['The renotropic growth factors (GFs), hepatocyte GF (HGF), epidermal GF (EGF), and insulin-like GF-I (IGF-I) accelerate renal regeneration in animal models after toxic or ischemic injury. These GFs initiate their biological effects on renal tubular cells by interaction with specific transmembrane receptor tyrosine kinases.', 'In the proximal tubular cell line PT-1, the biological effects of HGF, EGF, and IGF-I and the growth-inhibitory effects of different tyrosine kinase inhibitors (TKIs) were investigated. Receptor binding and tyrosine kinase phosphorylation were determined by ligand binding studies and Western blot analysis.', 'HGF, EGF, and IGF-I bound with nanomolar affinity to their specific cell membrane receptor tyrosine kinases. In contrast to EGF or IGF-I, HGF induced a variety of cell morphological changes, including cell scattering, formation of tubular structures, and expression of long microvilli on the apical cell membrane. HGF was a 10-fold more potent and more effective growth promoter than EGF or IGF-I. Among the TKIs tested, the mitogenic effect of HGF could be more specifically inhibited by emodin and tyrphostin, that of EGF by methyl-2,5-dihydroxycinnamate, lavendustin A, and genistein, and that of IGF-I by geldanamycin.'] Are renal proximal tubular cell growth and differentiation differentially modulated by renotropic growth factors and tyrosine kinase inhibitors?