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APO‐1(CD95)‐mediated apoptosis in Jurkat cells does not involve src kinases or CD45

机译:APO-1(CD95)介导的Jurkat细胞凋亡不涉及src激酶或CD45

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>Tyrosine phosphorylation has been reported to be an early event required for APO-1/Fas(CD95) signalling in lymphocytes [Eischen, C.M., Dick, C.J. and Leibson, P.J. (1994) J. Immunol. 153, 1947–1954]. We have compared two mutant Jurkat cells, one largely deficient in expression of CD45 (J45.01) and a second one deficient in expression of p56lck (JCaM1.6) with wild type Jurkat cells for their ability to undergo APO-1-induced apoptosis. No significant difference was observed among the three cell lines. In the mutant Jurkat cells APO-1 triggering did not result in increased tyrosine phosphorylation of cytosolic proteins. Furthermore, herbimycin A did not inhibit but rather augmented apoptosis at concentrations which effectively degraded the src related kinases lck and fyn. The data suggest that APO-1-mediated signalling is independent from src kinases and CD45.
机译:据报道酪氨酸磷酸化是淋巴细胞中APO-1 / Fas(CD95)信号转导所必需的早期事件[Eischen,C.M.,Dick,C.J. and Leibson,P.J.(1994)J.Immunol。 153,1947–1954年]。我们已经比较了两种突变的Jurkat细胞,其中一种在CD45(J45.01)的表达上有很大的缺陷,而另一种在p56 lck (JCaM1.6)的表达上却与野生型Jurkat细胞的能力有关。经历APO-1诱导的凋亡。在三种细胞系之间未观察到显着差异。在突变的Jurkat细胞中,APO-1触发不会导致胞浆蛋白酪氨酸磷酸化增加。此外,除草霉素A在有效降解src相关激酶lck和fyn的浓度下不抑制而是增加凋亡。数据表明,APO-1介导的信号独立于src激酶和CD45。

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    《FEBS Letters》 |1995年第3期|共页
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