对“PDK1 形成用于 NF-κB 激活的 T 细胞受体诱导信号复合物”的评论
Comment on "PDK1 nucleates T cell receptor-induced signaling complex for NF-kappaB activation".
作者信息
Gruber Thomas, Freeley Michael, Thuille Nikolaus, Heit Isabelle, Shaw Stephen, Long Aideen, Baier Gottfried
机构信息
Department for Medical Genetics, Molecular and Clinical Pharmacology, Innsbruck Medical University, Austria.
出版信息
Science. 2006 Apr 7;312(5770):55; author reply 55. doi: 10.1126/science.1115362.
We observe that protein kinase C (PKC) is phosphorylated on the activation loop at threonine 538 (Thr-538) before T cell activation. Our results are inconsistent with the conclusions of Lee et al. (Reports, 1 April 2005, p. 114) that the Thr-538 phosphorylation of PKC is regulated by T cell receptor activation. Other mechanisms, such as autophosphorylation of Thr-219, might orchestrate the cellular function of PKC in T cells.
我们观察到，在T细胞激活之前，蛋白激酶C（PKC）在激活环的苏氨酸538（Thr-538）位点发生磷酸化。我们的结果与Lee等人（《报告》，2005年4月1日，第114页）得出的结论不一致，他们认为PKC的Thr-538磷酸化受T细胞受体激活的调节。其他机制，如Thr-219的自磷酸化，可能在T细胞中协调PKC的细胞功能。
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