Effect of the Insulin-like Growth Factor I Receptor on Ionizing Radiation-Induced Cell Death in Mouse Embryo Fibroblasts

1997 ◽  
Vol 235 (1) ◽  
pp. 287-294 ◽  
Author(s):  
Shin Nakamura ◽  
Hiroshi Watanabe ◽  
Masahiko Miura ◽  
Takehito Sasaki
Keyword(s):  
Cell Death ◽  
Growth Factor ◽  
Ionizing Radiation ◽  
Mouse Embryo ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Mouse Embryo Fibroblasts ◽  
Radiation Induced ◽  
Growth Factor I ◽  
Embryo Fibroblasts

scholarly journals Insulin-like growth factor I receptor signaling in transformation by src oncogenes.

1997 ◽  
Vol 17 (7) ◽  
pp. 3744-3754 ◽  
Author(s):  
B Valentinis ◽  
A Morrione ◽  
S J Taylor ◽  
R Baserga
Keyword(s):  
Growth Factor ◽  
Mouse Embryo ◽  
Soft Agar ◽  
Insulin Like Growth Factor ◽  
Full Transformation ◽  
Factor I ◽  
Mouse Embryo Fibroblasts ◽  
Igf I ◽  
Growth Factor I ◽  
Embryo Fibroblasts

R- cells, a line of mouse embryo fibroblasts with a targeted disruption of the insulin-like growth factor I (IGF-I) receptor genes, are refractory to transformation by several viral and cellular oncogenes. Using colony formation in soft agar as a measure of full transformation, we report here that R- cells can be transformed by v-src, although they still cannot be transformed by the activated c-src527 (mutation at tyrosine 527 to phenylalanine), which readily transforms mouse embryo cells with a wild-type number of IGF-I receptors (W cells). Although v-src is a more potent inducer of tyrosine phosphorylation than c-src527, the extent of phosphorylation of either insulin receptor substrate 1 or Shc, two of the major substrates of the IGF-I receptor, does not seem sufficiently different to explain the qualitative difference in soft agar growth. v-src, however, is considerably more efficient than c-src527 in its ability to tyrosyl phosphorylate, in R- cells, the focal adhesion kinase, Stat1, and p130cas. These results indicate that v-src, but not c-src527, can bypass the requirement for a functional IGF-I receptor in the full transformation of mouse embryo fibroblasts and suggest that qualitative and quantitative differences between the two oncogenes can be used to identify some of the signals relevant to the mechanism(s) of transformation.

scholarly journals Transformation of Late Passage Insulin-Like Growth Factor-I Receptor Null Mouse Embryo Fibroblasts by SV40 T Antigen

2006 ◽  
Vol 66 (8) ◽  
pp. 4233-4239 ◽  
Author(s):  
Susan L. Spence ◽  
Arthur L. Shaffer ◽  
Louis M. Staudt ◽  
Sewit Amde ◽  
Sutana Manney ◽  
...  
Keyword(s):  
Growth Factor ◽  
Mouse Embryo ◽  
T Antigen ◽  
Null Mouse ◽  
Insulin Like Growth Factor ◽  
Sv40 T Antigen ◽  
Factor I ◽  
Mouse Embryo Fibroblasts ◽  
Late Passage ◽  
Growth Factor I

Insulin-like growth factor I receptor regulates the radiation-induced G2/M checkpoint in HeLa cells

2018 ◽  
Vol 503 (4) ◽  
pp. 2977-2983 ◽  
Author(s):  
Nisha Gowri Manila ◽  
Atsushi Kaida ◽  
Ken-ichi Nakahama ◽  
Masahiko Miura
Keyword(s):  
Growth Factor ◽  
Hela Cells ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Radiation Induced ◽  
Growth Factor I

Ethanol Promotes Cell Death by Inhibition of the Insulin-Like Growth Factor I Receptor

1997 ◽  
Vol 21 (6) ◽  
pp. 1121-1127 ◽  
Author(s):  
Shi-jun Cui ◽  
Manorama Tewari ◽  
Tim Schneider ◽  
Raphael Rubin
Keyword(s):  
Cell Death ◽  
Growth Factor ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Growth Factor I

scholarly journals Induction of apoptosis in cerebellar granule neurons by low potassium: inhibition of death by insulin-like growth factor I and cAMP

1993 ◽  
Vol 90 (23) ◽  
pp. 10989-10993 ◽  
Author(s):  
S R D'Mello ◽  
C Galli ◽  
T Ciotti ◽  
P Calissano
Keyword(s):  
Cell Death ◽  
Nervous System ◽  
Growth Factor ◽  
Cerebellar Granule Neurons ◽  
Granule Neurons ◽  
Insulin Like Growth Factor ◽  
Cerebellar Granule ◽  
Factor I ◽  
Growth Factor I ◽  
Low K

High levels of extracellular K+ ensure proper development and prolong survival of cerebellar granule neurons in culture. We find that when switched from a culture medium containing high K+ (25 mM) to one containing a low but more physiological K+ concentration (5 mM), differentiated granule neurons degenerate and die. Death induced by low K+ is due to apoptosis (programmed cell death), a form of cell death observed extensively in the developing nervous system and believed to be necessary for proper neurogenesis. The death process is accompanied by cleavage of genomic DNA into internucleosome-sized fragments, a hallmark of apoptosis. Inhibitors of transcription and translation suppress apoptosis induced by low K+, suggesting the necessity for newly synthesized gene products for activation of the process. Death can be prevented by insulin-like growth factor I but not by several other growth/neurotrophic factors. cAMP but not the protein kinase C activator phorbol 12-myristate 13-acetate can also support survival in low K+. In view of the large numbers of granule neurons that can be homogeneously cultured, our results offer the prospect of an excellent model system to study the mechanisms underlying apoptosis in the central nervous system and the suppression of this process by survival factors such as insulin-like growth factor I.

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