Anti-NCAM antibodies and soluble NCAM | NCAM-transfected COS-7 cells | Coprecipitates with NCAM140 | (Beggs et al., 1997) |
PDGF | Quiescent Swiss 3T3 vascular smooth muscle cells | Bell-shaped dose response BB-homodimer only | (Abedi et al., 1995; Rankin and Rozengurt, 1994) |
Vascular endothelial growth factor | Human umbilical vein endothelial cells | Rapid, partially PKC-dependent response | (Abedi and Zachary, 1997) |
Hepatocyte growth factor/scatter factor acting via the c-Met RTK | Human squamous carcinoma cells | Transient response, loss of phosphorylation corresponds with motile phenotype | (Matsumotoet al., 1994) |
Macrophage colony-stimulating factor via the M-CSF RTK | Human monocytes | Results in GRB2 binding to FAK | (Kharbanda et al., 1995) |
Bombesin, bradykinin, vasopressin, and endothelin acting via G-protein-coupled receptors | Quiescent Swiss 3T3 | Rapid response (seconds) | (Leeb-Lundberg et al., 1994; Zachary et al., 1992) |
Angiotensin II acting via G-protein-coupled receptor | Quiescent vascular smooth muscle cells | Rapid response | (Polte et al., 1994; Turner et al., 1995) |
Prolactin acting via a cytokine family receptor | Human breast carcinoma cells | Also results in paxillin phosphorylation | (Canbay et al., 1997) |
Intracellular acting bacterial toxin | Quiescent Swiss 3T3 | Response dissociated from PKC activation | (Lacerda et al., 1996) |
Bioactive lipids, e.g. sphingolipid metabolites and lysophosphatidic acid | Quiescent Swiss 3T3 | Rapid, response, independent of PKC activation and Ca2+ mobilization | (Seufferlein and Rozengurt, 1994a, b) |
Aggregation of the FcɛRI | Rat basophilic leukemia cells | Phosphorylation requires adherence | (Hamawy et al., 1993) |
Amyloid peptide | Differentiated neuroblastoma cultures | Effects with aggregated but not soluble peptide | (Zhanget al., 1994) |
Hyaluronan mediated by the HA receptor RHAMM | C-H-ras transformed 10T1/2 fibroblast cells | Rapid and transient response | (Hall et al., 1994) |