Role of Gene33/RALT in oxidative stress-induced signal transduction in cardiac cells.

我们发现氧化应激处理的大鼠胚胎心脏源性H9c2细胞显示出Ralt mRNA和蛋白的显著诱导。H9c2细胞中稳定的过表达Ralt可阻止hb - egf诱导的信号转导。为了鉴定心脏细胞中与Ralt结合的内源性蛋白，我们进行了蛋白质组学分析，发现Ralt特异性地与14-3-3蛋白的几种不同亚型结合，而不依赖于其磷酸化状态。

We found that rat embryonic heart-derived H9c2 cells treated with oxidative stress exhibited a significant induction in Ralt mRNA and protein. Stable overexpression of Ralt in H9c2 cells prevented HB-EGF-induced signal transduction. To identify endogenous proteins that bind to Ralt in cardiac cells, we carried out a proteomic analysis and found that Ralt specifically bound to several different isoforms of 14-3-3 proteins independently of its phosphorylation status.