Le Cam A, Le Cam G
Biochem J. 1985 Sep 15;230(3):603-7. doi: 10.1042/bj2300603.
The effect of acute inflammation on the production of the major phosphorylated protein (PP63) excreted by rat hepatocytes was investigated. Both intra- and extracellular forms of the protein labelled with [32P]Pi, [3H]fucose and [35S]methionine were immunoprecipitated with monospecific polyclonal antibodies, and relative rates of PP63 synthesis were measured. The hepatocytes of acutely inflamed rats produced and excreted 85% less 32P- and 3H-labelled PP63 than did control cells. This decreased amount of PP63 did not result from an impairment in the phosphorylation or glycosylation processes or from a blockade in excretion, but rather was found to be due to extensive shut-off in biosynthesis of the protein as measured by [35S]methionine incorporation. Thus PP63 would appear to represent a new negatively regulated acute-phase protein.
研究了急性炎症对大鼠肝细胞分泌的主要磷酸化蛋白（PP63）产生的影响。用[32P]Pi、[3H]岩藻糖和[35S]甲硫氨酸标记的该蛋白的细胞内和细胞外形式，均用单特异性多克隆抗体进行免疫沉淀，并测定PP63的相对合成速率。急性炎症大鼠的肝细胞产生和分泌的32P和3H标记的PP63比对照细胞少85%。PP63量的减少并非由于磷酸化或糖基化过程受损或排泄受阻，而是通过[35S]甲硫氨酸掺入测定发现是由于该蛋白生物合成的广泛关闭。因此，PP63似乎代表一种新的负调节急性期蛋白。
