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Takao Sakai, M.D., Ph.D.Assistant Staff
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Research Profile
Cells in all tissues are in contact with organized complexes of structural molecules called the extracellular matrix (ECM). The ECM induces a variety of signals that regulate the behavior of cells and fundamental physiological processes. As a consequence, tissues or organs keep their normal architecture and homeostasis. Aberrations in signal transduction from the ECM cause chronic degenerative and fibrotic disorders.
The overall long-term objective of my laboratory is to increase understanding of the molecular mechanisms underlying tissue-specific constitution induced by interactions between ECM and cell-surface receptor integrins and their downstream signaling molecules.
We study cell-ECM interactions during development, tissue repair, and carcinogenesis using in vivo transgenic mouse models.
We are also pursuing studies on tendon biology and tissue engineering to increase understanding of how tendon cells construct tendon tissues in normal and pathological conditions. We focus on the microenvironment during mesenchymal stem cell differentiation into tendon cells and on a basic helix-loop-helix type transcription factor, scleraxis, which is specifically expressed in tendon cells.
We use extensive mouse genetic approaches, including conditional knockout technology, as well as a wide range of biochemical, cellular, and molecular biological techniques.
Key References
- Honda K, et al. Epidermal hyperplasia and papillomatosis in mice with a keratinocyte-restrictive deletion of csk. Carcinogenesis 2007; 28:2074-81.
- Nyberg P, et al. Interactions with fibronectin attenuate the virulence of Streptococcus pyogenes. EMBO J 2004;23:2166-74.
- Bae E, Sakai T, Mosher DF. Assembly of exogenous fibronectin by fibronectin-null cells is dependent on the adhesive substrate. J Biol Chem 2004;279:35749-59.
- Sakai T, et al. Integrin-linked kinase (ILK) is required for polarizing the epiblast, cell adhesion and controlling actin accumulation. Genes Dev 2003;17:926-40.