Hoshino Y, Enomoto N, Sakamoto N, Kurosaki M, Ikeda T, Marumo F, Sato C
Second Department of Internal Medicine, Faculty of Medicine, Tokyo Medical and Dental University, Japan.
Cancer Lett. 1993 Jul 30;71(1-3):119-23. doi: 10.1016/0304-3835(93)90106-j.
The c-met oncogene product is a cell-surface receptor, which ligand is believed to be the hepatocyte growth factor. We studied the expression of c-met oncogene in the regenerating rat liver after either partial hepatectomy or CCl4-induced liver injury. Northern blot analysis showed that after partial hepatectomy the transcripts of c-met decreased at 8 h, reached the minimum at 36 h, and returned to the steady level on the seventh day. In contrast with the hepatectomized liver, the transcripts of c-met increased after CCl4 treatment. These observations suggest that c-met transcription may be regulated differently depending on regeneration signals.
c-met原癌基因产物是一种细胞表面受体，其配体被认为是肝细胞生长因子。我们研究了部分肝切除或四氯化碳诱导肝损伤后再生大鼠肝脏中c-met原癌基因的表达。Northern印迹分析表明，部分肝切除后，c-met的转录本在8小时时减少，在36小时时达到最低水平，并在第七天恢复到稳定水平。与肝切除的肝脏相反，四氯化碳处理后c-met的转录本增加。这些观察结果表明，c-met转录可能根据再生信号的不同而受到不同的调节。
