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首页> 外文期刊>Archives of Biochemistry and Biophysics >CAMP does not inhibit convulxin-induced tyrosyl-phosphorylation of human platelet proteins, including PLC gamma 2, but completely blocks the integrin alpha(IIb)beta(3)-dependent dephosphorylation step: Comparisons with RGDS peptide, cytochalasin D, a
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CAMP does not inhibit convulxin-induced tyrosyl-phosphorylation of human platelet proteins, including PLC gamma 2, but completely blocks the integrin alpha(IIb)beta(3)-dependent dephosphorylation step: Comparisons with RGDS peptide, cytochalasin D, a

机译：CAMP不会抑制惊厥毒素诱导的人类血小板蛋白（包括PLCγ2）的酪氨酰磷酸化，但会完全阻断整合素α（IIb）β（3）依赖性去磷酸化步骤：与RGDS肽，细胞松弛素D，

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Convulxin (Cvx) isolated from Crotalus durissus terrificus venom, induces platelet aggregation, phospholipase C (PLC) activation, and tyrosyl-phosphorylation (PTP) of multiple proteins, including PLC gamma 2 by a mechanism independent of integrin alpha(IIb)beta(3). However, PTP induced by Cvx is followed by a dephosphorylation step in a platelet aggregation-dependent manner. Here we show that increasing intraplatelet content of cAMP with forskolin is associated with the inhibition of Cvx-induced platelet aggregation, ATP secretion, and inositol-phosphates production. However, the early onset of Cvx-induced PTP is not sensitive to cAMP (including PLC gamma 2), and it also occurs in the presence of integrin alpha(IIb)beta(3)-antagonist (RGDS peptide, RGDS) or inhibitors of actin polymerization (cytochalasin D, CD) and tyrosine-phosphatases (phenylarsine oxide, PAO). However, forskolin, RGDS, and CD prevented the dephosphorylation step together with inhibition of platelet aggregation, whereas in the presence of phenylarsine oxide (PAO) the dephosphorylation step was replaced by an increase in the number and intensity of tyrosyl-phosphorylated proteins. Our data provide evidence to conclude that (i) cAMP inhibits platelet aggregation at a downstream site to PLC gamma 2 tyrosyl-phosphorylation; (ii) Cvx-induced PTP is independent on integrin alpha(IIb)beta(3) engagement, actin polymerization, and tyrosine-phosphatases activation; (iii) integrin alpha(IIb)beta(3) mediates the dephosphorylation step in a platelet aggregation-dependent manner; and (iv) Cvx and collagen stimulate platelets by a similar signal transduction pathway. (C) 1998 Academic Press. [References: 34]
机译：从猪屎豆的毒液中分离出的惊厥毒素（Cvx）通过独立于整联蛋白alpha（IIb）beta（3）的机制诱导血小板聚集，磷脂酶C（PLC）激活和酪氨酸磷酸化（PTP）包括PLCγ2在内的多种蛋白质。 ）。但是，由Cvx诱导的PTP之后是血小板聚集依赖性方式的去磷酸化步骤。在这里，我们显示与福司柯林一起提高cAMP的血小板内含量与抑制Cvx诱导的血小板聚集，ATP分泌和肌醇磷酸生成有关。但是，Cvx诱导的PTP的早期发作对cAMP（包括PLCγ2）不敏感，并且它也存在于整联蛋白α（IIb）β（3）拮抗剂（RGDS肽，RGDS）或CYP抑制剂的存在下肌动蛋白聚合反应（细胞松弛素D，CD）和酪氨酸磷酸酶（氧化苯砷酰，PAO）。但是，福司可林，RGDS和CD阻止了去磷酸化步骤并抑制了血小板凝集，而在存在苯ar氧化物（PAO）的情况下，去磷酸化步骤被酪氨酰磷酸化蛋白的数量和强度增加所取代。我们的数据提供了得出以下结论的证据：（i）cAMP抑制PLCγ2酪氨酰磷酸化下游位点的血小板聚集; （ii）Cvx诱导的PTP独立于整联蛋白alpha（IIb）beta（3）参与，肌动蛋白聚合和酪氨酸磷酸酶激活; （iii）整合素α（IIb）β（3）以血小板聚集依赖性的方式介导去磷酸化步骤; （iv）Cvx和胶原蛋白通过类似的信号转导途径刺激血小板。 （C）1998年学术出版社。 [参考：34]

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