,1) | Details |
| 15986093 | Kotsias BA, Peracchia C: Functional interaction between CFTR and Cx45 gap junction channels expressed in oocytes. J Membr Biol. 2005 Feb;203(3):143-50. In single oocytes expressing CFTR, an increase in cAMP caused by forskolin application induced a Cl (-) current and increased membrane conductance; application of diphenylamine carboxylic acid (CFTR blocker) readily blocked the Cl (-) current. |
37(0,1,1,7) | Details |
| 18850051 | Chen M, Du J, Jiang W, Zuo W, Wang F, Li M, Chan H, Zhou W: Functional expression of cystic fibrosis transmembrane conductance regulator in rat oviduct epithelium. Acta Biochim Biophys Sin. 2008 Oct;40(10):864-72. In whole-cell patch clamp, oviduct epithelial cells responded to 100 microM 8-bromoadenosine 3',5'-cyclic monophosphate (8-Br-cAMP) with a rise in inward current in Gap-free mode, which was inhibited successively by 5 microM CFTR (inh)-172, a CFTR specific inhibitor, and 1 mM diphenylamine-2-carboxylate (DPC), the Cl- channel blocker. |
36(0,1,1,6) | Details |
| 8772467 | Hanaoka K, Devuyst O, Schwiebert EM, Wilson PD, Guggino WB: A role for CFTR in human autosomal dominant polycystic kidney disease. . Am J Physiol. 1996 Jan;270(1 Pt 1):C389-99. 3',5'-cyclic monophosphate-activated Cl- currents are present in primary cultures of ADPKD cells and have characteristics such as a linear current-voltage relation, insensitivity to 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid, sensitivity to glibenclamide and diphenylamine carboxylic acid, and an anion selectivity sequence of Br- > Cl- > I- > all of which are identical to cystic fibrosis transmembrane conductance regulator (CFTR). |
34(0,1,1,4) | 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. |
34(0,1,1,4) | 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. |
38(0,1,1,8) | Details |
| 12202948 | Reddy MM, Quinton PM: Effect of anion transport blockers on CFTR in the human sweat duct. J Membr Biol. 2002 Sep 1;189(1):15-25. Studies using mostly ex vivo systems suggested diphenylamine-2-carboxylate (DPC), 5-nitro-2-(3-phenylpropylamino) (NPPB) and glybenclamide inhibit CFTR Cl- conductance (CFTR GCl). |
37(0,1,1,7) | 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. An inhibitor of CFTR-dependent Cl (-) flux, diphenylamine-2-carboxylate down-regulates mast cell mediator release. |
36(0,1,1,6) | Details |
| 17588945 | Hernandez-Gonzalez EO, Trevino CL, Castellano LE, de la Vega-Beltran JL, Ocampo AY, Wertheimer E, Visconti PE, Darszon A: Involvement of cystic fibrosis transmembrane conductance regulator in mouse sperm capacitation. J Biol Chem. 2007 Aug 17;282(33):24397-406. Epub 2007 Jun 22. Interestingly, the addition of a CFTR inhibitor (diphenylamine-2-carboxylic acid; 250 microM) inhibited the capacitation-associated hyperpolarization, prevented ENaC closure, and decreased the zona pellucida-induced acrosome reaction without affecting the increase in phosphorylation. |
35(0,1,1,5) | Details |
| 17596272 | Robert R, Savineau JP, Norez C, Becq F, Guibert C: Expression and function of cystic fibrosis transmembrane conductance regulator in rat intrapulmonary arteries. Eur Respir J. 2007 Nov;30(5):857-64. Epub 2007 Jun 27. Furthermore, the following effects were found: 1) inhibition of forskolin/-activated iodide efflux by glibenclamide, diphenylamine-2-carboxylic acid and CFTR-specific inhibitor (CFTR (inh))-172; 2) activation of iodide efflux by the benzoquinolizinium derivative CFTR activators MPB-07 and MPB-91; and 3) inhibition of MPB-dependent efflux by CFTR (inh)-172. |
87(1,1,1,7) | Details |
| 9518736 | Briel M, Greger R, Kunzelmann K: Cl- transport by cystic fibrosis transmembrane conductance regulator (CFTR) contributes to the inhibition of epithelial Na+ channels (ENaCs) in Xenopus oocytes co-expressing CFTR and ENaC. J Physiol. 1998 May 1;508 ( Pt 3):825-36. SCN- or or when CFTR was inhibited by diphenylamine-carboxylate (DPC, 1 mmol l-1). 4. |
90(1,1,1,10) | Details |
| 10600767 | Prat AG, Cunningham CC, Jackson GR Jr, Borkan SC, Wang Y, Ausiello DA, Cantiello HF: Actin filament organization is required for proper cAMP-dependent activation of CFTR. Am J Physiol. 1999 Dec;277(6 Pt 1):C1160-9. In contrast, cAMP induced a 10-fold increase in the diphenylamine-2-carboxylate (DPC)-sensitive whole cell Cl (-) currents of ABP (+)/CFTR (+) cells. |
