['Activation of hepatic stellate cells (HSC) plays an integral role in hepatic fibrosis. HSC activation increases fibronectin (alpha(5)beta(1)) receptor expression and interactions between alpha(5)beta(1) and the extracellular matrix increase collagen synthesis. It is unclear how signaling by the alpha(5)beta(1) receptor initiates these changes. We aimed to determine the signaling cascade after alpha(5)beta(1) stimulation in activated HSC.', 'HSC were isolated from male Sprague-Dawley rats. Activated HSC were exposed to beads coated with fibronectin (ligand for alpha(5)beta(1)) or D-polylysine (inert control). HSC were stained with FTC-labeled antibodies against classes of signaling molecules. Tyrosine phosphorylation was blocked using genistein or herbimycin A. The fraction of beads with localized immunostaining (indicating accumulation of signaling protein) was determined.', 'The majority of cytoskeletal proteins, Src substrates, Src kinases and members of the ERK and JNK signaling molecule families require actin cytoskeletal organization and tyrosine-kinase-mediated phosphorylation to accumulate. Several proteins (e.g. tensin, FAK) accumulated in the absence of tyrosine phosphorylation.'] Is initial signaling of the fibronectin receptor ( alpha5beta1 integrin ) in hepatic stellate cells independent of tyrosine phosphorylation?