PML‐like subnuclear bodies, containing XRCC1, juxtaposed to DNA replication‐based single‐strand breaks-Reference-Cited by-同舟云学术

PML‐like subnuclear bodies, containing XRCC1, juxtaposed to DNA replication‐based single‐strand breaks

Published:2018-09-27 Issue:2 Volume:33 Page:2301-2313
ISSN:0892-6638
Container-title:The FASEB Journal
language:en
Short-container-title:FASEB j.

Author:

Kordon Magdalena M.¹,Szczurek Aleksander¹²,Berniak Krzysztof¹,Szelest Oskar¹,Solarczyk Kamil¹,Tworzydło Magdalena³,Wachsmann-Hogiu Sebastian⁴,Vaahtokari Anne⁵,Cremer Christoph²,Pederson Thoru⁶,Dobrucki Jurek W.¹

Affiliation:

1. Department of Cell BiophysicsFaculty of Biochemistry, Biophysics, and BiotechnologyJagiellonian UniversityKrakówPoland

2. Superresolution Microscopy GroupInstitute of Molecular BiologyMainzGermany

3. Department of Physical BiochemistryFaculty of Biochemistry, Biophysics, and BiotechnologyJagiellonian UniversityKrakówPoland

4. Department of Pathology and Laboratory MedicineUniversity of California at DavisDavisCaliforniaUSA

5. The Francis Crick InstituteCancer Research UKLondonUnited Kingdom

6. Department of Biochemistry and Molecular PharmacologyUniversity of Massachusetts Medical SchoolWorcesterMassachusettsUSA

Funder

National Institutes of Health

National Institute on Drug Abuse

University of Massachusetts Medical School

Publisher

Wiley

Subject

Genetics,Molecular Biology,Biochemistry,Biotechnology

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1096/fj.201801379R

Reference57 articles.

1. In situ analysis of repair processes for oxidative DNA damage in mammalian cells

2. XRCC1 and PCNA are loading platforms with distinct kinetic properties and different capacities to respond to multiple DNA lesions

3. Damage response of XRCC1 at sites of DNA single strand breaks is regulated by phosphorylation and ubiquitylation after degradation of poly(ADP-ribose)

4. Inducing local DNA damage by visible light to study chromatin repair

5. Two stages of XRCC1 recruitment and two classes of XRCC1 foci formed in response to low level DNA damage induced by visible light, or stress triggered by heat shock

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