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Requirement of Nck adaptors for actin dynamics and cell migration stimulated by platelet-derived growth factor B

G M Rivera1, S Antoku, S Gelkop

  • 1Raymond and Beverly Sackler Laboratory of Genetics and Molecular Medicine, Department of Genetics and Developmental Biology and Center for Cell Analysis and Modeling, University of Connecticut Health Center, Farmington, CT 06030, USA.

Proceedings of the National Academy of Sciences of the United States of America
|June 14, 2006
PubMed

Insights

Mammalian Nck adaptors are crucial for platelet-derived growth factor (PDGF)-B signaling, linking the PDGF receptor to actin cytoskeleton reorganization and cell movement. This pathway involves the Crk-associated substrate (p130(Cas)) for proper cellular response.

Area of Science:

  • Cellular signaling
  • Cytoskeletal dynamics
  • Molecular adaptors

Background:

  • Nck adaptors (Src homology 2/3 domain) link extracellular signals to actin regulation.
  • Platelet-derived growth factor receptor (PDGFbetaR) signaling influences cell behavior.

Purpose of the Study:

  • Investigate the role of mammalian Nck adaptors in PDGFbetaR signaling to the actin cytoskeleton.
  • Elucidate the specific Nck-binding proteins involved in PDGF-B-stimulated cellular responses.

Main Methods:

  • Analysis of tyrosine-phosphorylated proteins in PDGF-B-stimulated cells.
  • Utilizing Nck- and p130(Cas)-deficient cell lines.
  • Microscopy to observe cytoskeletal rearrangements and protein colocalization.

Main Results:

  • Nck adaptors are essential for PDGF-B-induced cytoskeletal reorganization and chemotaxis.
  • Crk-associated substrate (p130(Cas)) is a major Nck SH2 domain-binding protein in these cells.
  • Absence of Nck or p130(Cas) prevents membrane ruffling and actin bundle disassembly.

Conclusions:

  • Nck adaptors link activated PDGFbetaR to actin dynamics via p130(Cas).
  • This signaling pathway is critical for cellular responses to PDGF-B.

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