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XRCC3 promotes homology-directed repair of DNA damage in mammalian cells.
TLDR
It is demonstrated here that error-free homology-directed repair of DNA double-strand breaks is decreased 25-fold in an XR CC3-deficient hamster cell line and can be restored to wild-type levels through XRCC3 expression.
Pathways of DNA Double-Strand Break Repair during the Mammalian Cell Cycle
TLDR
It is shown here that NHEJ-defective hamster cells (CHO mutant V3 cells) have strongly reduced repair in all cell cycle phases after 1 Gy of irradiation, and HR is particularly important in late S/G2, where both pathways contribute to repair and radioresistance.
Characterization of the XRCC1-DNA ligase III complex in vitro and its absence from mutant hamster cells.
TLDR
Immunodetection of XRCC1 on Western blots revealed that the level of this polypeptide was also decreased in EM9 and EM-C11, indicating that the XR CC1-DNA ligase III complex is much reduced in the two CHO mutants.
An interaction between the mammalian DNA repair protein XRCC1 and DNA ligase III
TLDR
The findings indicate that XRCC1 is required for normal levels of DNA ligase III activity, and they implicate a major role for thisDNA ligase in DNA base excision repair in mammalian cells.
XRCC1 keeps DNA from getting stranded.
Requirement for the Xrcc1 DNA base excision repair gene during early mouse development.
TLDR
Results show that an intact base excision repair pathway is essential for normal early postimplantation mouse development and implicate an endogenous source of DNA damage in the lethal phenotype of embryos lacking this repair capacity.
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