90(1,1,1,10) | Details |
| 10864573 | Hanaoka K, Guggino WB: cAMP regulates cell proliferation and cyst formation in autosomal polycystic kidney disease cells. J Am Soc Nephrol. 2000 Jul;11(7):1179-87. Fluid secretion into the cyst lumen was blocked by diphenylamine carboxylic acid (DPC) and glibenclamide in ADPKD cells but blocked only by DPC in HRCE cells. It was previously reported that the cystic fibrosis transmembrane conductance regulator (CFTR) is expressed in cysts from ADPKD patients and suggested that cAMP-stimulated Cl (-) and fluid secretion occurs through CFTR. |
1(0,0,0,1) | Details |
| 7573398 | Vandorpe D, Kizer N, Ciampollilo F, Moyer B, Karlson K, Guggino WB, Stanton BA: CFTR mediates electrogenic secretion in mouse inner medullary collecting duct (mIMCD-K2) cells. Am J Physiol. 1995 Sep;269(3 Pt 1):C683-9. In whole cell patch-clamp experiments, 8-(4-chlorophenylthio) 3',5'-cyclic monophosphate (CPT-cAMP) activated Cl- currents that were time and voltage independent, inhibited by diphenylamine 2-carboxylate (DPC), and had a linear current-voltage (I-V) relation. |
1(0,0,0,1) | Details |
| 16183882 | Fuller MD, Zhang ZR, Cui G, McCarty NA: The block of CFTR by scorpion venom is state-dependent. Biophys J. 2005 Dec;89(6):3960-75. Epub 2005 Sep 23. Application of either venom or diphenylamine-2-carboxylate to channels that were either activated (open) or resting (closed) indicate primarily closed state-dependent inhibition of CFTR by venom, whereas diphenylamine-2-carboxylate showed no state-dependence of block. |
6(0,0,0,6) | Details |
| 1372482 | Cunningham SA, Worrell RT, Benos DJ, Frizzell RA: cAMP-stimulated ion currents in Xenopus oocytes expressing CFTR cRNA. Am J Physiol. 1992 Mar;262(3 Pt 1):C783-8. In addition, the Cl channel blockers 5-nitro-2-(3-phenylpropylamino) (NPPB; 50 microM) and diphenylamine-2-carboxylic acid (DPC; 3 mM) reduced the cAMP-evoked currents by only approximately 10%. |
6(0,0,0,6) | Details |
| 7539220 | Dinudom A, Komwatana P, Young JA, Cook DI: A forskolin-activated Cl- current in mouse mandibular duct cells. Am J Physiol. 1995 May;268(5 Pt 1):G806-12. The current carried by this conductance is attenuated 65% by 1 mmol/l diphenylamine-2-carboxylate but is not affected by 0.1 mmol/l4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid or 0.1 mmol/l glibenclamide. We conclude that this adrenergically evoked conductance is due to CFTR, which has previously been shown to be expressed in salivary duct cells, and suggest that it may form part of the mechanism by which beta-adrenergic agonists modulate NaCl absorption by salivary ducts. |
1(0,0,0,1) | Details |
| 11159054 | Wang X, Zhang Y, Amberson A, Engelhardt JF: New models of the tracheal airway define the glandular contribution to airway surface fluid and electrolyte composition. Am J Respir Cell Mol Biol. 2001 Feb;24(2):195-202. Furthermore, a temperature labile factor secreted by submucosal glands appears to alter the baseline activation of 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid and/or diphenylamine-2-carboxylic acid-sensitive channels in the surface airway epithelium. Submucosal glands, a predominant site of cystic fibrosis transmembrane conductance regulator (CFTR) protein expression in the airway, have been hypothesized to play an important role in protection of the airway. |
1(0,0,0,1) | 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. To establish whether cystic fibrosis transmembrane conductance regulator (CFTR) is functionally expressed in the testis, we subjected spermatogenic cells from rat testes to analysis of CFTR mRNA, protein and channel activity. The current displayed a linear I / V relationship and was inhibited by diphenylamine-2-carboxylate (DPC), a chloride channel blocker. |
5(0,0,0,5) | Details |
| 11078708 | Bulteau L, Derand R, Mettey Y, Metaye T, Morris MR, McNeilly CM, Folli C, Galietta LJ, Zegarra-Moran O, Pereira MM, Jougla C, Dormer RL, Vierfond JM, Joffre M, Becq F: Properties of CFTR activated by the derivative X-33 in human airway Calu-3 cells. Am J Physiol Cell Physiol. 2000 Dec;279(6):C1925-37. Whole cell current activated by X-33 or IBMX is linear, inhibited by glibenclamide and diphenylamine-2-carboxylate but not by DIDS or TS-TM calix [4] arene. |
