Name | protein kinase C (protein family or complex) |
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Synonyms | Protein kinase C; PKC |
Name | diphenylamine |
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CAS |
PubMed | Abstract | RScore(About this table) | |
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7562609 | Gosling M, Smith JW, Poyner DR: Characterization of a volume-sensitive 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. |
current in rat 0(0,0,0,0) | Details |
1323920 | Tamaoki J, Kanemura T, Sakai N, Isono K, Chiyotani A, Yamauchi F, Takizawa T, Konno K: secretion across canine tracheal epithelium through cyclo-oxygenase stimulation and cAMP production. Acta Physiol Scand. 1992 May;145(1):1-6. The -induced increase in Isc was not altered by preincubation of cells with autonomic antagonists (phentolamine, atropine), the lipoxygenase inhibitor AA-861, the protein kinase C inhibitor H-7, or the Na channel blocker amiloride, but it was inhibited by each of indomethacin, piroxicam, the Cl channel blocker diphenylamine-2-carboxylate, the Cl transport inhibitor and Cl-free medium. |
increases Cl 0(0,0,0,0) | Details |
7932649 | Bescond J, Bois P, Petit-Jacques J, Lenfant J: Characterization of an angiotensin-II-activated current in rabbit sino-atrial cells. J Membr Biol. 1994 Jun;140(2):153-61. Anthracene-9-carboxylic acid and diphenylamine-2-carboxylic acid channels blockers) were found to be effective in blocking the AII-sensitive current. The linear segment of the current-voltage relation can be totally inhibited by the competitive AII-receptor (AT1) antagonist losartan and by the presence of intracellular protein kinase C inhibitor, whereas the outward rectification is only slightly changed. |
2(0,0,0,2) | Details |
8203530 | Sahi J, Goldstein JL, Layden TJ, Rao MC: Cyclic AMP- and phorbol ester-regulated Cl- permeabilities in primary cultures of human and rabbit colonocytes. Am J Physiol. 1994 May;266(5 Pt 1):G846-55. Depending on the secretagogue, this influx was inhibited 50-90% by the Cl- channel blocker diphenylamine-2-carboxylate (DPC; 50 microM) and > or = 65% by the Na-K-2Cl cotransport inhibitor (10 microM). Phorbol 12,13-dibutyrate, an activator of protein kinase C, increased Cl- permeability 3.8-fold in human and 2.4-fold in rabbit colonocytes. |
2(0,0,0,2) | Details |
8376764 | Illera VA, Perandones CE, Stunz LL, Mower DA Jr, Ashman RF: Apoptosis in splenic B lymphocytes. J Immunol. 1993 Sep 15;151(6):2965-73. Regulation by protein kinase C and IL-4.. The percentage of apoptotic cells measured by flow cytometry and the percentage of fragmented DNA measured by the diphenylamine method were nearly equal, regardless of the method of apoptotic regulation. |
2(0,0,0,2) | Details |
8942733 | Desai GN, Sahi J, Reddy PM, Venkatasubramanian J, Vidyasagar D, Rao MC: transport in primary cultures of rabbit colonocytes at different stages of development. Gastroenterology. 1996 Dec;111(6):1541-50. Influx was inhibited significantly by the Cl- channel (50 mumol/L diphenylamine-2-carboxylate) and the Na (+)-K (+)- 2Cl- cotransport (10 mumol/L inhibitors. The 3',5'-cyclic monophosphate (cAMP)-dependent secretagogues, (1 mumol/L), forskolin (1 mumol/L), and 8-bromo-cAMP (100 mumol/L), and the protein kinase C activator, phorbol 12-13 dibutyrate (1 mumol/L), increased Cl- influx significantly in all groups with adults showing greatest stimulation. |
1(0,0,0,1) | Details |
8747558 | Weber WM, Liebold KM, Reifarth FW, Clauss W: The Ca (2+)-induced leak current in Xenopus oocytes is indeed mediated through a Cl- channel. J Membr Biol. 1995 Dec;148(3):263-75. Injection of phorbol 12- 13- (PMA), a protein kinase C activating phorbol ester, stimulated the Cl- current. |
1(0,0,0,1) | Details |
1284079 | Kubo M, Okada Y: Volume-regulatory Cl- channel currents in cultured human epithelial cells. . J Physiol. 1992 Oct;456:351-71. The outward and inward currents were equally inhibited by a carboxylate analogue Cl- channel blocker, 5-nitro-2-(3-phenylpropylamino)- (NPPB) or diphenylamine-2-carboxylate (DPC) at higher doses (IC50 = 25 for NPPB or 350 microM for DPC). was still effective in the presence of inhibitors of lipoxygenase (nordihydroguaiaretic acid, 10 microM), cyclo-oxygenase (indomethacin, 10 microM) and protein kinase C (polymyxin B, 30 microM). |
1(0,0,0,1) | 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]. Secretion of ACTH in response to cAMP-independent stimulants such as the protein kinase C activator 12-O-tetradecanoylphorbol-13- or the calcium channel agonist BAY K 8644 were blocked by compound 131 as was the secretory response to 8-bromoadenosine 3',5'-cyclic monophosphate. |
1(0,0,0,1) | 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. Phorbol 12,13-dibutyrate also stimulated cotransport activity (P < 0.03), which was abolished by protein kinase C (PKC) blockade by staurosporine. |
1(0,0,0,1) | Details |
7777588 | LaVoie HA, Witorsch RJ: Investigation of intracellular signals mediating the anti-apoptotic action of prolactin in Nb2 lymphoma cells. Proc Soc Exp Biol Med. 1995 Jul;209(3):257-69. A short-term assay was implemented that quantitates fragmented DNA released from the genome by reaction with diphenylamine. Signals previously implicated in prolactin induction of mitogenesis in Nb2 cells were investigated for their role in prolactin inhibition of apoptosis including: protein kinase C activation, arachidonic acid metabolism, polyamine production, phosphorylation, and extracellular |
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. Spontaneous apoptosis was decreased in spleen T cells by protein kinase C activation, and was increased by H7 and staurosporine, which inhibits protein kinases, in contrast with the behavior of thymocytes. 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 |
7756457 | Chan HC, Hon FK, Wong PY: Stimulatory and inhibitory effects of a phorbol ester on secretion by rat epididymal epithelium. Biol Reprod. 1995 Mar;52(3):638-44. The effects of a protein kinase C (PKC) activator, phorbol 12- 13- (PMA), on Cl- secretion by rat cauda epididymal epithelium were studied through use of the short-circuit current (Isc) technique. The PMA-induced Isc was blocked by the Cl channel blocker, diphenylamine-2-carboxylate, but not by 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid. |
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. 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). |
0(0,0,0,0) | 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). |
0(0,0,0,0) | Details |