Murray, S. A., Zheng, H. W., Gu, L., Xiao, Z. X. J.
(March 2003)
IGF-1 activates p21 to inhibit UV-induced cell death.
Oncogene, 22 (11).
pp. 1703-1711.
ISSN 0950-9232
Abstract
The insulin-like growth factor-1 (IGF-1) and its downstream effector Akt have been documented as survival factors in response to a variety of stress signals. In this study, we show that IGF-1 activates p21 protein expression in a p53-dependent manner. Inhibition of PI-3 kinase or ectopic expression of a dominant-negative Akt blocks the effect of IGF-1 on the upregulation of p21 expression. In addition, IGF-1 prevents the UV irradiation-mediated suppression of p21 and MDM2 expression. Furthermore, p21 is important for IGF-1-mediated cell survival upon UV irradiation. Taken together, these data indicate that IGF-1 may activate p21 in executing its survival function upon genotoxic insults.
| Item Type: |
Paper
|
| Uncontrolled Keywords: |
IGF-1
Akt
p53
p21
UV and apoptosis
SERINE-THREONINE KINASE
MYC-INDUCED APOPTOSIS
NF-KAPPA-B
P53-INDUCED
APOPTOSIS
TUMOR-SUPPRESSOR
CANCER-CELLS
TRANSCRIPTION FACTOR
GROWTH-FACTORS
DNA-DAMAGE
P53
Biochemistry & Molecular Biology
Oncology
Cell Biology
Genetics &
Heredity |
| Subjects: |
bioinformatics > genomics and proteomics > genetics & nucleic acid processing > protein structure, function, modification > protein types > enzymes > Akt
organs, tissues, organelles, cell types and functions > cell types and functions > cell functions > apoptosis
bioinformatics > genomics and proteomics > genetics & nucleic acid processing > DNA, RNA structure, function, modification > genes, structure and function > genes: types > p21
bioinformatics > genomics and proteomics > genetics & nucleic acid processing > DNA, RNA structure, function, modification > genes, structure and function > genes: types > p53 |
| CSHL Authors: |
|
| Communities: |
CSHL labs > Zheng lab |
| Depositing User: |
Matt Covey
|
| Date: |
March 2003 |
| Date Deposited: |
22 Aug 2014 15:43 |
| Last Modified: |
22 Aug 2014 15:43 |
| Related URLs: |
|
| URI: |
https://repository.cshl.edu/id/eprint/30710 |
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