D'Ambrosio D, Cantrell D A, Frati L, Santoni A, Testi R
Department of Experimental Medicine, University of Rome La Sapienza, Italy.
Eur J Immunol. 1994 Mar;24(3):616-20. doi: 10.1002/eji.1830240319.
The involvement of p21ras in the induction of the early activation antigen CD69 was investigated in T cells. Expression of a v-Ha-ras coding for a constitutively active ras protein in Jurkat cells resulted in CD69 induction on the cell surface. Transfected ras was shown to be constitutively activated and functionally efficient, since it could be immunoprecipitated in the guanosine triphosphate (GTP)-bound form and it induced transactivation of an AP-1 consensus-chloramphenicol acetyltransferase reporter gene. The requirement for ras activation in T cell receptor (TcR) CD3-mediated CD69 induction was also investigated. The expression of a dominant negative c-Ha-ras-N17 mutant markedly reduced the amount of GTP that could be immunoprecipitated from ras proteins after TcR/CD3 triggering in Jurkat cells, and concomitantly decreased TcR/CD3-mediated CD69 induction. These results suggest a central role for ras in TcR/CD3-mediated CD69 expression in T cells.
研究了p21ras在T细胞中诱导早期激活抗原CD69过程中的作用。在Jurkat细胞中表达编码组成型活性ras蛋白的v-Ha-ras，导致细胞表面CD69的诱导表达。转染的ras被证明是组成型激活且功能有效的，因为它可以以结合鸟苷三磷酸（GTP）的形式被免疫沉淀，并且它能诱导AP-1共有序列-氯霉素乙酰转移酶报告基因的反式激活。还研究了T细胞受体（TcR）-CD3介导的CD69诱导中ras激活的必要性。在Jurkat细胞中，TcR/CD3触发后，显性负性c-Ha-ras-N17突变体的表达显著减少了从ras蛋白中可免疫沉淀的GTP量，并同时降低了TcR/CD3介导的CD69诱导。这些结果表明ras在T细胞中TcR/CD3介导的CD69表达中起核心作用。
