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Mol Cell Biol
1994 Jan 01;141:68-76. doi: 10.1128/mcb.14.1.68-76.1994.
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An interaction between the mammalian DNA repair protein XRCC1 and DNA ligase III.
Caldecott KW
,
McKeown CK
,
Tucker JD
,
Ljungquist S
,
Thompson LH
.
???displayArticle.abstract??? XRCC1, the human gene that fully corrects the Chinese hamster ovary DNA repair mutant EM9, encodes a protein involved in the rejoining of DNA single-strand breaks that arise following treatment with alkylating agents or ionizing radiation. In this study, a cDNA minigene encoding oligohistidine-tagged XRCC1 was constructed to facilitate affinity purification of the recombinant protein. This construct, designated pcD2EHX, fully corrected the EM9 phenotype of high sister chromatid exchange, indicating that the histidine tag was not detrimental to XRCC1 activity. Affinity chromatography of extract from EM9 cells transfected with pcD2EHX resulted in the copurification of histidine-tagged XRCC1 and DNA ligase III activity. Neither XRCC1 or DNA ligase III activity was purified during affinity chromatography of extract from EM9 cells transfected with pcD2EX, a cDNA minigene that encodes untagged XRCC1, or extract from wild-type AA8 or untransfected EM9 cells. The copurification of DNA ligase III activity with histidine-tagged XRCC1 suggests that the two proteins are present in the cell as a complex. Furthermore, DNA ligase III activity was present at lower levels in EM9 cells than in AA8 cells and was returned to normal levels in EM9 cells transfected with pcD2EHX or pcD2EX. These findings indicate that XRCC1 is required for normal levels of DNA ligase III activity, and they implicate a major role for this DNA ligase in DNA base excision repair in mammalian cells.
Barnes,
Mutations in the DNA ligase I gene of an individual with immunodeficiencies and cellular hypersensitivity to DNA-damaging agents.
1992, Pubmed
Barnes,
Mutations in the DNA ligase I gene of an individual with immunodeficiencies and cellular hypersensitivity to DNA-damaging agents.
1992,
Pubmed
Bradford,
A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding.
1976,
Pubmed
Caldecott,
Construction of human XRCC1 minigenes that fully correct the CHO DNA repair mutant EM9.
1992,
Pubmed
Chaganti,
A manyfold increase in sister chromatid exchanges in Bloom's syndrome lymphocytes.
1974,
Pubmed
Chan,
Defective DNA ligase I in Bloom's syndrome cells. Simultaneous analysis using immunoblotting and the ligase-[32P]AMP adduct assay.
1988,
Pubmed
Chan,
Altered DNA ligase I activity in Bloom's syndrome cells.
,
Pubmed
Chan,
DNA-ligase activities appear normal in the CHO mutant EM9.
1984,
Pubmed
Dillehay,
DNA-strand breaks associated with halogenated pyrimidine incorporation.
1984,
Pubmed
Franke,
Expression and single-step purification of enzymatically active vaccinia virus thymidine kinase containing an engineered oligohistidine domain by immobilized metal affinity chromatography.
1993,
Pubmed
Ikejima,
Poly(ADP-ribose) metabolism appears normal in EM9, a mutagen-sensitive mutant of CHO cells.
1984,
Pubmed
Janknecht,
Rapid and efficient purification of native histidine-tagged protein expressed by recombinant vaccinia virus.
1991,
Pubmed
Jessberger,
A mammalian protein complex that repairs double-strand breaks and deletions by recombination.
1993,
Pubmed
Krepinsky,
Sensitivity of Bloom's syndrome lymphocytes to ethyl methanesulfonate.
1979,
Pubmed
Kurihara,
Hypersensitivity of Bloom's syndrome fibroblasts to N-ethyl-N-nitrosourea.
1987,
Pubmed
La Belle,
Apurinic/apyrimidinic endonuclease activities appear normal in the CHO-cell ethyl methanesulfonate-sensitive mutant, EM9.
1984,
Pubmed
Lindahl,
Instability and decay of the primary structure of DNA.
1993,
Pubmed
McDaniel,
Elevated sister chromatid exchange phenotype of Bloom syndrome cells is complemented by human chromosome 15.
1992,
Pubmed
Minkler,
An ultraviolet light source for consistent differential staining of sister chromatids.
1978,
Pubmed
Perry,
New Giemsa method for the differential staining of sister chromatids.
1974,
Pubmed
Ray,
Different mutations are responsible for the elevated sister-chromatid exchange frequencies characteristic of Bloom's syndrome and hamster EM9 cells.
1987,
Pubmed
Siciliano,
Assignment of a human DNA-repair gene associated with sister-chromatid exchange to chromosome 19.
1986,
Pubmed
Söderhäll,
Mammalian DNA ligases. Serological evidence for two separate enzymes.
1975,
Pubmed
Studier,
Use of T7 RNA polymerase to direct expression of cloned genes.
1990,
Pubmed
Studier,
Use of bacteriophage T7 RNA polymerase to direct selective high-level expression of cloned genes.
1986,
Pubmed
Thompson,
DNA-mediated transfer of a human DNA repair gene that controls sister chromatid exchange.
1985,
Pubmed
Thompson,
A CHO-cell strain having hypersensitivity to mutagens, a defect in DNA strand-break repair, and an extraordinary baseline frequency of sister-chromatid exchange.
1982,
Pubmed
Thompson,
Molecular cloning of the human XRCC1 gene, which corrects defective DNA strand break repair and sister chromatid exchange.
1990,
Pubmed
Tomkinson,
Three distinct DNA ligases in mammalian cells.
1991,
Pubmed
,
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Tomkinson,
Mammalian DNA ligases. Catalytic domain and size of DNA ligase I.
1990,
Pubmed
Weiss,
Enzymatic breakage and joining of deoxyribonucleic acid. VI. Further purification and properties of polynucleotide ligase from Escherichia coli infected with bacteriophage T4.
1968,
Pubmed
Willis,
Structural alterations of DNA ligase I in Bloom syndrome.
1987,
Pubmed
Willis,
DNA ligase I deficiency in Bloom's syndrome.
,
Pubmed
Wilson,
The structure of an antigenic determinant in a protein.
1984,
Pubmed
Yoo,
Alterations in expression and structure of the DNA repair gene XRCC1.
1992,
Pubmed
Zdzienicka,
A Chinese hamster ovary cell mutant (EM-C11) with sensitivity to simple alkylating agents and a very high level of sister chromatid exchanges.
1992,
Pubmed