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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2006.9
- 수록면
- 215 - 219 (5page)
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It has been reported that liver is a primary organ producing insulin like growth factor-1 (IGF-1). Cell proliferation has been regulated by diverse growth factors. Thus, we examined the effect of IGF-1 on cell proliferation and its related signal pathways in primary cultured rat hepatocytes. In the present study, IGF-1 stimulates [³H]-thymidine incorporation. The treatement of IGF-1 also increased expression of CDK-2 and CDK-4 but decreased expression of p27 Kip1 and p21WAF1/Cip1. IGF-1-induced stimulation of cell proliferation was prevented by genistein and herbymycin A (tyrosine kinase inhibitors). In addition, IGF-1-induced stimulation of [³H]-thymidine incorporation was blocked by neomycin, U73122 (phospholipase C inhibitors), staurosporine, H-7, and bisindolylmaleimide I(protein kinase C inhibitors). Moreover, the treatment of PD98059 (a p44/42 MAPK inhibitor) and SP600125 (a SAPK/JNK inhibitor), but not SB203580 (a p38 MAPK inhibitor) blocked IGF-1-induced stimulation of cell proliferation. In conclusion, IGF-1 stimulates cell proliferation via PKC and MAPK activation in hepatocytes.
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UCI(KEPA) : I410-ECN-0101-2009-510-016363042