作者: Mariana Resnicoff , Andres Ferber , Renato Baserga , Consuelo D'Ambrosio
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摘要: Abstract By a frame-shift mutation, we have engineered human IGF-I receptor (IGF-IR) cDNA that produces 486 amino acids long (plus the 30 of signal peptide). This receptor, which designated as 486/STOP, is partially secreted into medium cells in culture and markedly inhibits autophosphorylation endogenous IGF-IRs well activation signaling pathway. The 486/STOP acts strong dominant negative for several growth functions: (a) it monolayers; (b) transformed soft agar; (c) induces extensive apoptosis vivo; (d) tumorigenesis syngeneic rats. first demonstration IGF-IR can induce massive tumor vivo.