Fibronectin and Integrins in Cell Adhesion, Signaling, and Morphogenesis

Authors

  • SHINGO MIYAMOTO,

    1. Craniofacial Developmental Biology and Regeneration Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892-4370. USA
    2. National Kyusyu Cancer Center, Notame 3-1-1, Minami-ku, Fukuoka 815, Japan
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  • BEN-ZION KATHZ,

    1. Craniofacial Developmental Biology and Regeneration Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892-4370. USA
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  • ROBERT M. LAFRENIE,

    1. Northeastern Ontario Regional Cancer Centre, Sudbury, Ontario, P3E 5J1 Canada
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  • KENNETH M. YAMADA

    Corresponding author
    1. Craniofacial Developmental Biology and Regeneration Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892-4370. USA
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Address for communication: Kenneth Yamada, Building 30, Room 421, 30 Convent Dr. MSC 4370, Bethesda, MD 20892-4370. Phone: 301/496-9124; fax: 301/402-0897; e-mail: ky4w@nih.gov

Abstract

ABSTRACT: Fibronectin and integrins play crucial roles in a variety of morphogenetic processes, in which they mediate cell adhesion, migration, and signal transduction. They induce hierarchical transmembrane organization of cytoskeletal and signaling molecules into multimolecular complexes of more than 30 proteins. Organization of these complexes is a synergistic process dependent on integrin aggregation and occupancy, as well as tyrosine phosphorylation. Integrins also cooperate with growth-factor receptors to enhance signaling. Fibronectin and integrins induce a variety of downstream effects, including enhanced transcription factor activity, induction of over 30 genes (>half novel), and altered expression of over 100 proteins. Fibronectin and integrins therefore trigger a hierarchy of signaling responses involved in regulating processes crucial for normal morphogenesis, including cell adhesion, migration, and specific gene expression.

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