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 |
|---|---|
| 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.
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
Keywords
- Alopecia
- Chemotherapy-induced alopecia
- Cyclophosphamide
- Knockout
- XEDAR
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