p53-dependent transcriptional regulation of EDA2R and its involvement in chemotherapy-induced hair loss

被引：42

作者：

Brosh, Ran ^{[1
]}

Sarig, Rachel ^{[1
]}

Bar Natan, Elad ^{[1
]}

Molchadsky, Alina ^{[1
]}

Madar, Shalom ^{[1
]}

Bornstein, Chamutal ^{[1
]}

Buganim, Yosef ^{[1
]}

Shapira, Tirosh ^{[1
]}

Goldfinger, Naomi ^{[1
]}

Paus, Ralf ^{[2
,3
]}

Rotter, Varda ^{[1
]}

机构：

[1] Weizmann Inst Sci, Dept Mol Cell Biol, IL-76100 Rehovot, Israel

[2] Univ Lubeck, Dept Dermatol, Lubeck, Germany

[3] Univ Manchester, Sch Translat Med, Manchester, Lancs, England

来源：

FEBS LETTERS | 2010年 / 584卷 / 11期

关键词：

XEDAR; Alopecia; Cyclophosphamide; Knockout; Chemotherapy-induced alopecia; ECTODERMAL DYSPLASIA RECEPTOR; INDUCED ALOPECIA; P53; APOPTOSIS; INDUCTION; FOLLICLE; ACTIVATION; PATHWAY; XEDAR; MICE;

D O I：

10.1016/j.febslet.2010.04.058

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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. (C) 2010 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.

引用

页码：2473 / 2477

页数：5

共 23 条

[1] ATM is a target for positive regulation by E2F-1 [J].