5(0,0,0,5) | Details |
| 11457796 | Crews A, Taylor AE, Ballard ST: Liquid transport properties of porcine tracheal epithelium. J Appl Physiol. 2001 Aug;91(2):797-802. Absorptive J (V) was not significantly affected by 300 microM 5-nitro-2-(3-phenylpropylamino) or 100 microM diphenylamine-2-carboxylic acid, both cystic fibrosis transmembrane conductance regulator protein (CFTR) inhibitors, in the instillate but was significantly reduced by 60% when the luminal solution was Cl (-)-free Krebs solution. |
0(0,0,0,0) | Details |
| 9618558 | Mitchell CH, Carre DA, McGlinn AM, Stone RA, Civan MM: A release mechanism for stored ATP in ocular ciliary epithelial cells. . Proc Natl Acad Sci U S A. 1998 Jun 9;95(12):7174-8. In contrast, the P-glycoprotein inhibitors tamoxifen and and the cystic fibrosis transmembrane conductance regulator (CFTR) blockers glybenclamide and diphenylamine-2-carboxylate did not affect ATP release from either cell type. |
0(0,0,0,0) | Details |
| 16038730 | Assef YA, Cavarra SM, Damiano AE, Ibarra C, Kotsias BA: Ionic currents in multidrug resistant K562 human leukemic cells. Leuk Res. 2005 Sep;29(9):1039-47. Epub 2005 Apr 19. In this study, the expression and functional characterization of currents through the CFTR (cystic fibrosis transmembrane regulator) and ORCC (outwardly rectifying channels) were determined in wild-type K562 chronic human leukemia cells (K562-WT) and in its resistant counterpart, the vincristine resistant cell line (K562-Vinc). A fraction of the activated whole cell currents was inhibited by 500 microM 4,4-diisothiocyanatostilbene-2,2-disulfonic acid (DIDS) and subsequent addition of 500 microM diphenylamine-2-carboxylate (DPC plus DIDS) further inhibited the remaining currents. |
5(0,0,0,5) | Details |
| 11319159 | Leung GP, Gong XD, Cheung KH, Cheng-Chew SB, Wong PY: Expression of cystic fibrosis transmembrane conductance regulator in rat efferent duct epithelium. Biol Reprod. 2001 May;64(5):1509-15. The expression of cystic fibrosis transmembrane conductance regulator (CFTR) was studied in rat efferent ducts. The current was inhibited by the Cl (-) channel blocker diphenylamine 2,2'-dicarboxylic acid (DPC) in a voltage-dependent manner and reversed at 24 +/- 0.5 mV, close to the equilibrium potential for Cl (-) (30 mV), suggesting that the current was Cl (-) selective. |
5(0,0,0,5) | Details |
| 7522483 | McDonough S, Davidson N, Lester HA, McCarty NA: Novel pore-lining residues in CFTR that govern permeation and open-channel block. Neuron. 1994 Sep;13(3):623-34. |
4(0,0,0,4) | Details |
| 9108631 | Iwase N, Sasaki T, Shimura S, Yamamoto M, Suzuki S, Shirato K: ATP-induced Cl- secretion with suppressed Na+ absorption in rabbit tracheal epithelium. Respir Physiol. 1997 Feb;107(2):173-80. The initial increase by ATP (10 (-4) M) was significantly inhibited by a Cl (-) -channel inhibitor diphenylamine-2-carboxylate (DPC, 5 x 10 (-4) M) and Cl (-) -substitution with in the bath solution, while a cystic fibrosis transmembrane regulator (CFTR) Cl (-) -channel inhibitor glibenclamide (10 (-4) M), a Na (+)-channel inhibitor amiloride (10 (-4) M) and a K (+) -channel inhibitor quinidine (10 (-4) M) all failed to alter it. |
0(0,0,0,0) | Details |
| 7543241 | Faller DP, Egan DA, Ryan MP: Evidence for location of the CFTR in human placental apical membrane vesicles. Am J Physiol. 1995 Jul;269(1 Pt 1):C148-55. The sensitivities of 36Cl uptake to the inhibitors 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), bumetanide, and diphenylamine-2-carboxylate were investigated. |
5(0,0,0,5) | Details |
| 9435576 | Moon S, Singh M, Krouse ME, Wine JJ: -stimulated Cl- secretion in Calu-3 human airway cells requires CFTR. Am J Physiol. 1997 Dec;273(6 Pt 1):L1208-19. Thapsigargin stimulated large, sustained changes (delta) in Isc and Gte, whereas forskolin stimulated variable and smaller increases. delta Isc was decreased by basolateral bumetanide, quinidine, barium, or diphenylamine-2-carboxylate (DPAC) but was unaffected by high apical concentrations of 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), 4,4'-dinitrostilbene-2,2'-disulfonic acid, and calixarene. |
