Disease relevance of Ywhaz

• This response was insensitive to pertussis toxin and was partially blocked by the protein kinase C inhibitor H7 [1].
• H7 (20 mg/kg body weight IP, 30 min prior to DPH), a protein kinase C inhibitor, was able to prevent the DPH-induced GSH depletion only at the lower DPH dose used [2].
• Staurosporine, a toxin isolated from Streptomyces staurospores bacteria, is widely used as a protein kinase C inhibitor in signal transduction research [3].
• Staurosporine, a protein kinase C inhibitor, eliminated the hypertrophy and the effect on L-type Ca2+ current [4].

High impact information on Ywhaz

• The protein kinase C inhibitor staurosporine (20 nmol/L) but neither indomethacin nor L-NAME also inhibited captopril-induced upregulation of beta-ARs [5].
• The protective effects of IB-MECA against stunning were completely blocked by pretreatment with the nonselective adenosine receptor antagonist 8-p-sulfophenyl theophylline or the specific protein kinase C inhibitor chelerythrine [6].
• The thapsigargin-induced secretion in adherent cells was inhibited by protein kinase C down-regulation and by the protein kinase C inhibitor GF 109203X, but not by calphostin C [7].
• These reactions, however, were not dependent on protein kinase C; the cascade was totally resistant to the actions of a selective protein kinase C inhibitor, Ro31-7549, whereas release of the secretory granule marker, hexosaminidase, was blocked by this agent [8].
• Moreover, a protein kinase C inhibitor, calphostin C, dramatically suppressed IL-6 release, whereas a protein kinase A inhibitor H-89 and a Ca2+ chelator EGTA failed [9].

Biological context of Ywhaz

• PMA- but not SP-induced NK-1 R desensitization and phosphorylation were abolished by the protein kinase C inhibitor bisindolylmaleimide 1 [10].
• Stimulation of apoptosis by staurosporine, a protein kinase C inhibitor, reduces the LPR in Rat1-Myc cells in a dose-dependent manner [11].
• Sex differences in rat hepatic cytolethality of the protein kinase C inhibitor safingol: role of biotransformation [12].
• Nifedipine (an L-type Ca2+ channel blocker), manganese acetate (an inorganic Ca2+ channel blocker), and staurosporine (a nonselective protein kinase C inhibitor), but not the selective protein kinase C inhibitor chelerythrine, inhibited the enhancement of vasoconstriction by MEPE [13].
• The aim of the present work was to examine the effects of 4'-N-benzoyl staurosporine (CGP 41251), a protein kinase C inhibitor with broad antiproliferative activity in many cell lines, on the rat isolated heart contractility under normoxic and hypoxic conditions [14].

Anatomical context of Ywhaz

• The activation of JNK by ethanol or acetaldehyde was insensitive to the treatment of hepatocytes with genistein (tyrosine kinase inhibitor) and 2-[1-(3-dimethylaminopropyl)-1H-indol-3-yl]-3-(1H-indol-3-yl)maleimide (GF109203X) (protein kinase C inhibitor) [15].
• Calphostin C (500 nM), a protein kinase C inhibitor, caused a leftward shift of the curve in prostates from diabetic, but not control, rats [16].
• Preincubation of striatal synaptosomes with 10 microM of the protein kinase C inhibitor, Ro-31-8220, blocked the amphetamine-mediated increases in the levels of both phosphoser41-neuromodulin and site 3-phospho-synapsin I [17].
• The 110 kDa polypeptide and its fragments were phosphorylated by a nuclear envelope kinase and this phosphorylation was inhibited by a monoclonal antibody against protein kinase C and by a specific protein kinase C inhibitor obtained from bovine brain [18].
• Neither phorbol 12-myristate 13-acetate, dibutyryl cAMP, indomethacin nor a protein kinase C inhibitor H-7 affected NO production by Kupffer cells [19].

Associations of Ywhaz with chemical compounds

• Calphostin C, a protein kinase C inhibitor, attenuated the effect of insulin and IGF-I, whereas wortmannin, a phosphatidylinositol 3-kinase inhibitor, was ineffective [20].
• 5. Intracellular application of H-7 (20 microM; a protein kinase C inhibitor) reversed adenosine inhibition of IGABA while inclusion of cAMP (1 mM), H-9 (20 microM; a protein kinase A inhibitor) and BAPTA (10 mM; a chelator of calcium ions) in the recording pipette did not affect the depression of IGABA by adenosine [21].
• The ZG proliferogenic action of 10(-8) M ET-1 was reversed by both the protein kinase C inhibitor Ro31-8220 and the tyrosine kinase inhibitor tyrphostin-23; a complete blockade was obtained at a 10(-6)-M concentration of each inhibitor [22].
• The cyclo-oxygenase and lipoxygenase inhibitors indomethacin and nordihydroguaiaretic acid, and the protein kinase C inhibitor staurosporine, had no effect on the extent of arachidonic acid inhibition of transport, which suggests that the inhibitory effects of arachidonic acid result from a direct interaction with the transporter [23].
• CIE was also abolished by intra-floccular microinjection of the metabotropic glutamate receptor (mGluR) antagonist AIDA, and the protein kinase C inhibitor bisindolymaleimide I (BIS-I) [24].

Regulatory relationships of Ywhaz

• Moreover, pretreatment with the protein kinase C inhibitor (chelerythrine chloride) reduced the ischemia-induced activation of Pyk2 [25].
• Effects of pentoxifylline and protein kinase C inhibitor on phorbol ester-induced intercellular adhesion molecule-1 expression in brain microvascular endothelial cells [26].

Other interactions of Ywhaz

• Also, Ro-32-0432 (3-[8-[(dimethylamino)methyl]-6,7,8,9-tetrahydropyrido-[1,2-a]indol-10-yl]-4-(1-methyl-3-indolyl)-H-pyrrole-2,5-dione hydrochloride) (100nM), a protein kinase C inhibitor, completely inhibited ET-1-induced increases in TH activity and mRNA level [27].
• A protein kinase C inhibitor, calphostin C, suppressed endothelin-3-enhanced inducible NO synthase expression [28].
• TNF-alpha enhancement of IL-1beta-induced NO(-)(2) production was blocked by PD-98059, a selective mitogen-activated protein (MAP) kinase kinase inhibitor, but not calphostin C (Cal C), a protein kinase C inhibitor [29].
• The augmentation of flinching by CPT is also eliminated following a spinal pretreatment with MK-801 (NMDA receptor antagonist), cyclohexyladenosine (adenosine A(1) receptor agonist), N(G)-nitro-L-arginine methyl ester HCl (nitric oxide synthetase inhibitor), and chelerythrine (protein kinase C inhibitor) [30].

Analytical, diagnostic and therapeutic context of Ywhaz

• In the presence of calcium channel antagonist verapamil or protein kinase C inhibitor staurosporine, ACh produced a significant drop in heart rate but did not significantly affect coronary perfusion pressure and force of contraction [31].
• The sarafotoxin 6c-induced contraction after 24 hours of organ culture was attenuated by the transcriptional inhibitor actinomycin D and the translational inhibitor cycloheximide as well as the protein kinase C inhibitor Ro-31-8220 [32].

References