AI Article Synopsis
- - The p53 tumor suppressor regulates various cellular functions primarily through activating gene transcription, including the activation of the ectodysplasin A2 receptor (EDA2R) in different cells and tissues.
- - Treatment of cancer cells with EDA-A2, which activates EDA2R, leads to cell death that relies on p53, indicating a link between EDA2R and the p53 tumor suppressor pathway.
- - The study also reveals that EDA2R is activated by p53 during chemotherapy-induced hair loss, though it's not essential for this hair loss process, highlighting a complex role for EDA2R in p53 activity.
Article 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.
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| http://dx.doi.org/10.1016/j.febslet.2010.04.058 | DOI Listing |
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