(Q41087679)

English

Identification of defective illegitimate recombinational repair of oxidatively-induced DNA double-strand breaks in ataxia-telangiectasia cells

scientific article published on September 1997

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scholarly article

1 reference

Europe PubMed Central

PubMed publication ID

26 September 2017

Identification of defective illegitimate recombinational repair of oxidatively-induced DNA double-strand breaks in ataxia-telangiectasia cells (English)

1 reference

Europe PubMed Central

PubMed publication ID

26 September 2017

author name string

M E Dar

1

1 reference

Europe PubMed Central

PubMed publication ID

26 September 2017

T A Winters

2

1 reference

Europe PubMed Central

PubMed publication ID

26 September 2017

T J Jorgensen

3

1 reference

Europe PubMed Central

PubMed publication ID

26 September 2017

language of work or name

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publication date

1 September 1997

1 reference

Europe PubMed Central

PubMed publication ID

26 September 2017

Mutation Research

1 reference

Europe PubMed Central

PubMed publication ID

26 September 2017

384

1 reference

Europe PubMed Central

PubMed publication ID

26 September 2017

3

1 reference

Europe PubMed Central

PubMed publication ID

26 September 2017

169-179

1 reference

Europe PubMed Central

PubMed publication ID

26 September 2017

The nature of ataxia-telangiectasia: problems and perspectives

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Breast and other cancers in families with ataxia-telangiectasia

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Incidence of cancer in 161 families affected by ataxia-telangiectasia

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A single ataxia telangiectasia gene with a product similar to PI-3 kinase

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The complete sequence of the coding region of the ATM gene reveals similarity to cell cycle regulators in different species

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DNA-dependent protein kinase catalytic subunit: a relative of phosphatidylinositol 3-kinase and the ataxia telangiectasia gene product

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The ATM gene and the radiobiology of ataxia-telangiectasia

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Analysis of mutations caused by DNA double-strand breaks produced by a restriction enzyme in shuttle vector plasmids propagated in ataxia telangiectasia cells

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Abnormal processing of transfected plasmid DNA in cells from patients with ataxia telangiectasia

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Ataxia telangiectasia: An investigation of the repair defect in the cell line AT5BIVA by plasmid reconstitution

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High spontaneous intrachromosomal recombination rates in ataxia-telangiectasia

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High frequency and error-prone DNA recombination in ataxia telangiectasia cell lines

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Deletions at short direct repeats and base substitutions are characteristic mutations for bleomycin-induced double- and single-strand breaks, respectively, in a human shuttle vector system

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Mutations caused by gamma-radiation-induced double-strand breaks in a shuttle plasmid replicated in human lymphoblasts

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Formation of large deletions by illegitimate recombination in the HPRT gene of primary human fibroblasts

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Nonhomologous recombination in mammalian cells: role for short sequence homologies in the joining reaction

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Illegitimate recombination induced by DNA double-strand breaks in a mammalian chromosome

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Predominance of null mutations in ataxia-telangiectasia

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Use of supF, an Escherichia coli tyrosine suppressor tRNA gene, as a mutagenic target in shuttle-vector plasmids.

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Removal of 3'-phosphoglycolate from DNA strand-break damage in an oligonucleotide substrate by recombinant human apurinic/apyrimidinic endonuclease 1

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DNA sequencing with dye-labeled terminators and T7 DNA polymerase: effect of dyes and dNTPs on incorporation of dye-terminators and probability analysis of termination fragments

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Determination of the spectrum of mutations induced by defined-wavelength solar UVB (313-nm) radiation in mammalian cells by use of a shuttle vector

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Bleomycin-dependent damage to the bases in DNA is a minor side reaction

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Analysis of products formed during bleomycin-mediated DNA degradation

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Human HeLa cell enzymes that remove phosphoglycolate 3'-end groups from DNA

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Repair and misrepair of site-specific DNA double-strand breaks by human cell extracts

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Mutation spectrum in gamma-irradiated shuttle vector replicated in ataxia-telangiectasia lymphoblasts

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Mechanisms involved in rejoining DNA double-strand breaks induced by ionizing radiation and restriction enzymes

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Relationship of the ataxia-telangiectasia protein ATM to phosphoinositide 3-kinase

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Absence of p350 subunit of DNA-activated protein kinase from a radiosensitive human cell line

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DNA-dependent kinase (p350) as a candidate gene for the murine SCID defect

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Identification of a nonsense mutation in the carboxyl-terminal region of DNA-dependent protein kinase catalytic subunit in the scid mouse

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The scid mutation in mice causes a general defect in DNA repair

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scid mutation in mice confers hypersensitivity to ionizing radiation and a deficiency in DNA double-strand break repair

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A link between double-strand break-related repair and V(D)J recombination: the scid mutation

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Relative increase of T cells expressing the gamma/delta rather than the alpha/beta receptor in ataxia-telangiectasia

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Disorders of B cells and helper T cells in the pathogenesis of the immunoglobulin deficiency of patients with ataxia telangiectasia

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Specific cleavage of model recombination and repair intermediates by the yeast Rad1-Rad10 DNA endonuclease

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Effect of mutations in genes affecting homologous recombination on restriction enzyme-mediated and illegitimate recombination in Saccharomyces cerevisiae

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Human Rad50 is physically associated with human Mre11: identification of a conserved multiprotein complex implicated in recombinational DNA repair

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Atm-deficient mice: a paradigm of ataxia telangiectasia

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DNA damage and the DNA-activated protein kinase

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Repair of double-stranded DNA breaks by homologous DNA fragments during transfer of DNA into mouse L cells

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Two alternative pathways of double-strand break repair that are kinetically separable and independently modulated

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Identifiers

10.1016/S0921-8777(97)00021-9

1 reference

Europe PubMed Central

PubMed publication ID

26 September 2017

PubMed publication ID

1 reference

Europe PubMed Central

PubMed publication ID

26 September 2017

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