Suppression of apoptosis by survival factors is important for the maintenance of normal tissue homoeostasis and the response to infection or injury. Survival factors such as insulin-like growth factor-I (IGF-I) initiate a signalling cascade that starts by tyrosine phosphorylation of substrates leading to the activation of serine kinases that modulate the activity of members of the Bcl-2 family, which regulates the apoptotic machinery in most cells. Tumour cells often have enhanced survival mechanisms due either to up-regulation of the IGF-I receptor and its ligands or to loss of function of a phosphatase (PTEN) that regulates part of this survival pathway. The C-terminus of the IGF-I receptor appears to be a regulatory domain for the anti-apoptotic activity of this receptor, and certain residues within the C-terminus are essential for this regulatory activity. Knowledge of the proteins and pathways, which interact with these C-terminal domains, should lead us to ways of modulating IGF-I-mediated survival in tumours.
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Conference Article|
February 01 2000
Regulation of survival signals from the insulin-like growth factor-I receptor
R. O'Connor;
R. O'Connor
1Cell Biology Laboratory, Department of Biochemistry, University College Cork, Lee Maltings, Cork, Ireland
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C. Fennelly;
C. Fennelly
1Cell Biology Laboratory, Department of Biochemistry, University College Cork, Lee Maltings, Cork, Ireland
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D. Krause
D. Krause
1Cell Biology Laboratory, Department of Biochemistry, University College Cork, Lee Maltings, Cork, Ireland
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Publisher: Portland Press Ltd
Received:
September 09 1999
Online ISSN: 1470-8752
Print ISSN: 0300-5127
© 2000 Biochemical Society
2000
Biochem Soc Trans (2000) 28 (2): 47–51.
Article history
Received:
September 09 1999
Citation
R. O'Connor, C. Fennelly, D. Krause; Regulation of survival signals from the insulin-like growth factor-I receptor. Biochem Soc Trans 1 February 2000; 28 (2): 47–51. doi: https://doi.org/10.1042/bst0280047
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