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CHK2 sets the stage for CK1 in oocyte quality control

CHK2 sets the stage for CK1 in oocyte quality control Cell Death & Differentiation (2018) 25:1007–1009 https://doi.org/10.1038/s41418-018-0107-6 COMMENT 1,2 1 1 ● ● Sebastian Kehrloesser Marcel Tuppi Volker Dötsch Published online: 17 April 2018 © ADMC Associazione Differenziamento e Morte Cellulare 2018 TAp63α has been identified as the major quality control the active tetramer with a 20-fold higher DNA binding factor in the female germline more than a decade ago by the affinity [7]. Activated TAp63α then orchestrates the group of Frank McKeon. DNA damage in primary oocytes, induction of apoptosis by driving transcription of genes within primordial follicles, that constitute the ovarian coding for the BH3 only proteins PUMA and NOXA [8]. reserve in women, results in the phosphorylation-dependent Although several kinases and phosphorylation sites have activation of p63 that in turn induces apoptosis of the been suggested, the exact activation mechanism for affected oocytes [1]. Although this mechanism is crucial to TAp63α remained enigmatic and in part controversially ensure oocyte quality throughout the reproductive lifespan, discussed [9, 10]. Although CHK2 has been identified as a female cancer patients treated with DNA damaging che- kinase essential for activation of TAp63α [11], we report motherapy or pelvic radiotherapy frequently suffer from now that phosphorylation at S582 is essential but http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Cell Death & Differentiation Springer Journals

CHK2 sets the stage for CK1 in oocyte quality control

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References (15)

Publisher
Springer Journals
Copyright
Copyright © 2018 by ADMC Associazione Differenziamento e Morte Cellulare
Subject
Life Sciences; Life Sciences, general; Biochemistry, general; Cell Biology; Stem Cells; Apoptosis; Cell Cycle Analysis
ISSN
1350-9047
eISSN
1476-5403
DOI
10.1038/s41418-018-0107-6
Publisher site
See Article on Publisher Site

Abstract

Cell Death & Differentiation (2018) 25:1007–1009 https://doi.org/10.1038/s41418-018-0107-6 COMMENT 1,2 1 1 ● ● Sebastian Kehrloesser Marcel Tuppi Volker Dötsch Published online: 17 April 2018 © ADMC Associazione Differenziamento e Morte Cellulare 2018 TAp63α has been identified as the major quality control the active tetramer with a 20-fold higher DNA binding factor in the female germline more than a decade ago by the affinity [7]. Activated TAp63α then orchestrates the group of Frank McKeon. DNA damage in primary oocytes, induction of apoptosis by driving transcription of genes within primordial follicles, that constitute the ovarian coding for the BH3 only proteins PUMA and NOXA [8]. reserve in women, results in the phosphorylation-dependent Although several kinases and phosphorylation sites have activation of p63 that in turn induces apoptosis of the been suggested, the exact activation mechanism for affected oocytes [1]. Although this mechanism is crucial to TAp63α remained enigmatic and in part controversially ensure oocyte quality throughout the reproductive lifespan, discussed [9, 10]. Although CHK2 has been identified as a female cancer patients treated with DNA damaging che- kinase essential for activation of TAp63α [11], we report motherapy or pelvic radiotherapy frequently suffer from now that phosphorylation at S582 is essential but

Journal

Cell Death & Differentiation – Springer Journals

Published: Apr 17, 2018

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