p73β is a member of the p53 family of transcription factors involved in cellular responses to stress and development. The p73 protein is expressed at very low levels in normal tissues and is differentially expressed in a number of tumors. P73β is strongly involved in malignancy acquisition and maintenance (1). p73 is a stress-response gene that activates transcription of p53-responsive genes and inhibits cell growth in a p53-like manner by inducing apoptosis (2). p73 is a component of a mismatch repair-dependent apoptosis pathway, which contributes to cisplatin-induced cytotoxicity. The regulation of p73 by c-Abl in response to DNA damage was also demonstrated by a failure of ionizing radiation-induced apoptosis after disruption of c-Abl-p73 interaction.
1. Jost. C. A. et.al: p73 is a human p53-related protein that can induce apoptosis. Nature 389: 191-194, 1997.
2. Gong, J. et.al: The tyrosine kinase c-Abl regulates p73 in apoptotic response to cisplatin-induced DNA damage. Nature 399: 806-809, 1999.
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Apoptosis/Autophagy, Cancer, Cardiovascular Disease, Cell Cycle, Cellular Stress, Inflammation, JNK/SAPK Pathway, Metabolic Disorder, Neurobiology, p38 Pathway