5(0,0,0,5) | Details |
| 11845302 | Duszyk M: CFTR and lysozyme secretion in human airway epithelial cells. . Pflugers Arch. 2001;443 Suppl 1:S45-9. Epub 2001 Aug 4. Similarly, blockers of Cl (-) secretion, such as diphenylamine-2-carboxylate (DPC), also reduced lysozyme secretion. |
5(0,0,0,5) | Details |
| 11845319 | Chan LN, Wang XF, Tsang LL, So SC, Chung YW, Liu CQ, Chan HC: Inhibition of amiloride-sensitive Na (+) absorption by activation of CFTR in mouse endometrial epithelium. Pflugers Arch. 2001;443 Suppl 1:S132-6. Epub 2001 Jul 10. When the contribution of Cl (-) to the I (sc) was eliminated by diphenylamine 2,2'-dicarboxylic acid (DPC, 2 mM) or Cl (-) replacement, forskolin now decreased, rather than increased the I (sc), demonstrating the inhibition of Na (+) absorption upon stimulation. |
5(0,0,0,5) | Details |
| 10516209 | Ballard ST, Trout L, Bebok Z, Sorscher EJ, Crews A: CFTR involvement in and liquid secretion by airway submucosal glands. Am J Physiol. 1999 Oct;277(4 Pt 1):L694-9. Pretreatment with diphenylamine-2-carboxylate, a relatively nonselective Cl (-)-channel blocker, significantly reduced liquid secretion by 86%, whereas pretreatment with DIDS, which inhibits a variety of Cl (-) channels but not CFTR, had no effect. |
5(0,0,0,5) | Details |
| 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. |
4(0,0,0,4) | Details |
| 9120009 | Iwase N, Sasaki T, Shimura S, Fushimi T, Okayama H, Hoshi H, Irokawa T, Sasamori K, Takahashi K, Shirato K: Signature current of SO2-induced bronchitis in rabbit. J Clin Invest. 1997 Apr 1;99(7):1651-61. This pathological ATP response was abolished by diphenylamine 2-carboxylate or Cl--free bath solution. The Northern blot analysis showed a strong expression of cystic fibrosis transmembrane conductance regulator (CFTR) mRNA in SO2-exposed epithelium. |
3(0,0,0,3) | Details |
| 10611078 | Leung GP, Wong PY: Activation of cystic fibrosis transmembrane conductance regulator in rat epididymal epithelium by Biol Reprod. 2000 Jan;62(1):143-9. The effect of on anion secretion via cystic fibrosis transmembrane conductance regulator (CFTR) in cultured rat cauda epididymal epithelia was studied by short-circuit current (Isc) technique. The response could be blocked by the nonspecific Cl (-) channel blocker, diphenylamine-2-carboxylate (DPC), but not by the Ca (2+)-activated Cl (-) channel blocker, 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS). |
3(0,0,0,3) | Details |
| 10913005 | Goddard CA, Evans MJ, Colledge WH: activates CFTR-mediated Cl (-) secretion in the murine trachea and colon. Am J Physiol Cell Physiol. 2000 Aug;279(2):C383-92. This increase was inhibited by diphenylamine-2-carboxylate, and glibenclamide, but not by DIDS. |
3(0,0,0,3) | Details |
| 11914383 | Marshall WS, Howard JA, Cozzi RR, Lynch EM: NaCl and fluid secretion by the intestine of the teleost Fundulus heteroclitus: involvement of CFTR. J Exp Biol. 2002 Mar;205(Pt 6):745-58. Mucosal application of the anion channel blocker 1 mmol l (-1) diphenylamine-2-carboxylate (DPC) after ionomycin + db-cAMP + IBMX treatment significantly reduced serosal-to-mucosal unidirectional Cl (-) flux (P <0.001), net Cl (-) flux (P <0.05), short-circuit current (I (sc), P <0.001) and tissue conductance (G (t), P <0.001), while 0.1 mmol l (-1) 4,4'-diisothiocyano-2,2'-stilbene-disulphonic acid (DIDS, a blocker of anion exchange) was without effect. |
3(0,0,0,3) | Details |
| 7530244 | Jovov B, Ismailov II, Benos DJ: Cystic fibrosis transmembrane conductance regulator is required for protein kinase A activation of an outwardly rectified anion channel purified from bovine tracheal epithelia. J Biol Chem. 1995 Jan 27;270(4):1521-8. This small conductance channel was inhibited by 300 microM diphenylamine-2-carboxylic acid. Immunoprecipitation experiments with anti-CFTR antibodies indicate that the 174-kDa phosphoprotein was CFTR. |
3(0,0,0,3) | Details |
| 10794662 | Bertog M, Smith DJ, Bielfeld-Ackermann A, Bassett J, Ferguson DJ, Korbmacher C, Harris A: Ovine male genital duct epithelial cells differentiate in vitro and express functional CFTR and ENaC. Am J Physiol Cell Physiol. 2000 May;278(5):C885-94. The remaining amiloride-insensitive I (sc) component in epididymis and vas deferens cells was partially inhibited by apical application of the Cl (-) channel blocker diphenylamine-2-carboxylic acid (1 mM). |
