| Name | cAMP dependent protein kinase (protein family or complex) |
|---|---|
| Synonyms | Protein kinase A; cAMP dependent protein kinase; cAMP dependent protein kinases |
| Name | diphenylamine |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 9649581 | Sorensen JB, Larsen EH: Patch clamp on the luminal membrane of exocrine gland acini from frog skin (Rana esculenta) reveals the presence of cystic fibrosis transmembrane conductance regulator-like Cl- channels activated by cyclic AMP. J Gen Physiol. 1998 Jul;112(1):19-31. In excised inside-out patches with 25 mM Cl- on the inside, activity of small (8-pS) linear Cl--selective channels was dependent upon bath ATP (1.5 mM) and increased upon exposure to cAMP-dependent protein kinase. In inside-out patches, the channels were blocked reversibly by 5-nitro-2-(3-phenylpropylamino) glibenclamide, and diphenylamine-2-carboxylic acid, whereas 4, 4-diisothiocyanatostilbene-2,2-disulfonic acid blocked channel activity completely and irreversibly. |
1(0,0,0,1) | 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. Despite negligible intracellular cAMP, the protein kinase A inhibitor H89 blocked basal and hCG-stimulated steroidogenesis. 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. |
1(0,0,0,1) | 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). H-89, a selective protein kinase A (PKA) inhibitor, blocked the vasorelaxant responses to |
1(0,0,0,1) | 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. |
0(0,0,0,0) | Details |
| 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. 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. In addition, a 13-pS conductance Cl- channel was measured in excised membrane patches exposed to the catalytic subunit of protein kinase A. |
1(0,0,0,1) | Details |
| 7658386 | Guinamard R, Chraibi A, Teulon J: A small-conductance Cl- channel in the mouse thick ascending limb that is activated by ATP and protein kinase A. J Physiol. 1995 May 15;485 ( Pt 1):97-112. The Cl- channel blockers 5-nitro-2-(3-phenylpropylamine)- (NPPB), 4,4'-diisothiocyanatostilbene-2,2'-disulphonic acid (DIDS) or glibenclamide, all at 0.1 mmol l-1, and diphenylamine-2-carboxylic acid (DPC), at 1 mmol l-1, inhibited the small channel activity by 80-100% in inside-out patches. 7. |
1(0,0,0,1) | Details |
| 8568854 | Chan HC, Zhou WL, Wong PY: Extracellular ATP activates both Ca (2+)- and cAMP-dependent Cl- conductances in rat epididymal cells. J Membr Biol. 1995 Sep;147(2):185-93. When applied to the later phase of the ATP-activated whole-cell current, the disulfonic acid stilbene DIDS (200 microM) could only inhibit 64% of the current while diphenylamine-dicarboxylic acid (DPC, 1 mM) completely inhibited it. |
0(0,0,0,0) | 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. |
0(0,0,0,0) | 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. 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). |
0(0,0,0,0) | 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. |
0(0,0,0,0) | 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. Immunoprecipitation and in vitro protein kinase A phosphorylation show the appearance of mature band C of CFTR. 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. |
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 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. |
1(0,0,0,1) | 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. Present evidence suggests that in mouse sperm the capacitation-associated membrane hyperpolarization is regulated by a cAMP/protein kinase A-dependent pathway involving activation of inwardly rectifying K+ channels and inhibition of epithelial channels (ENaCs). 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. |
1(0,0,0,1) | 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. CFTR expression, localisation and function were analysed in cultured smooth muscle cells using Reverse transcriptase (RT)-PCR and immunoprecipitation followed by protein kinase A phosphorylation, immunolocalisation and an iodide efflux assay, respectively. 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. |
1(0,0,0,1) | 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. Cystic fibrosis transmembrane conductance regulator (CFTR) is a protein kinase A (PKA) and ATP regulated Cl- channel. 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). |
1(0,0,0,1) | 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. Like H2O2, treatment induced a twofold increase in Isc that was reduced by the protein kinase A (PKA) inhibitors H-89 and KT5720. |
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. |
162(2,2,2,2) | 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)). |
81(1,1,1,1) | Details |
| 8769983 | Amlal H, Legoff C, Vernimmen C, Paillard M, Bichara M: Na (+)-K+(NH4+)-2Cl- cotransport in medullary thick ascending limb: control by PKA, PKC, and 20-HETE. Am J Physiol. 1996 Aug;271(2 Pt 1):C455-63. Cell pH was monitored in suspensions of medullary thick ascending limbs (MTALs) of rat kidney to determine possible effects of various transduction pathways on apical Na (+)-K+ (NH4+)-2Cl- cotransport, the activity of which was measured as the bumetanide-sensitive component of cell acidification caused by abrupt exposure to 4 mM NH4Cl. 8-Bromoadenosine 3',5'-cyclic monophosphate stimulated cotransport activity through activation of 3',5'-cyclic monophosphate (cAMP)-dependent protein kinase (PKA), since the cAMP effect was abolished by N-[2-(p- bromocinnamylamino) ethyl]-5-isoquinolinesulfonamide (H-89); stimulation by cAMP (P < 0.02) was observed even when other Na+, Cl-, and K+ carriers were blocked by ouabain, diphenylamine-2-carboxylate, and barium, which indicates that cotransport was directly affected by PKA. |
