(Q40639081)

English

Efficient repair of cyclobutane pyrimidine dimers at mutational hot spots is restored in complemented Xeroderma pigmentosum group C and trichothiodystrophy/xeroderma pigmentosum group D cells

scientific article published on September 2003

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scholarly article

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Europe PubMed Central

PubMed publication ID

22 September 2017

Efficient repair of cyclobutane pyrimidine dimers at mutational hot spots is restored in complemented Xeroderma pigmentosum group C and trichothiodystrophy/xeroderma pigmentosum group D cells (English)

1 reference

Europe PubMed Central

PubMed publication ID

22 September 2017

xeroderma pigmentosum

1 reference

based on heuristic

inferred from title

xeroderma pigmentosum group C

1 reference

based on heuristic

inferred from title

author name string

Ning Ye Zhou

1

1 reference

Europe PubMed Central

PubMed publication ID

22 September 2017

Steven E Bates

2

1 reference

Europe PubMed Central

PubMed publication ID

22 September 2017

Mohammed Bouziane

3

1 reference

Europe PubMed Central

PubMed publication ID

22 September 2017

Anne Stary

4

1 reference

Europe PubMed Central

PubMed publication ID

22 September 2017

Alain Sarasin

5

1 reference

Europe PubMed Central

PubMed publication ID

22 September 2017

Timothy R O'Connor

6

1 reference

Europe PubMed Central

PubMed publication ID

22 September 2017

language of work or name

0 references

publication date

1 September 2003

1 reference

Europe PubMed Central

PubMed publication ID

22 September 2017

Journal of Molecular Biology

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Europe PubMed Central

PubMed publication ID

22 September 2017

332

1 reference

Europe PubMed Central

PubMed publication ID

22 September 2017

2

1 reference

Europe PubMed Central

PubMed publication ID

22 September 2017

337-351

1 reference

Europe PubMed Central

PubMed publication ID

22 September 2017

Nucleotide excision repair and human syndromes

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How nucleotide excision repair protects against cancer

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Defective Repair Replication of DNA in Xeroderma Pigmentosum

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Xeroderma pigmentosum: a human disease in which an initial stage of DNA repair is defective

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DNA Damage and Repair in Light-Sensitive Human Skin Disease

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Absence of excision of ultraviolet-induced cyclobutane dimers in xeroderma pigmentosum

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Functional retroviral vector for gene therapy of xeroderma pigmentosum group D patients

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Five complementation groups in xeroderma pigmentosum

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DNA excision repair

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DNA repair in eukaryotes

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Trichothiodystrophy: update on the sulfur-deficient brittle hair syndromes

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Centrosome protein centrin 2/caltractin 1 is part of the xeroderma pigmentosum group C complex that initiates global genome nucleotide excision repair

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HHR23B, a human Rad23 homolog, stimulates XPC protein in nucleotide excision repair in vitro

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Xeroderma pigmentosum group C protein complex is the initiator of global genome nucleotide excision repair

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The xeroderma pigmentosum group C protein complex XPC-HR23B plays an important role in the recruitment of transcription factor IIH to damaged DNA

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Human xeroderma pigmentosum group D gene encodes a DNA helicase

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XPD mutations prevent TFIIH-dependent transactivation by nuclear receptors and phosphorylation of RARalpha

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Complementation of transformed fibroblasts from patients with combined xeroderma pigmentosum-Cockayne syndrome

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Low amounts of the DNA repair XPA protein are sufficient to recover UV-resistance.

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Long-term complementation of DNA repair deficient human primary fibroblasts by retroviral transduction of the XPD gene

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Retroviral-mediated correction of DNA repair defect in xeroderma pigmentosum cells is associated with recovery of catalase activity

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Retrovirus-mediated gene transfer corrects DNA repair defect of xeroderma pigmentosum cells of complementation groups A, B and C

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Retrovirus-mediated DNA repair gene transfer into xeroderma pigmentosum cells: perspectives for a gene therapy

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Cancer-susceptibility genes. Gatekeepers and caretakers

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Formation and processing of UV photoproducts: effects of DNA sequence and chromatin environment

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Distribution and repair of photolesions in DNA: genetic consequences and the role of sequence context

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The DNA damage spectrum produced by simulated sunlight

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Cyclobutane pyrimidine dimers are responsible for the vast majority of mutations induced by UVB irradiation in mammalian cells

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TP53 mutations in human skin cancers.

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Formation and repair of DNA lesions in the p53 gene: relation to cancer mutations?

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Preferential formation of benzo[a]pyrene adducts at lung cancer mutational hotspots in P53.

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UVB-induced cyclobutane pyrimidine dimer frequency correlates with skin cancer mutational hotspots in p53

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TP53 mutation spectrum in lung cancers and mutagenic signature of components of tobacco smoke: lessons from the IARC TP53 mutation database

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Human cells compromised for p53 function exhibit defective global and transcription-coupled nucleotide excision repair, whereas cells compromised for pRb function are defective only in global repair

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PCR-based approaches to adduct analysis

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Slow repair of pyrimidine dimers at p53 mutation hotspots in skin cancer

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Identifiers

10.1016/S0022-2836(03)00793-9

1 reference

Europe PubMed Central

PubMed publication ID

22 September 2017

PubMed publication ID

1 reference

Europe PubMed Central

PubMed publication ID

22 September 2017

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