IGF-1 activates p21 to inhibit UV-induced cell death

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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