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Role of TGF‐β in EGF‐induced transformation of NRK cells is sustaining high‐level EGF‐signaling 1
Author(s) -
Kizaka-Kondoh Shinae,
Akiyama Nobutake,
Okayama Hiroto
Publication year - 2000
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(99)01784-6
Subject(s) - epidermal growth factor , mutant , transforming growth factor , transformation (genetics) , microbiology and biotechnology , signal transduction , transforming growth factor beta , receptor , cell growth , tgf alpha , epidermal growth factor receptor , autocrine signalling , biology , chemistry , biochemistry , gene
We have been isolating and analyzing NRK cell mutants, which fail to transform by epidermal growth factor (EGF) and transforming growth factor (TGF)‐β. One such mutant, R14, can respond to the growth inhibitory signal of TGF‐β to the same extent as parental NRK but fail to respond to the growth stimulatory signal of EGF. This mutant has a defect in EGF receptor (EGFR) expression. When R14 mutant expressed a high level of EGFR, however, EGF not only induced proliferation in this mutant but also induced transformation without the aid of TGF‐β. These findings suggest that the major role of TGF‐β in this transformation system should be to counteract the ligand‐dependent down‐regulation of EGFR, thereby sustaining high‐level EGF‐signaling.