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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 저널정보
- 대한약학회 Archives of pharmacal research : a publication of the Pharmaceutical Society of Korea Archives of pharmacal research : a publication of the Pharmaceutical Society of Korea 제30권 제6호
- 발행연도
- 2007.1
- 수록면
- 739 - 742 (4page)
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이 논문의 연구 히스토리 (4)
2003
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Although it has been demonstrated that p21$^{WAF1/Cip1}$ could be induced by transforming growth factor-${\beta}$1 (TGF-${\beta}$1) in a Smad-dependent manner, the cross-talk of Smad signaling Pathway with other signaling pathways still remains poorly understood. In this study, we investigated a possible role of protein kinase C (PKC) signaling pathway in TGF-${\beta}$1 induction of p21$^{WAF1/Cip1}$ in human keratinocytes HaCaT cells. Our data show that PKC is required for TGF-${\beta}$1 induction of p21$^{WAF1/Cip1}$, as evidenced by the fact that specific inhibition of PKC leads to a decrease in p21$^{WAF1/Cip1}$ protein and mRNA expression induced by TGF-${\beta}$1. And this notion is further supported by the observation that activation of p21$^{WAF1/Cip1}$ promoter activity is dramatically attenuated by treatment with PKC inhibitor. However, PKC signaling pathway is not associated with TGF-${\beta}$1 activation of Smad signaling pathway, because inhibitor of PKC signaling pathway does not affect nuclear translocation of Smads induced by TGF-${\beta}$1, Taken together, our data suggest that PKC signaling pathway is required for p21$^{WAF1/Cip1}$ expression by TGF-${\beta}$1 , which is independent of Smad signaling pathway.
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