Disease relevance of YWHAG

• Our data show that Hodgkin's disease derived B-cell lines uniformly proved resistant to staurosporine, a protein kinase C inhibitor that preferentially stimulates the mitochondrial apoptotic pathway [1].
• Only tyrosine phosphorylation was significantly inhibited by pertussis toxin and by the protein kinase C inhibitor GF109203X [2].
• The protein kinase C inhibitor, CGP 41 251, reverses decreased daunomycin uptake in a human drug-resistant ovarian carcinoma cell line [3].
• The protein kinase C inhibitor H-7 (2-20 microM) inhibited dose-dependently the infectivity of the vesicular stomatitis virus on cultured human fibroblasts [4].
• Finally, although the protein kinase C stimulator phorbol-12-myristate-13-acetate enhanced EAAT2 mRNA levels after hypoxia, protein kinase C inhibitor bisindolylmaleimide I had the opposite effect [5].

Psychiatry related information on YWHAG

• Death by protein kinase C inhibitor: a stressful event [6].

High impact information on YWHAG

• Thus, pretreatment of platelets with the cyclooxygenase (COX) inhibitor, indomethacin (20 microM), the thromboxane antagonist SQ29,548 (1 microM), or the protein kinase C inhibitor GF109203X (5 microM) prevents platelet activation by microparticles [7].
• The rapid biogenesis of secretory lysosomes was blocked by specific protein kinase C inhibitor but not by brefeldin A [8].
• Tyrosine phosphorylation elicited by carbachol, but not by cell adhesion to fibronectin, is reduced by the protein kinase C inhibitor GF 109203X [9].
• The impact of continuous intracoronary infusion of 10(-7) mol/L staurosporine, a potent protein kinase C inhibitor, on global and regional myocardial function (sonomicrometry), subendocardial blood flow (ENDO, microspheres), and infarct size (IS, triphenyltetrazolium chloride staining after 120 minutes of reperfusion) was analyzed [10].
• We also examined effects of 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H-7), another protein kinase C inhibitor, on responses to bradykinin and adenosine [11].

Chemical compound and disease context of YWHAG

• The selective protein kinase C inhibitor GF 109203X inhibits phorbol ester-induced morphological and functional differentiation of SH-SY5Y human neuroblastoma cells [12].

Biological context of YWHAG

• PKCI increased radiation induced apoptosis in LM cells (5% to 20%) but reduced apoptosis slightly in AT cells [13].
• The signal of low pH value was blocked by the protein kinase inhibitor H-7 or Calphostin C (protein kinase C inhibitor), indicating the involvement of protein kinase C in the alternative splicing [14].
• CD2 up-regulation appeared to be elicited by a protein kinase C-dependent mechanism because it was abrogated by staurosporine, a potent protein kinase C inhibitor [15].
• We wished to test the effect of a protein kinase C inhibitor staurosporine (100 nmol/l) on the elevated antiport activity, and the degree of stimulation achieved by exogenous diacyl glycerol [16].
• These phenomena appear to involve protein kinase C; two PMA analogs, 4 alpha-phorbol and 4 alpha-PMA, lacking the ability to activate protein kinase C fail to induce elevated levels of gene expression, and the protein kinase C inhibitor, H7 [1-(5-isoquinolinylsulfonyl)-2-methylpiperazine dihydrochloride[, inhibits the enhancement induced by PMA [17].

Anatomical context of YWHAG

• The human 14-3-3gamma gene (HGMW-approved symbol YWHAG) is highly expressed in brain, skeletal muscle, and heart [18].
• These results demonstrate that the protein kinase C inhibitor H-7 has a specific and rapid effect on the actin cytoskeleton, and furthermore H-7 may have biochemical effects beyond those mediated by inhibition of protein kinase C or the cyclic nucleotide dependent kinases [19].
• Protein kinase C inhibitor H-7 alters the actin cytoskeleton of cultured cells [19].
• Forty-five minutes of exposure of Swiss 3T3 cells to 200 microM of either HA1004 (which is comparable to H-7 with respect to inhibition of cyclic nucleotide dependent kinases) or to the protein kinase C inhibitor sangivamycin did not induce the actin alterations characteristic of H-7 [19].
• Contrasting actions of staurosporine, a protein kinase C inhibitor, on human neutrophils and primary mouse epidermal cells [20].

Associations of YWHAG with chemical compounds

• The protein kinase C inhibitor, sphingosine (10(-6) M), markedly attenuated responses to bradykinin [11].
• Unlike ADP- or thrombin-induced PA, BL6 cell-induced PA was not inhibited by Calphostin-C (a potent protein kinase C inhibitor) or cilostazol (a potent inhibitor of PA based on inhibition of cyclic AMP phosphodiesterase) [21].
• In contrast, no significant inhibition of clustering was observed with protein kinase C inhibitor GF109203X, rapamycin, or heparin [22].
• Incubation in protein kinase C inhibitor chelerythrine killed androgen-independent but not androgen-dependent cells [23].
• Benoxaprofen-mediated activation of lucigenin-enhanced chemiluminescence by PMNL was increased by UV radiation and was particularly sensitive to inhibition by the selective protein kinase C inhibitor H-7 [24].

Analytical, diagnostic and therapeutic context of YWHAG

• The protein kinase C inhibitor staurosporine does not prevent ischemic preconditioning in swine [10].
• Sequence analysis of the ryanodine receptor: possible association with a 12K, FK506-binding immunophilin/protein kinase C inhibitor [25].
• The presence of a protein kinase C inhibitor, H7 or calphostin C, in the medium eliminated the stimulatory effects of P. gingivalis fimbriae on Fc rosette formation [26].
• Northern blot analysis showed that cytokine-induced tissue factor mRNA was significantly reduced in human umbilical vein endothelial cells treated with calphostin C, a specific protein kinase C inhibitor [27].
• Key words for the literature search were 'diabetic', 'retinopathy', 'treatment', 'laser photocoagulation', 'vitrectomy', 'corticosteroid', 'protein kinase C inhibitor', and 'VEGF inhibitor'. DATA EXTRACTION [28].

References