Localized Movement and Levels of 53BP1 Protein Are Changed by gamma-irradiation in PML Deficient Cells

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68081707%3A_____%2F16%3A00464620" target="_blank" >RIV/68081707:_____/16:00464620 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00216224:14330/16:00087865 RIV/00216208:11110/16:10328049

Výsledek na webu

<a href="http://dx.doi.org/10.1002/jcb.25551" target="_blank" >http://dx.doi.org/10.1002/jcb.25551</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1002/jcb.25551" target="_blank" >10.1002/jcb.25551</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Localized Movement and Levels of 53BP1 Protein Are Changed by gamma-irradiation in PML Deficient Cells

Popis výsledku v původním jazyce

We studied epigenetics, distribution pattern, kinetics, and diffusion of proteins recruited to spontaneous and -radiation-induced DNA lesions. We showed that PML deficiency leads to an increased number of DNA lesions, which was accompanied by changes in histone signature. In PML wt cells, we observed two mobile fractions of 53BP1 protein with distinct diffusion in spontaneous lesions. These protein fractions were not detected in PML-deficient cells, characterized by slow-diffusion of 53BP1. Single particle tracking analysis revealed limited local motion of 53BP1 foci in PML double null cells and local motion 53BP1 foci was even more reduced after -irradiation. However, radiation did not change co-localization between 53BP1 nuclear bodies and interchromatin granule-associated zones (IGAZs), nuclear speckles, or chromocenters. This newly observed interaction pattern imply that 53BP1 protein could be a part of not only DNA repair, but also process mediated via components accumulated in IGAZs, nuclear speckles, or paraspeckles. Together, PML deficiency affected local motion of 53BP1 nuclear bodies and changed composition and a number of irradiation-induced foci. J. Cell. Biochem. 117: 2583-2596, 2016. (c) 2016 Wiley Periodicals, Inc.

Název v anglickém jazyce

Localized Movement and Levels of 53BP1 Protein Are Changed by gamma-irradiation in PML Deficient Cells

Popis výsledku anglicky

We studied epigenetics, distribution pattern, kinetics, and diffusion of proteins recruited to spontaneous and -radiation-induced DNA lesions. We showed that PML deficiency leads to an increased number of DNA lesions, which was accompanied by changes in histone signature. In PML wt cells, we observed two mobile fractions of 53BP1 protein with distinct diffusion in spontaneous lesions. These protein fractions were not detected in PML-deficient cells, characterized by slow-diffusion of 53BP1. Single particle tracking analysis revealed limited local motion of 53BP1 foci in PML double null cells and local motion 53BP1 foci was even more reduced after -irradiation. However, radiation did not change co-localization between 53BP1 nuclear bodies and interchromatin granule-associated zones (IGAZs), nuclear speckles, or chromocenters. This newly observed interaction pattern imply that 53BP1 protein could be a part of not only DNA repair, but also process mediated via components accumulated in IGAZs, nuclear speckles, or paraspeckles. Together, PML deficiency affected local motion of 53BP1 nuclear bodies and changed composition and a number of irradiation-induced foci. J. Cell. Biochem. 117: 2583-2596, 2016. (c) 2016 Wiley Periodicals, Inc.

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

BO - Biofyzika

OECD FORD obor

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Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2016

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Journal of Cellular Biochemistry

ISSN

0730-2312

e-ISSN

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Svazek periodika

117

Číslo periodika v rámci svazku

11

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

14

Strana od-do

2583-2596

Kód UT WoS článku

000383626800015

EID výsledku v databázi Scopus

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