53BP1: pro choice in DNA repair

J 2014

53BP1: pro choice in DNA repair

ZIMMERMANN, Michal a T. DE LANGE

Základní údaje

Originální název

53BP1: pro choice in DNA repair

Autoři

ZIMMERMANN, Michal (203 Česká republika, garant, domácí) a T. DE LANGE (840 Spojené státy)

Vydání

TRENDS IN CELL BIOLOGY, LONDON, ELSEVIER SCIENCE LONDON, 2014, 0962-8924

Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

Genetika a molekulární biologie

Stát vydavatele

Velká Británie a Severní Irsko

Utajení

není předmětem státního či obchodního tajemství

Odkazy

URL

Impakt faktor

Impact factor: 12.007

Kód RIV

RIV/00216224:14740/14:00074404

Organizační jednotka

Středoevropský technologický institut

DOI

http://dx.doi.org/10.1016/j.tcb.2013.09.003

UT WoS

000332498100003

Klíčová slova anglicky

53BP1; Rif1; PTIP; NHEJ; HDR; PARPi; telomere; CSR; V(D)J; BRCA1; resection

Štítky

kontrola MP, MP, rivok

Příznaky

Mezinárodní význam, Recenzováno

Změněno: 23. 2. 2015 10:01, Martina Prášilová

Anotace

V originále

The DNA damage response factor 53BP1 functions at the intersection of two major double strand break (DSB) repair pathways - promoting nonhomologous end-joining (NHEJ) and inhibiting homology-directed repair (HDR) - and integrates cellular inputs to ensure their timely execution in the proper cellular contexts. Recent work has revealed that 53BP1 controls 5' end resection at DNA ends, mediates synapsis of DNA ends, promotes the mobility of damaged chromatin, improves DSB repair in heterochromatic regions, and contributes to lethal mis-repair of DSBs in BRCA1-deficient cells. Here we review these aspects of 53BP1 and discuss new data revealing how 53BP1 is loaded onto chromatin and uses its interacting factors Rif1 and PTIP to promote NHEJ and inhibit HDR.

Návaznosti

GAP205/12/0550, projekt VaV

Název: Dynamika vzniku shelterinového komplexu

Investor: Grantová agentura ČR, Dynamika vzniku shelterinového komplexu

Citovat

ZIMMERMANN, Michal a T. DE LANGE. 53BP1: pro choice in DNA repair. TRENDS IN CELL BIOLOGY. LONDON: ELSEVIER SCIENCE LONDON, 2014, roč. 24, č. 2, s. 108-117. ISSN 0962-8924. Dostupné z: https://dx.doi.org/10.1016/j.tcb.2013.09.003.

@article{1227550,
   author = {Zimmermann, Michal and de Lange, T.},
   article_location = {LONDON},
   article_number = {2},
   doi = {http://dx.doi.org/10.1016/j.tcb.2013.09.003},
   keywords = {53BP1; Rif1; PTIP; NHEJ; HDR; PARPi; telomere; CSR; V(D)J; BRCA1; resection},
   language = {eng},
   issn = {0962-8924},
   journal = {TRENDS IN CELL BIOLOGY},
   title = {53BP1: pro choice in DNA repair},
   url = {http://ac.els-cdn.com/S0962892413001554/1-s2.0-S0962892413001554-main.pdf?_tid=66e12f66-bb3a-11e4-abe9-00000aacb360&acdnat=1424682203_f8bd4c3cd228cef3ed42bebd7ad4b631},
   volume = {24},
   year = {2014}
}

TY  - JOUR
ID  - 1227550
AU  - Zimmermann, Michal - de Lange, T.
PY  - 2014
TI  - 53BP1: pro choice in DNA repair
JF  - TRENDS IN CELL BIOLOGY
VL  - 24
IS  - 2
SP  - 108-117
EP  - 108-117
PB  - ELSEVIER SCIENCE LONDON
SN  - 09628924
KW  - 53BP1
KW  - Rif1
KW  - PTIP
KW  - NHEJ
KW  - HDR
KW  - PARPi
KW  - telomere
KW  - CSR
KW  - V(D)J
KW  - BRCA1
KW  - resection
UR  - http://ac.els-cdn.com/S0962892413001554/1-s2.0-S0962892413001554-main.pdf?_tid=66e12f66-bb3a-11e4-abe9-00000aacb360&acdnat=1424682203_f8bd4c3cd228cef3ed42bebd7ad4b631
L2  - http://ac.els-cdn.com/S0962892413001554/1-s2.0-S0962892413001554-main.pdf?_tid=66e12f66-bb3a-11e4-abe9-00000aacb360&acdnat=1424682203_f8bd4c3cd228cef3ed42bebd7ad4b631
N2  - The DNA damage response factor 53BP1 functions at the intersection of two major double strand break (DSB) repair pathways - promoting nonhomologous end-joining (NHEJ) and inhibiting homology-directed repair (HDR) - and integrates cellular inputs to ensure their timely execution in the proper cellular contexts. Recent work has revealed that 53BP1 controls 5' end resection at DNA ends, mediates synapsis of DNA ends, promotes the mobility of damaged chromatin, improves DSB repair in heterochromatic regions, and contributes to lethal mis-repair of DSBs in BRCA1-deficient cells. Here we review these aspects of 53BP1 and discuss new data revealing how 53BP1 is loaded onto chromatin and uses its interacting factors Rif1 and PTIP to promote NHEJ and inhibit HDR.
ER  -

ZIMMERMANN, Michal a T. DE LANGE. 53BP1: pro choice in DNA repair. \textit{TRENDS IN CELL BIOLOGY}. LONDON: ELSEVIER SCIENCE LONDON, 2014, roč.~24, č.~2, s.~108-117. ISSN~0962-8924. Dostupné z: https://dx.doi.org/10.1016/j.tcb.2013.09.003.

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