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 |
| 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. |
31(0,1,1,1) | 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. 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. Rut treatment resulted in the increase in intracellular cAMP levels and the activation of protein kinase A. |
2(0,0,0,2) | 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 channel-like nature of the cAMP-induced ATP-permeable pathway was also determined by assessing protein kinase A-activated single channel Cl (-) and ATP currents in excised inside-out patches of NRCM. |
1(0,0,0,1) | Details |
| 7562609 | Gosling M, Smith JW, Poyner DR: Characterization of a volume-sensitive current in rat osteoblast-like (ROS 17/2.8) cells. J Physiol. 1995 Jun 15;485 ( Pt 3):671-82. The current was relatively insensitive to diphenylamine-2-carboxylate (DPC), 500 microM producing only 22.5 +/- 4.0% inhibition. 5. Inhibitors of protein kinase A (H-89, 1 microM) and kinase (tyrphostin A25, 200 microM) were without effect upon activation of Cl- currents in response to hypotonic shock. |
1(0,0,0,1) | 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. This requires a low level of phosphorylation of CFTR by basal protein kinase A activity. 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). |
1(0,0,0,1) | 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. At the single-channel level, protein kinase A plus ATP activated single Cl (-) channels only in excised patches from ABP (+)/CFTR (+) cells. |
1(0,0,0,1) | Details |
| 1362444 | Huang SJ, Leung AY, Fu WO, Chung YW, Zhou TS, Chan PS, Wong PY: Electrophysiological studies of anion secretion in cultured human epididymal cells. J Physiol. 1992 Sep;455:455-69. The effect of on the whole-cell current was found to be mimicked by forskolin and could be abolished by including GDP beta S or a protein kinase A inhibitor in the pipette solution. This increase was blockable by diphenylamine-2-carboxylate (DPC, 1 mmol l-1). |
1(0,0,0,1) | Details |
| 8376790 | Perandones CE, Illera VA, Peckham D, Stunz LL, Ashman RF: Regulation of apoptosis in vitro in mature murine spleen T cells. . J Immunol. 1993 Oct 1;151(7):3521-9. The protein kinase A/G inhibitor HA1004 also decreased spleen T cell apoptosis. Assays for apoptosis included internucleosomal DNA cleavage by gel electrophoresis, percent fragmentation of DNA by the diphenylamine method, and percent of cells with hypodiploid DNA by flow cytometry. |
1(0,0,0,1) | Details |
| 7505913 | Becq F, Hollande E, Gola M: Phosphorylation-regulated low-conductance Cl- channels in a human pancreatic duct cell line. Pflugers Arch. 1993 Oct;425(1-2):1-8. The PKA-activated Cl- channel was 4,4'-diisothiocyanatostilbene-2,2'-disulphonic acid (DIDS, 100 mumol/l) and 4-acetamido-4'-isothiocyanatostilbene-2,2'-disulphonic acid (SITS, 100 mumol/l) insensitive, but was blocked by diphenylamine-2-carboxylic acid (DPC, 100 mumol/l). Reactivation of silent excised channels was achieved by adding protein kinase A (PKA, in the presence of ATP, cAMP and Mg2+). |
1(0,0,0,1) | 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. OBJECTIVES: The aim of this study was to determine the effects of Cl- channel blockers on the cardiac cystic fibrosis transmembrane conductance regulator (CFTR) Cl- current (ICl) and the protein kinase A-regulated L-type current (PKA-ICa). 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. |
1(0,0,0,1) | 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. Epithelial Na+ channels (ENaCs) are inhibited by the cystic fibrosis transmembrane conductance regulator (CFTR) when CFTR is activated by protein kinase A. SCN- or or when CFTR was inhibited by diphenylamine-carboxylate (DPC, 1 mmol l-1). 4. |
1(0,0,0,1) | 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. Protein kinase A (PKA)-activation of epithelial Na+ channels requires actin filaments. 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. |
1(0,0,0,1) | 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. |
1(0,0,0,1) | Details |
| 9124289 | Cantiello HF, Jackson GR Jr, Prat AG, Gazley JL, Forrest JN Jr, Ausiello DA: cAMP activates an ATP-conductive pathway in cultured shark rectal gland cells. Am J Physiol. 1997 Feb;272(2 Pt 1):C466-75. The cAMP-inducible ATP currents were insensitive to the Cl- channel blockers 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid, diphenylamine-2-carboxylate, and anthracene-9-carboxylic acid but were readily blocked by nifedipine (400 microM) and glibenclamide (400 microM). The nature of the electrodiffusional ATP movement was further assessed by single-channel analysis of either MgATP or Tris-ATP currents in excised inside-out patches, both spontaneous and after activation with protein kinase A. |
1(0,0,0,1) | Details |