p53-dependent transcriptional regulation of EDA2R and its involvement in chemotherapy-induced hair loss.
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.
Brosh
Ran
R
Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot, Israel. ran.brosh@weizmann.ac.il
Sarig
Rachel
R
Natan
Elad Bar
EB
Molchadsky
Alina
A
Madar
Shalom
S
Bornstein
Chamutal
C
Buganim
Yosef
Y
Shapira
Tirosh
T
Goldfinger
Naomi
N
Paus
Ralf
R
Rotter
Varda
V
D000505:Alopecia / Q000235:genetics*; D016923:Cell Death / Q000235:genetics; D005786:Gene Expression Regulation; D016158:Genes, p53 / Q000235:genetics*; D015533:Transcriptional Activation; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000502:physiology*; D053340:Xedar Receptor / Q000378:metabolism*
D016159:Tumor Suppressor Protein p53; D053340:Xedar Receptor