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Signal transduction cascade shared by epidermal growth factor and platelet-derived growth factor is a major pathway for oncogenic transformation in NRK cells.
- A. Masuda, S. Kizaka-Kondoh, H. Miwatani, Y. Terada, H. Nojima, H. Okayama
- BiologyThe New biologist
- 1 May 1992
Analysis of two recessive, mutually complementary NRK cell mutants that are refractory to transformation by epidermal growth factor (EGF) and transforming growth factor-beta suggests that the EGF/PDGF cascade branches into mitogenic and oncogenic signals, the latter of which is required for soft agar growth and focus formation.
Oncogenic signal-induced ability to enter S phase in the absence of anchorage is the mechanism for the growth of transformed NRK cells in soft agar.
Cell cycle analysis of a rat cell line NRK-49F and its transformation-deficient mutants indicates that oncogenic signals confer on NRK the ability to enter S phase in the absence of anchorage and that this is the principal mechanism for its ability to grow in soft agar.
Targeted introduction of a diphtheria toxin-resistant point mutation into the chromosomal EF-2 locus by in vivo homologous recombination.
- M. Kido, H. Miwatani, K. Kohno, T. Uchida, Y. Okada
- BiologyCell structure and function
- 1 December 1991
This result shows that the specific point mutation was co-introduced with a second selective marker into an endogenous chromosomal gene and that the modified gene was expressed.
Secretion of Mr 46,000 protein from human hepatoma cells treated with tumor promotors is regulated by c-myc gene expression.
Results suggested that the expression of p46 was regulated by a factor that was activated in the growth state and by TPA treatment, and the effect of introduction of the competence gene c-myc into Huh-7 Cl-4 cells was examined.