scholarly journals Localization of xeroderma pigmentosum group A protein and replication protein A on damaged DNA in nucleotide excision repair

2010 ◽  
Vol 38 (22) ◽  
pp. 8083-8094 ◽  
Author(s):  
Yuliya S. Krasikova ◽  
Nadejda I. Rechkunova ◽  
Ekaterina A. Maltseva ◽  
Irina O. Petruseva ◽  
Olga I. Lavrik
Keyword(s):  
Nucleotide Excision Repair ◽  
Xeroderma Pigmentosum ◽  
Excision Repair ◽  
Protein A ◽  
Replication Protein A ◽  
Replication Protein ◽  
Nucleotide Excision ◽  
Group A ◽  
Xeroderma Pigmentosum Group A ◽  
Damaged Dna

scholarly journals Relationship of the Xeroderma Pigmentosum Group E DNA Repair Defect to the Chromatin and DNA Binding Proteins UV-DDB and Replication Protein A

1998 ◽  
Vol 18 (6) ◽  
pp. 3182-3190 ◽  
Author(s):  
Vesna RapićOtrin ◽  
Isao Kuraoka ◽  
Tiziana Nardo ◽  
Mary McLenigan ◽  
A. P. M. Eker ◽  
...  
Keyword(s):  
Dna Binding ◽  
Nucleotide Excision Repair ◽  
Xeroderma Pigmentosum ◽  
Excision Repair ◽  
Protein A ◽  
Replication Protein A ◽  
Replication Protein ◽  
Cell Extracts ◽  
Nucleotide Excision ◽  
Repair Defect

ABSTRACT Cells from complementation groups A through G of the heritable sun-sensitive disorder xeroderma pigmentosum (XP) show defects in nucleotide excision repair of damaged DNA. Proteins representing groups A, B, C, D, F, and G are subunits of the core recognition and incision machinery of repair. XP group E (XP-E) is the mildest form of the disorder, and cells generally show about 50% of the normal repair level. We investigated two protein factors previously implicated in the XP-E defect, UV-damaged DNA binding protein (UV-DDB) and replication protein A (RPA). Three newly identified XP-E cell lines (XP23PV, XP25PV, and a line formerly classified as an XP variant) were defective in UV-DDB binding activity but had levels of RPA in the normal range. The XP-E cell extracts did not display a significant nucleotide excision repair defect in vitro, with either UV-irradiated DNA or a uniquely placed cisplatin lesion used as a substrate. Purified UV-DDB protein did not stimulate repair of naked DNA by DDB− XP-E cell extracts, but microinjection of the protein into DDB−XP-E cells could partially correct the repair defect. RPA stimulated repair in normal, XP-E, or complemented extracts from other XP groups, and so the effect of RPA was not specific for XP-E cell extracts. These data strengthen the connection between XP-E and UV-DDB. Coupled with previous results, the findings suggest that UV-DDB has a role in the repair of DNA in chromatin.

scholarly journals DNA Replication but Not Nucleotide Excision Repair Is Required for UVC-Induced Replication Protein A Phosphorylation in Mammalian Cells

2000 ◽  
Vol 20 (8) ◽  
pp. 2696-2705 ◽  
Author(s):  
Gregory Rodrigo ◽  
Sophie Roumagnac ◽  
Marc S. Wold ◽  
Bernard Salles ◽  
Patrick Calsou
Keyword(s):  
Dna Damage ◽  
Dna Replication ◽  
Nucleotide Excision Repair ◽  
Mammalian Cells ◽  
Excision Repair ◽  
Protein A ◽  
Replication Protein A ◽  
Replication Protein ◽  
Dependent Manner ◽  
Nucleotide Excision

ABSTRACT Exposure of mammalian cells to short-wavelength light (UVC) triggers a global response which can either counteract the deleterious effect of DNA damage by enabling DNA repair or lead to apoptosis. Several stress-activated protein kinases participate in this response, making phosphorylation a strong candidate for being involved in regulating the cellular damage response. One factor that is phosphorylated in a UVC-dependent manner is the 32-kDa subunit of the single-stranded DNA-binding replication protein A (RPA32). RPA is required for major cellular processes like DNA replication, and removal of DNA damage by nucleotide excision repair (NER). In this study we examined the signal which triggers RPA32 hyperphosphorylation following UVC irradiation in human cells. Hyperphosphorylation of RPA was observed in cells from patients with either NER or transcription-coupled repair (TCR) deficiency (A, C, and G complementation groups of xeroderma pigmentosum and A and B groups of Cockayne syndrome, respectively). This exclude both NER intermediates and TCR as essential signals for RPA hyperphosphorylation. However, we have observed that UV-sensitive cells deficient in NER and TCR require lower doses of UV irradiation to induce RPA32 hyperphosphorylation than normal cells, indicating that persistent unrepaired lesions contribute to RPA phosphorylation. Finally, the results of UVC irradiation experiments on nonreplicating cells and S-phase-synchronized cells emphasize a major role for DNA replication arrest in the presence of UVC lesions in RPA UVC-induced hyperphosphorylation in mammalian cells.

Differential binding kinetics of replication protein A during replication and the pre- and post-incision steps of nucleotide excision repair

DNA Repair ◽  
2014 ◽  
Vol 24 ◽  
pp. 46-56 ◽  
Author(s):  
Audrey M. Gourdin ◽  
Loes van Cuijk ◽  
Maria Tresini ◽  
Martijn S. Luijsterburg ◽  
Alex L. Nigg ◽  
...  
Keyword(s):  
Nucleotide Excision Repair ◽  
Excision Repair ◽  
Protein A ◽  
Replication Protein A ◽  
Binding Kinetics ◽  
Replication Protein ◽  
Nucleotide Excision ◽  
Differential Binding ◽  
Kinetics Of

scholarly journals High-Mobility Group A1 Proteins Inhibit Expression of Nucleotide Excision Repair Factor Xeroderma Pigmentosum Group A

2007 ◽  
Vol 67 (13) ◽  
pp. 6044-6052 ◽  
Author(s):  
Jennifer E. Adair ◽  
Scott C. Maloney ◽  
Gregory A. Dement ◽  
Kelsey J. Wertzler ◽  
Michael J. Smerdon ◽  
...  
Keyword(s):  
Nucleotide Excision Repair ◽  
Xeroderma Pigmentosum ◽  
Excision Repair ◽  
High Mobility ◽  
High Mobility Group ◽  
Nucleotide Excision ◽  
Group A ◽  
Repair Factor ◽  
Xeroderma Pigmentosum Group A ◽  
Nucleotide Excision Repair Factor
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