Brancolini C, Bottega S, Schneider C
International Center for Genetic Engineering and Biotechnology (I.C.G.E.B.) Trieste, Italy.
J Cell Biol. 1992 Jun;117(6):1251-61. doi: 10.1083/jcb.117.6.1251.
In this report we analyze the protein product of a growth arrest-specific gene, gas2, by means of an affinity-purified antibody raised against the protein produced in bacteria. The regulation of Gas2 biosynthesis reflects the pattern of mRNA expression (Schneider, C., R. King, and L. Philipson. 1988. Cell. 54:787-793): its relative level is tightly associated with growth arrest. Gas2 seems to be regulated also at the posttranslational level via a phosphorylation mechanism. Gas2 is well conserved during the evolution with the same apparent molecular mass (36 kD) between mouse and human. We also demonstrate that Gas2 is a component of the microfilament system. It colocalizes with actin fiber, at the cell border and also along the stress fiber, in growth-arrested NIH 3T3 cells. The pattern of distribution, detected in arrested cells, can also be observed in growing cells when they are microinjected with the purified GST-Gas2 protein. In none of the analyzed oncogene-transformed NIH 3T3 cell lines was Gas2 expression induced under serum starvation.
在本报告中，我们通过针对细菌中产生的蛋白质制备的亲和纯化抗体，分析了一种生长停滞特异性基因gas2的蛋白质产物。Gas2生物合成的调节反映了mRNA表达模式（施奈德，C.，R.金，和L.菲利普森。1988年。《细胞》。54:787 - 793）：其相对水平与生长停滞紧密相关。Gas2似乎也通过磷酸化机制在翻译后水平受到调节。Gas2在进化过程中高度保守，在小鼠和人类之间具有相同的表观分子量（36 kD）。我们还证明Gas2是微丝系统的一个组成部分。在生长停滞的NIH 3T3细胞中，它与肌动蛋白纤维共定位，位于细胞边界以及应力纤维上。在停滞细胞中检测到的分布模式，当向生长中的细胞显微注射纯化的GST - Gas2蛋白时也能观察到。在分析的任何一种癌基因转化的NIH 3T3细胞系中，血清饥饿条件下均未诱导Gas2表达。
