Cellular and molecular actions of CCN2/CTGF and its role under physiological and pathological conditions
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- Satoshi Kubota
- Department of Biochemistry and Molecular Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Advanced Research Center for Oral and Craniofacial Sciences (ARCOCS), Okayama University Dental School, 2-5-1 Shikata-cho, Kita-ku, Okayama 700-8525, Japan
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- Masaharu Takigawa
- Department of Biochemistry and Molecular Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Advanced Research Center for Oral and Craniofacial Sciences (ARCOCS), Okayama University Dental School, 2-5-1 Shikata-cho, Kita-ku, Okayama 700-8525, Japan
書誌事項
- 公開日
- 2014-10-03
- 資源種別
- journal article
- DOI
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- 10.1042/cs20140264
- 公開者
- Portland Press Ltd.
この論文をさがす
説明
<jats:p>CCN family protein 2 (CCN2), also widely known as connective tissue growth factor (CTGF), is one of the founding members of the CCN family of matricellular proteins. Extensive investigation on CCN2 over decades has revealed the novel molecular action and functional properties of this unique signalling modulator. By its interaction with multiple molecular counterparts, CCN2 yields highly diverse and context-dependent biological outcomes in a variety of microenvironments. Nowadays, CCN2 is recognized to conduct the harmonized development of relevant tissues, such as cartilage and bone, in the skeletal system, by manipulating extracellular signalling molecules involved therein by acting as a hub through a web. However, on the other hand, CCN2 occasionally plays profound roles in major human biological disorders, including fibrosis and malignancies in major organs and tissues, by modulating the actions of key molecules involved in these clinical entities. In this review, the physiological and pathological roles of this unique protein are comprehensively summarized from a molecular network-based viewpoint of CCN2 functionalities.</jats:p>
収録刊行物
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- Clinical Science
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Clinical Science 128 (3), 181-196, 2014-10-03
Portland Press Ltd.