3(0,0,0,3) | Details |
| 10898729 | Lader AS, Xiao YF, O'Riordan CR, Prat AG, Jackson GR Jr, Cantiello HF: cAMP activates an ATP-permeable pathway in neonatal rat cardiac myocytes. . Am J Physiol Cell Physiol. 2000 Jul;279(1):C173-87. Spontaneous ATP release by NRCM was significantly increased after cAMP stimulation under physiological conditions. cAMP stimulation also induced an anion-selective electrodiffusional pathway that elicited linear, diphenylamine-2-carboxylate (DPC)-inhibitable Cl (-) currents in either symmetrical MgCl (2) or NaCl. The cAMP-induced ATP currents were inhibited by DPC and glibenclamide and by a monoclonal antibody raised against the R domain of the cystic fibrosis transmembrane conductance regulator (CFTR). |
3(0,0,0,3) | 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. Bioelectrical properties measured using the nasal transepithelial potential difference (TEPD) assay are believed to reflect these cystic fibrosis transmembrane conductance regulator (CFTR)-dependent transport defects. 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). |
3(0,0,0,3) | Details |
| 9916004 | Chan LN, Chung YW, Leung PS, Liu CQ, Chan HC: Activation of an 3',5'-cyclic monophosphate-dependent Cl- conductance in response to neurohormonal stimuli in mouse endometrial epithelial cells: the role of cystic fibrosis transmembrane conductance regulator. Biol Reprod. 1999 Feb;60(2):374-80. The observed electrophysiological properties of the agonist-induced Cl- conductance were consistent with those reported for the cystic fibrosis transmembrane conductance regulator (CFTR), a cAMP-activated Cl- channel expressed in many epithelia. The agonist-induced current was inhibited by the Cl- channel blocker diphenylamine 2,2'-dicarboxylic acid (DPC), but not by the Cl- channel blocker 4,4'-diisothiocyanatostibene-2, 2'-disulfonic acid (DIDS). |
3(0,0,0,3) | Details |
| 9699500 | Mailleau C, Capeau J, Brahimi-Horn MC: Interrelationship between the Na+/ cotransporter and CFTR in Caco-2 cells: relevance to cystic fibrosis. J Cell Physiol. 1998 Sep;176(3):472-81. We also demonstrated that inhibition of CFTR by glibenclamide or diphenylamine-2-carboxylate did not modify the activity of SGLT1 and inhibition of SGLT1 by phlorizin did not modify the activity of CFTR, although it resulted in inhibition of glycoconjugate synthesis. |
3(0,0,0,3) | Details |
| 7491973 | Shen BQ, Mrsny RJ, Finkbeiner WE, Widdicombe JH: Role of CFTR in secretion across human tracheal epithelium. Am J Physiol. 1995 Nov;269(5 Pt 1):L561-6. In support of the first hypothesis, we found 1) when the level of differentiation of cultures was varied by varying the culture conditions, there was a significant positive correlation between the levels of CFTR and the magnitude of mediator-induced Cl secretion. 2) Amiloride-insensitive baseline short-circuit current (Isc) and mediator-induced increases in Isc were inhibited by diphenylamine-2-carboxylic acid (DPAC) but not by 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), a pharmacology consistent with passage of apical membrane Cl current through CFTR; Ca-activated Cl channels are inhibited by DIDS but not by DPAC. 3) Raising temperature from 22 degrees to 37 degrees C increased 125I efflux, and this increase was inhibited by DPAC and blockers of protein kinase A, but not by DIDS or 1,2-bis (2-aminophenoxy) ethane-N,N,N',N'-tetraacetic acid-acetoxymethyl ester. |
2(0,0,0,2) | Details |
| 8766016 | Poulsen JH, Machen TE: HCO3-dependent pHi regulation in tracheal epithelial cells. . Pflugers Arch. 1996 Jul;432(3):546-54. Thus, the HCO3-dependent, Na- and Cl-independent, DPC-blockable pHi recovery may be largely due to an influx of HCO3 via CFTR Cl channels. 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. |
2(0,0,0,2) | 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. Potent CFTR inhibitors, such as glibenclamide and diphenylamine-2-carboxylic acid, triggered stomatal opening in darkness. |
33(0,1,1,3) | 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. |
32(0,1,1,2) | Details |
