Receptor binding and biological effects of insulin and insulin-like growth factor I during the cell cycle in a human leukemic cell line

1988 ◽  
Vol 117 (4_Suppl) ◽  
pp. S2-S3
Author(s):  
R. GOSSLA ◽  
W. HARTMANN ◽  
J . ◽  
J. ZAPE ◽  
U. VETTER
Keyword(s):  
Cell Cycle ◽  
Growth Factor ◽  
Cell Line ◽  
Receptor Binding ◽  
Biological Effects ◽  
Leukemic Cell ◽  
Insulin Like Growth Factor ◽  
Leukemic Cell Line ◽  
Factor I ◽  
Human Leukemic Cell Line

Characteristics of 25-Hydroxycholesterol-Induced Apoptosis in the Human Leukemic Cell Line CEM

1997 ◽  
Vol 235 (1) ◽  
pp. 35-47 ◽  
Author(s):  
Sylvette Ayala-Torres ◽  
Peter C. Moller ◽  
Betty H. Johnson ◽  
E.Brad Thompson
Keyword(s):  
Cell Line ◽  
Leukemic Cell ◽  
Leukemic Cell Line ◽  
Human Leukemic Cell ◽  
Human Leukemic Cell Line ◽  
Induced Apoptosis

scholarly journals Insulin-like growth factor-I signaling is modified during chondrocyte differentiation

2004 ◽  
Vol 183 (3) ◽  
pp. 477-486 ◽  
Author(s):  
Chanika Phornphutkul ◽  
Ke-Ying Wu ◽  
Xu Yang ◽  
Qian Chen ◽  
Philip A Gruppuso
Keyword(s):  
Growth Factor ◽  
Cell Line ◽  
Chondrocyte Differentiation ◽  
Erk Pathway ◽  
Insulin Like Growth Factor ◽  
Erk Activation ◽  
Atdc5 Cell ◽  
Factor I ◽  
Proliferation And Differentiation ◽  
Igf I

Insulin-like growth factor-I (IGF-I) is a critical regulator of skeletal growth. While IGF-I has been shown to be a potent chondrocyte mitogen in vitro, its role in chondrocyte differentiation is less well characterized. We chose to study the action of IGF-I on an accepted model of chondrocyte differentiation, the ATDC5 cell line. Insulin concentrations sufficiently high to interact with the IGF-I receptor are routinely used to induce ATDC5 cells to differentiate. Therefore, we first examined the ability of IGF-I to promote chondrocyte differentiation at physiological concentrations. IGF-I could induce differentiation of these cells at concentrations below 10 nM. However, increasing IGF-I concentrations were less potent at inducing differentiation. We hypothesized that mitogenic effects of IGF-I might inhibit its differentiating effects. Indeed, the extracellular-signal-regulated kinase (ERK)-pathway inhibitor PD98059 inhibited ATDC5 cell DNA synthesis while enhancing differentiation. This suggested that the ability of IGF-I to promote both proliferation and differentiation might require that its signaling be modulated through the differentiation process. We therefore compared IGF-I-mediated ERK activation in proliferating and hypertrophic chondrocytes. IGF-I potently induced ERK activation in proliferating cells, but minimal ERK response was seen in hypertrophic cells. In contrast, IGF-I-mediated Akt activation was unchanged by differentiation, indicating intact upstream IGF-I receptor signaling. Similar findings were observed in the RCJ3.1C5.18 chondrogenic cell line and in primary chick chondrocytes. We conclude that IGF-I promotes both proliferation and differentiation of chondrocytes and that the differentiation effects of IGF-I may require uncoupling of signaling to the ERK pathway.

scholarly journals The insulin-like growth factor-I receptor inhibitor NVP-AEW541 provokes cell cycle arrest and apoptosis in multiple myeloma cells

2008 ◽  
Vol 141 (4) ◽  
pp. 470-482 ◽  
Author(s):  
Patricia Maiso ◽  
Enrique M. Ocio ◽  
Mercedes Garayoa ◽  
Juan C. Montero ◽  
Francesco Hofmann ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Multiple Myeloma ◽  
Growth Factor ◽  
Cell Cycle Arrest ◽  
Insulin Like Growth Factor ◽  
Myeloma Cells ◽  
Factor I ◽  
Cycle Arrest ◽  
Growth Factor I ◽  
Receptor Inhibitor
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