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First published online 27 May 2008
doi: 10.1242/jcs.024620

Journal of Cell Science 121, 2008-2017 (2008)
Published by The Company of Biologists 2008
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Research Article

Involvement of the nectin-afadin complex in PDGF-induced cell survival

Noriyuki Kanzaki1, Hisakazu Ogita1, Hitomi Komura1, Misa Ozaki1, Yasuhisa Sakamoto1, Takashi Majima1, Takeshi Ijuin2, Tadaomi Takenawa2 and Yoshimi Takai1,3,*

1 Department of Molecular Biology and Biochemistry, Osaka University Graduate School of Medicine/Faculty of Medicine, Osaka, Japan
2 Division of Lipid Biochemistry, Department of Biochemistry and Molecular Biology, Kobe University Graduate School of Medicine, 7-5-1, Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan
3 Division of Molecular and Cellular Biology, Department of Biochemistry and Molecular Biology, Kobe University Graduate School of Medicine, 7-5-1, Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan

* Author for correspondence (e-mail: ytakai{at}med.kobe-u.ac.jp)

Accepted 22 March 2008

The nectin-afadin complex is involved in the formation of cell-cell junctions, such as adherens junctions (AJs) and tight junctions (TJs). Nectins are Ca2+-independent immunoglobulin-like cell-cell adhesion molecules, whereas afadin is an intracellular nectin-binding protein that connects nectins to the cadherin-catenin system at AJs and to the claudin–zona-occludens (ZO) protein system at TJs. Afadin–/– mice show embryonic lethality, resulting from impaired migration and improper differentiation of cells due to disorganization of cell-cell junctions during gastrulation. However, it remains to be elucidated whether disruption of afadin affects apoptosis. In the present study, we first found that embryoid bodies derived from afadin-knockout embryonic stem (ES) cells contained many more apoptotic cells than those derived from wild-type ES cells. We also revealed that apoptosis induced by serum starvation or Fas-ligand stimulation was increased in cultured NIH3T3 cells when afadin or nectin-3 was knocked down. The nectin-afadin complex was involved in the platelet-derived growth factor (PDGF)-induced activation of phosphatidylinositol 3-kinase (PI3K)-Akt signaling for cell survival. This complex was associated with PDGF receptor on the plasma membrane at cell-cell adhesion sites. Thus, the nectin-afadin complex is involved in PDGF-induced cell survival, at least through the PI3K-Akt signaling pathway.

Key words: Afadin, Akt, Cell survival, Growth factor, Nectin, Phosphatidylinositol 3-kinase


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