| 12562898 | Paradiso AM, Coakley RD, Boucher RC: Polarized distribution of HCO3- transport in human normal and cystic fibrosis nasal epithelia. J Physiol. 2003 Apr 1;548(Pt 1):203-18. Epub 2003 Jan 31. Recovery from this alkaline shift was dependent on mucosal Cl-, was insensitive to the AE inhibitor 4,4'-diisothiocyanatodihydrostilbene-2,2'-disulfonic acid (H2DIDS; 1.5 mM), but was sensitive to the cystic fibrosis transmembrane conductance regulator (CFTR) channel inhibitor diphenylamine-2-carboxylate (DPC; 100 microM). |
31(0,1,1,1) | 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. |
31(0,1,1,1) | 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 gene product affected in cystic fibrosis, the cystic fibrosis transmembrane conductance regulator (CFTR), is a chlorideselective ion channel that is regulated by cAMP-dependent protein kinase-mediated phosphorylation, ATP binding and ATP hydrolysis. 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. |
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| 9038891 | Nguyen TD, Koh DS, Moody MW, Fox NR, Savard CE, Kuver R, Hille B, Lee SP: Characterization of two distinct channels in cultured dog pancreatic duct epithelial cells. Am J Physiol. 1997 Jan;272(1 Pt 1):G172-80. In cystic fibrosis, for example, impaired function of the cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channel results in decreased pancreatic secretion and secondary pancreatic insufficiency. The Cl- conductances activated by cAMP and Ca2+ were distinct, since they were differentially inhibited by 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid and, to a lesser extent, by 5-nitro-2-(3-phenylpropylamino) and diphenylamine-2 carboxylate. |
2(0,0,0,2) | Details |
| 11117534 | Selvaraj NG, Omi E, Gibori G, Rao MC: Janus kinase 2 (JAK2) regulates prolactin-mediated transport in mouse mammary epithelial cells through phosphorylation of Na+-K+-2Cl- cotransporter. Mol Endocrinol. 2000 Dec;14(12):2054-65. Epithelial (Cl-) transport is achieved by the coordinated action of symporters such as the Na+-K+-2Cl- cotransporter (NKCC1) and channels such as the cystic fibrosis transmembrane conductance regulator (CFTR). This was inhibited by the NKCC1 blocker, and by the Cl- channel inhibitor, diphenylamine 2-carboxylate. |
2(0,0,0,2) | Details |
| 17128288 | Ostroumov K, Grandolfo M, Nistri A: The effects induced by the sulphonylurea glibenclamide on the neonatal rat spinal cord indicate a novel mechanism to control neuronal excitability and inhibitory neurotransmission. Br J Pharmacol. 2007 Jan;150(1):47-57. Epub 2006 Nov 27. The action of glibenclamide was mimicked by (500 microM) or the CFTR blocker diphenylamine-2,2-dicarboxylic acid (500 microM). |
11(0,0,1,6) | 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. The protein cystic fibrosis transmembrane conductance regulator (CFTR), the gene product defective in cystic fibrosis, functions as a cAMP-activated chloride channel in the plasma membrane. |
9(0,0,0,9) | Details |
| 15020588 | Robert R, Thoreau V, Norez C, Cantereau A, Kitzis A, Mettey Y, Rogier C, Becq F: Regulation of the cystic fibrosis transmembrane conductance regulator channel by beta-adrenergic agonists and vasoactive intestinal peptide in rat smooth muscle cells and its role in vasorelaxation. J Biol Chem. 2004 May 14;279(20):21160-8. Epub 2004 Mar 11. Here we show expression of the cystic fibrosis transmembrane conductance regulator (CFTR) Cl (-) channel in rat aortic smooth muscle cells. Smooth muscle CFTR possesses all of the pharmacological attributes of its epithelial homologues: stimulation by the CFTR pharmacological activators MPB-07 (EC (50) = 158 microm) and MPB-91 (EC (50) = 20 microm) and inhibition by glibenclamide and diphenylamine-2-carboxylic acid but not by 5,11,17,23-tetrasulfonato-25,26,27,28-tetramethoxy-calix [4] arene. |
