Acidic fibroblast growth factor (aFGF), fused to diphtheria toxin and
translocated into cells, stimulated DNA synthesis in toxin-resistant c
ells lacking functional aFGF receptors while having a high number of d
iphtheria toxin receptors. In NIH 3T3 cells that lack diphtheria toxin
receptors, but have receptors for aFGF, both aFGF and the fusion prot
ein induced tyrosine phosphorylation, but only aFGF as such entered th
e nuclei and stimulated DNA synthesis. The results indicate that signa
ling occurs partly through cell surface receptors and partly by transp
ort of the growth factor into the cell.