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Bovine X-ray repair complementing defective repair in Chinese hamster cells 3 (XRCC3) ELISA kit, Species Bovine, Sample Type serum, plasma

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[#CSB-EL026231BO] Bovine X-ray repair complementing defective repair in Chinese hamster cells 3 (XRCC3) ELISA kit, Species Bovine, Sample Type serum, plasma

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CSB-EL026231BO | Bovine X-ray repair complementing defective repair in Chinese hamster cells 3 (XRCC3) ELISA kit, Species Bovine, Sample Type serum, plasma, 96T
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(1) Quantification of XRCC and DNA-PK proteins in cancer cell lines and human tumors by LC-MS/MS.[TOP]

Pubmed ID :24785829
Publication Date : //
The x-ray repair cross-complementing (XRCC) proteins and a catalytic subunit of nuclear DNA-dependent serine/threonine protein kinase (DNA-PK) play important roles in cancer biology. Understanding the protein expression levels allows us to reconstruct in vivo functionality and to qualify protein biomarkers.

Authors : Myers Matthew V, Maxwell Stephen E, Wang Xiaomin,



(2) Mammary carcinogenesis in transgenic mice expressing a dominant-negative mutant of DNA polymerase beta in their mammary glands.[TOP]

Pubmed ID :17166880
Publication Date : //
DNA polymerase beta (polbeta) is a major contributor to mammalian DNA damage repair through its gap-filling DNA synthesis and 5'-deoxyribose phosphate lyase activities. In this way, polbeta plays pivotal roles in the repair of oxidative DNA damage, replication, embryonic survival, neuronal development, meiosis, apoptosis and telomere function. A 36 kDa truncated polbetaDelta protein is expressed in human colorectal, breast, lung and renal carcinomas, but not in normal matched tissues. Interestingly, a binary protein-protein complex of polbetaDelta and X-ray cross-complementing group 1 acts as dominant-negative mutant. In this study, the potential tumorigenic activity of polbetaDelta was examined in nude and transgenic mouse models. Mouse embryonic fibroblasts (MEFs) expressing polbetaDelta in the absence of endogenous polbeta exhibited increased susceptibility to N-methyl-N-nitrosourea (MNU)-induced morphological transformation as compared with cells expressing wild-type (WT) polbeta. This was accompanied by reduced gap-filling DNA synthesis activity. Anchorage-independent transformed cells derived from polbetaDelta-expressing MEFs induced 100% tumor occurrence in nude mice. To support these data, we established transgenic mice expressing polbetaDelta specifically in the mammary glands from a whey acidic protein promoter-driven transgene. This is the first report of transgenic mice with tissue-specific expression of polbetaDelta. MNU-induced tumor formation was analyzed in transgenic mice expressing polbetaDelta together with endogenous WT polbeta in their mammary glands and in normal control mice expressing only WT polbeta. The latent period of tumor appearance was markedly shorter and tumor incidence was significantly higher in transgenic animals than in control animals treated under the same conditions. These results indicate that cells expressing the mutant polbetaDelta display an enhanced sensitivity to MNU that probably underlies an increased susceptibility to tumorigenesis.

Authors : Wang Liming, Bhattacharyya Nandan, Rabi Thangaiyan, Wang Li, Banerjee Sipra,



(3) XRCC3 is required for efficient repair of chromosome breaks by homologous recombination.[TOP]

Pubmed ID :10725659
Publication Date : //
XRCC3 was originally identified as a human gene able to complement the DNA damage sensitivity, chromosomal instability and impaired growth of the mutant hamster cell line irs1SF. More recently, it has been cloned, sequenced and found to bear sequence homology to the highly conserved eukaryotic repair and recombination gene RAD51. The phenotype of irs1SF and the identification of XRCC3 as a member of the RAD51 gene family have suggested a role for XRCC3 in repair of DNA damage by homologous recombination. Homologous recombinational repair (HRR) of a specifically induced chromosomal double-strand break (DSB) was assayed in irs1SF cells with and without transient complementation by human XRCC3. Complementation with XRCC3 increased the frequencies of repair by 34- to 260-fold. The results confirm a role for XRCC3 in HRR of DNA DSB, and the importance of this repair pathway for the maintenance of chromosomal integrity in mammalian cells.

Authors : Brenneman M A, Weiss A E, Nickoloff J A, Chen D J,