The roles of LAT in platelet signaling induced by collagen, TxA2, or ADP.
The roles of LAT in platelet signaling induced by collagen, TxA2, or ADP.
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LAT 在胶原蛋白、TxA2 或 ADP 诱导的血小板信号传导中的作用。
DOI：
10.1006/bbrc.2002.6738
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发表时间：
2002
期刊：
影响因子：
--
通讯作者：
KentGartner,T
中科院分区：
文献类型：
--
作者：
Cho,MoonJ;Pestina,TamaraI;Steward,ShirleyA;Jackson,CarlW;KentGartner,T
The work presented here demonstrates that platelets from mice lacking LAT (linker for the activation of T cells) show reversible aggregation in response to concentrations of collagen that cause TxA2/ADP-dependent irreversible aggregation of control platelets. The aggregation defect of the LAT-deficient platelets was shown to be the result of almost no TxA2 production and significantly diminished ADP secretion. In contrast, the LAT deficiency does not affect aggregation induced by high concentrations of collagen because that aggregation is not dependent on TxA2 and/or ADP. Even though ADP and TxA2 provide amplification signals for platelet activation in response to low concentrations of collagen, LAT-deficient platelets hyperaggregate to low levels of U46619, a TxA2 analog, or ADP. Though the mechanism(s) of costimulatory signals by collagen, ADP, and TxA2 remains unidentified, it is clear that LAT plays a positive role in collagen-induced, TxA2/ADP-dependent aggregation, and a negative role in TxA2 or ADP-induced platelet aggregation.
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DOI：
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发表时间：
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