Cullin3-KLHL15 ubiquitin ligase mediates CtIP protein turnover to fine-tune DNA-end resection

Autor: Lorenza P. Ferretti, Sarah-Felicitas Himmels, Anika Trenner, Christina Walker, Christine von Aesch, Aline Eggenschwiler, Olga Murina, Radoslav I. Enchev, Matthias Peter, Raimundo Freire, Antonio Porro, Alessandro A. Sartori

Publikováno v: Nature Communications, Vol 7, Iss 1, Pp 1-16 (2016)

CtIP has a key role in DNA double-strand break repair as its role in resecting DNA at the break commits a cell to homologous recombination. Here the authors show that KLHL15 interacts with CtIP and regulates repair by controlling protein turnover.

Externí odkaz: https://doaj.org/article/205a013d59044243b694ef6cde84318a

Cullin3-KLHL15 ubiquitin ligase mediates CtIP protein turnover to fine-tune DNA-end resection

Autor: Sarah-Felicitas Himmels, Antonio Porro, Matthias Peter, Raimundo Freire, Alessandro A. Sartori, Christina Walker, Olga Murina, Aline Eggenschwiler, Lorenza P. Ferretti, Radoslav I. Enchev, Christine von Aesch, Anika Trenner

Publikováno v: Nature Communications, Vol 7, Iss 1, Pp 1-16 (2016)
Ferretti, L P, Himmels, S-F, Trenner, A, Walker, C, von Aesch, C, Eggenschwiler, A, Murina, O, Enchev, R I, Peter, M, Freire, R, Porro, A & Sartori, A A 2016, ' Cullin3-KLHL15 ubiquitin ligase mediates CtIP protein turnover to fine-tune DNA-end resection ', Nature Communications, vol. 7, pp. 12628 . https://doi.org/10.1038/ncomms12628
Nature Communications, 7
Nature Communications

Human CtIP is a decisive factor in DNA double-strand break repair pathway choice by enabling DNA-end resection, the first step that differentiates homologous recombination (HR) from non-homologous end-joining (NHEJ). To coordinate appropriate and tim

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::36dd6af941fc34b9d8140e4ab6963b9d
https://doaj.org/article/205a013d59044243b694ef6cde84318a