ニフジ アキラ
Nifuji Akira
二藤 彰 所属 鶴見大学 歯学部 歯学科 薬理学 職種 教授 |
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論文種別 | 【査読あり】 研究論文(学術雑誌) |
言語種別 | 英語 |
査読の有無 | 査読あり |
表題 | Overexpression of cas-interacting zinc finger protein (CIZ) suppresses proliferation and enhances expression of type I collagen gene in osteoblast-like MC3T3E1 cells |
掲載誌名 | 正式名:EXPERIMENTAL CELL RESEARCH ISSNコード:00144827 |
出版社 | ACADEMIC PRESS INC |
巻・号・頁 | 261(2),pp.329-335 |
著者・共著者 | K Furuya,T Nakamoto,ZJ Shen,K Tsuji,A Nifuji,H Hirai,M Noda |
発行年月 | 2000/12 |
概要 | Osteoblasts are the cells which form bone under the regulation not only by hormones and cytokines but also by ECM molecules via their attachment. To obtain insights into the role of intracellular signaling molecules operating to mediate the attachment-related regulation of osteoblastic functions, we investigated in osteoblast-like MC3T3E1 cells the effects of the overexpression of CIZ, a novel signaling protein which interacts with p130(Cas). In MC3T3E1 cells, CIZ mRNA is expressed constitutively, Endogenous CIZ was localized in the MC3T3E1 cells with relatively high levels of accumulation at the attachment sites when the cells were cultured on fibronectin, collagen, or BSA CIZ overexpression increased the number of adhesion plaques and reduced proliferation of the cells compared to that of control cells transfected with an empty vector, Furthermore, CIZ overexpression enhanced type I collagen mRNA expression, the most abundant constituent of bone matrix and a major product of osteoblasts. Analysis of the promoter region of type I collagen gene identified the presence of a consensus CIZ-binding sequence, which indeed conferred responsiveness to CIZ overexpression to a heterologous |