Targeting Pyk2 to beta1-integrin-containing focal contacts rescues fibronectin-stimulated signaling and haptotactic motility defects of focal adhesion kinase-null cells

Focal adhesion kinase-null (FAK-/-) fibroblasts exhibit morphological and motility defects that are reversed by focal adhesion kinase (FAK) reexpression. The FAK-related kinase, proline-rich tyrosine kinase 2 (Pyk2), is expressed in FAK-/- cells, yet it exhibits a perinuclear distribution and does n...

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Veröffentlicht in:The Journal of cell biology 2001-01, Vol.152 (1), p.97
Hauptverfasser: Klingbeil, Candice K, Hauck, Christof R, Hsia, Datsun A, Jones, K C
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Sprache:eng
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Zusammenfassung:Focal adhesion kinase-null (FAK-/-) fibroblasts exhibit morphological and motility defects that are reversed by focal adhesion kinase (FAK) reexpression. The FAK-related kinase, proline-rich tyrosine kinase 2 (Pyk2), is expressed in FAK-/- cells, yet it exhibits a perinuclear distribution and does not functionally substitute for FAK.
ISSN:0021-9525
1540-8140