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| 8807590 | Davidow CJ, Maser RL, Rome LA, Calvet JP, Grantham JJ: The cystic fibrosis transmembrane conductance regulator mediates transepithelial fluid secretion by human autosomal dominant polycystic kidney disease epithelium in vitro. Kidney Int. 1996 Jul;50(1):208-18. We now report that forskolin, which stimulates adenylate cyclase, increased the efflux rate constant for 36Cl in monolayers of ADPKD cells in vitro from 0.23 +/- 0.02 min-1 to 0.44 +/- 0.05 min-1 (N = 4) and that diphenylamine 2-carboxylate (DPC), which blocks channels, eliminated the forskolin-stimulated efflux from these cells. To establish whether the cAMP-regulated transporter, cystic fibrosis transmembrane conductance regulator (CFTR), may potentially be involved in the transport and fluid secretion of ADPKD epithelia, we examined CFTR mRNA and protein in these cultures. |
6(0,0,0,6) | Details |
| 18187619 | Wu D, Hu Z: Rutaecarpine induces secretion across rat isolated distal colon. . J Pharmacol Exp Ther. 2008 Apr;325(1):256-66. Epub 2008 Jan 10. Depolarizing the basolateral membrane with high K (+) showed that Rut-stimulated apical Cl (-) current was largely prevented by cystic fibrosis transmembrane conductance regulator (CFTR) inhibitors. Evidence that Rut-stimulated I (SC) was due to Cl (-) secretion is based on 1) inhibition of current by bumetanide; 2) Cl (-) channel blockers diphenylamine-2-carboxylate, 5-nitro-2-(3-phenylpropylamino)- and glibenclamide; and 3) removal of Cl (-) ions in bath solution. |
2(0,0,0,2) | Details |
| 11498992 | Zhou SS, Zang YM: [Effects of monocarboxylic acid derivatives on cardiac ventricular CFTR Cl- channels in guinea pig]. Sheng Li Xue Bao. 1999 Jun;51(3):297-302. Anthracene-9-carboxylic acid (9-AC) added to the bath solution further enhanced the outward component of isoproterenol-induced currents in a reversible manner, whereas 5-nitro-2-(3-phenylpropylamino) (NPPB) or diphenylamine-2-carboxylic acid (DPC) induced a biphasic effect on the currents. |
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. |
8(0,0,1,3) | Details |
| 7517633 | Ohrui T, Skach W, Thompson M, Matsumoto-Pon J, Calayag C, Widdicombe JH: Radiotracer studies of cystic fibrosis transmembrane conductance regulator expressed in Xenopus oocytes. Am J Physiol. 1994 Jun;266(6 Pt 1):C1586-93. We measured fluxes of radiotracers in Xenopus oocytes expressing the cystic fibrosis transmembrane conductance regulator (CFTR). Increases in halide efflux were blocked by diphenylamine-2-carboxylic acid but not by 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid. |
8(0,0,0,8) | 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. |
2(0,0,0,2) | Details |
| 16015685 | He Q, Zhu JX, Xing Y, Tsang LL, Yang N, Rowlands DK, Chung YW, Chan HC: Tetramethylpyrazine stimulates cystic fibrosis transmembrane conductance regulator-mediated anion secretion in distal colon of rodents. World J Gastroenterol. 2005 Jul 21;11(27):4173-9. The TMP-elicited I (SC) as well as forskolin- or IBMX-induced I (SC) were abolished in mice with homozygous mutation of the cystic fibrosis transmembrane conductance regulator (CFTR) presenting defective CFTR functions and secretions. RESULTS: TMP stimulated a concentration-dependent rise in I (SC), which was dependent on both Cl (-) and HCO (3)(-), and inhibited by apical application of diphenylamine-2,2'-dicarboxylic acid (DPC) and glibenclamide, but resistant to 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid disodium salt hydrate (DIDS). |
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| 1705554 | Montrose-Rafizadeh C, Guggino WB, Montrose MH: Cellular differentiation regulates expression of Cl- transport and cystic fibrosis transmembrane conductance regulator mRNA in human intestinal cells. J Biol Chem. 1991 Mar 5;266(7):4495-9. The gene defective in cystic fibrosis has recently been shown to code for a membrane protein designated the "cystic fibrosis transmembrane conductance regulator" (CFTR) protein. Cellular differentiation also causes a 5-fold increase in second messenger-regulated Cl- transport which is sensitive to a Cl- channel blocker (diphenylamine 2-carboxylate). |
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| 10788432 | Jiang Q, Li J, Dubroff R, Ahn YJ, Foskett JK, Engelhardt J, Kleyman TR: Epithelial channels regulate cystic fibrosis transmembrane conductance regulator channels in Xenopus oocytes. J Biol Chem. 2000 May 5;275(18):13266-74. The cystic fibrosis transmembrane conductance regulator (CFTR), in addition to its well defined Cl (-) channel properties, regulates other ion channels. The forskolin/3-isobutyl-1-methylxanthine-stimulated whole-cell conductance in hCFTR-mENaC co-injected oocytes was amiloride-insensitive, indicating an inhibition of mENaC following hCFTR activation, and it was blocked by DPC (diphenylamine-2-carboxylic acid) and was DIDS (4, 4'-diisothiocyanatostilbene-2,2'-disulfonic acid)-insensitive. |
