Abstract
The p53 tumor suppressor coordinates a multitude of cellular and organismal processes and exerts its activities mainly by activation of gene transcription. Here we describe the transcriptional activation of ectodysplasin A2 receptor (EDA2R) by p53 in a variety of cell types and tissues. We demonstrate that treatment of cancer cells with the ligand EDA-A2, known to specifically activate EDA2R, results in p53-dependent cell death. Moreover, we show that EDA2R is transactivated by p53 during chemotherapy-induced hair-loss, although its presence is not necessary for this process. These data shed new light on the role of EDA2R in exerting p53 function.
Original language | English |
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Pages (from-to) | 2473-2477 |
Number of pages | 5 |
Journal | FEBS Letters |
Volume | 584 |
Issue number | 11 |
DOIs | |
State | Published - Jun 2010 |
Externally published | Yes |
Bibliographical note
Funding Information:Supported by a Center of Excellence grant from the Flight Attendant Medical Research Institute. V.R. is the incumbent of the Norman and Helen Asher Professorial Chair Cancer Research at the Weizmann institute.
Keywords
- Alopecia
- Chemotherapy-induced alopecia
- Cyclophosphamide
- Knockout
- XEDAR