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| 8661992 | Tauc M, Bidet M, Poujeol P: currents activated by calcitonin and cAMP in primary cultures of rabbit distal convoluted tubule. J Membr Biol. 1996 Apr;150(3):255-73. This current was inhibited by 10 (-3) M diphenylamine-2-carboxylate (DPC) and 10 (-4) M 5-nitro-2-(3-phenylpropylamino)- (NPPB) and was insensitive to 10 (-3) M 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS). These characteristics are similar to those described for the cystic fibrosis transmembrane conductance regulator (CFTR) Cl- conductance. |
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| 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. This suggests that a DIDS-insensitive Cl- channel other than CFTR is active in the SP response. 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 |
| 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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| 7504926 | McCray PB Jr, Bettencourt JD, Bastacky J, Denning GM, Welsh MJ: Expression of CFTR and a cAMP-stimulated secretory current in cultured human fetal alveolar epithelial cells. Am J Respir Cell Mol Biol. 1993 Dec;9(6):578-85. Apical diphenylamine-2-carboxylate (DPC), a Cl- channel inhibitor, caused no significant change in basal Isc. |
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| 9575788 | Boockfor FR, Morris RA, DeSimone DC, Hunt DM, Walsh KB: Sertoli cell expression of the cystic fibrosis transmembrane conductance regulator. Am J Physiol. 1998 Apr;274(4 Pt 1):C922-30. Mutations of the cystic fibrosis transmembrane conductance regulator (CFTR) gene have been associated with a number of male reproductive problems, including testis abnormalities and a reduction in germ cell quality and number. Application of the membrane-soluble cAMP analog, 8-chlorophenyl-thio-cAMP, resulted in the activation of a Cl- current that displayed a permeability sequence of Br- > I- > or = Cl- and was blocked by diphenylamine-2-carboxylate and glibenclamide. |
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| 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. The cystic fibrosis transmembrane conductance regulator (CFTR) or the small conductance cAMP-activated chloride channel encoded by the CFTR gene has been shown to play an important role in the formation of the epididymal fluid microenvironment. 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. |
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| 16183670 | Ballard ST, Trout L, Garrison J, Inglis SK: Ionic mechanism of forskolin-induced liquid secretion by porcine bronchi. Am J Physiol Lung Cell Mol Physiol. 2006 Jan;290(1):L97-104. Epub 2005 Sep 23. This pathway is thought to be CFTR dependent and thus defective in cystic fibrosis; however, the ionic mechanism that drives this secretion process is incompletely understood. The forskolin-induced Jv was significantly inhibited by the anion channel blockers 5-nitro-2-(3-phenylpropylamino) diphenylamine-2-carboxylate, and glibenclamide. |
1(0,0,0,1) | Details |
| 18833323 | Yang ZH, Yu HJ, Pan A, Du JY, Ruan YC, Ko WH, Chan HC, Zhou WL: Cellular mechanisms underlying the laxative effect of flavonol on rat constipation model. PLoS One. 2008 Oct 3;3(10):e3348. METHODS/PRINCIPAL FINDINGS: In isolated rat colonic crypts, mucosal addition of (100 microM) elicited a concentration-dependent and sustained increase in the short-circuit current (I (SC)), which could be inhibited in Cl- free solution or by bumetanide and DPC (diphenylamine-2-carboxylic acid), but not by DIDS (4, 4'- diisothiocyanatostilbene-2, 2'-disulfonic acid). -evoked whole cell current which exhibited a linear I-V relationship and time-and voltage- independent characteristics was inhibited by DPC, indicating that the cAMP activated Cl- conductance most likely CFTR (cystic fibrosis transmembrane conductance regulator) was involved. |
1(0,0,0,1) | Details |