“DNA ligase III is recruited to DNA strand breaks by a zinc finger motif homologous to that of poly(ADP-ribose) polymerase. Identification of two functionally distinct DNA binding regions within DNA ligase III”. Journal of Biological Chemistry274 (31): 21679–87. (July 1999). doi:10.1074/jbc.274.31.21679. PMID10419478.
“Interactions of the DNA ligase IV-XRCC4 complex with DNA ends and the DNA-dependent protein kinase”. Journal of Biological Chemistry275 (34): 26196–205. (August 2000). doi:10.1074/jbc.M000491200. PMID10854421.
“XRCC1 protein interacts with one of two distinct forms of DNA ligase III”. Biochemistry36 (17): 5207–11. (April 1997). doi:10.1021/bi962281m. PMID9136882.
“XRCC1 phosphorylation by CK2 is required for its stability and efficient DNA repair”. DNA Repair (Amst.)9 (7): 835–41. (July 2010). doi:10.1016/j.dnarep.2010.04.008. PMID20471329.
“Involvement of XRCC1 and DNA ligase III gene products in DNA base excision repair”. Journal of Biological Chemistry272 (38): 23970–5. (September 1997). doi:10.1074/jbc.272.38.23970. PMID9295348.
“DNA ligase III as a candidate component of backup pathways of nonhomologous end joining”. Cancer Res.65 (10): 4020–30. (May 2005). doi:10.1158/0008-5472.CAN-04-3055. PMID15899791.
“Analysis of DNA ligase IV mutations found in LIG4 syndrome patients: the impact of two linked polymorphisms”. Human Molecular Genetics13 (20): 2369–76. (October 2004). doi:10.1093/hmg/ddh274. PMID15333585.
“DNA ligase IV mutations identified in patients exhibiting developmental delay and immunodeficiency”. Molecular Cell8 (6): 1175–85. (December 2001). doi:10.1016/S1097-2765(01)00408-7. PMID11779494.
“Mutations in the DNA ligase I gene of an individual with immunodeficiencies and cellular hypersensitivity to DNA-damaging agents”. Cell69 (3): 495–503. (May 1992). doi:10.1016/0092-8674(92)90450-Q. PMID1581963.
“The neurodegenerative disease protein aprataxin resolves abortive DNA ligation intermediates”. Nature443 (7112): 713–6. (October 2006). doi:10.1038/nature05164. PMID16964241.
“Early-onset ataxia with ocular motor apraxia and hypoalbuminemia is caused by mutations in a new HIT superfamily gene”. Nature Genetics29 (2): 184–8. (October 2001). doi:10.1038/ng1001-184. PMID11586299.
“The gene mutated in ataxia-ocular apraxia 1 encodes the new HIT/Zn-finger protein aprataxin”. Nature Genetics29 (2): 189–93. (October 2001). doi:10.1038/ng1001-189. PMID11586300.
“Defective DNA single-strand break repair in spinocerebellar ataxia with axonal neuropathy-1”. Nature434 (7029): 108–13. (March 2005). doi:10.1038/nature03314. PMID15744309.
“DNA ligase III is recruited to DNA strand breaks by a zinc finger motif homologous to that of poly(ADP-ribose) polymerase. Identification of two functionally distinct DNA binding regions within DNA ligase III”. Journal of Biological Chemistry274 (31): 21679–87. (July 1999). doi:10.1074/jbc.274.31.21679. PMID10419478.
“Interactions of the DNA ligase IV-XRCC4 complex with DNA ends and the DNA-dependent protein kinase”. Journal of Biological Chemistry275 (34): 26196–205. (August 2000). doi:10.1074/jbc.M000491200. PMID10854421.
“XRCC1 protein interacts with one of two distinct forms of DNA ligase III”. Biochemistry36 (17): 5207–11. (April 1997). doi:10.1021/bi962281m. PMID9136882.
“XRCC1 phosphorylation by CK2 is required for its stability and efficient DNA repair”. DNA Repair (Amst.)9 (7): 835–41. (July 2010). doi:10.1016/j.dnarep.2010.04.008. PMID20471329.
“Involvement of XRCC1 and DNA ligase III gene products in DNA base excision repair”. Journal of Biological Chemistry272 (38): 23970–5. (September 1997). doi:10.1074/jbc.272.38.23970. PMID9295348.
“DNA ligase III as a candidate component of backup pathways of nonhomologous end joining”. Cancer Res.65 (10): 4020–30. (May 2005). doi:10.1158/0008-5472.CAN-04-3055. PMID15899791.
“Analysis of DNA ligase IV mutations found in LIG4 syndrome patients: the impact of two linked polymorphisms”. Human Molecular Genetics13 (20): 2369–76. (October 2004). doi:10.1093/hmg/ddh274. PMID15333585.
“DNA ligase IV mutations identified in patients exhibiting developmental delay and immunodeficiency”. Molecular Cell8 (6): 1175–85. (December 2001). doi:10.1016/S1097-2765(01)00408-7. PMID11779494.
“Mutations in the DNA ligase I gene of an individual with immunodeficiencies and cellular hypersensitivity to DNA-damaging agents”. Cell69 (3): 495–503. (May 1992). doi:10.1016/0092-8674(92)90450-Q. PMID1581963.
“The neurodegenerative disease protein aprataxin resolves abortive DNA ligation intermediates”. Nature443 (7112): 713–6. (October 2006). doi:10.1038/nature05164. PMID16964241.
“Early-onset ataxia with ocular motor apraxia and hypoalbuminemia is caused by mutations in a new HIT superfamily gene”. Nature Genetics29 (2): 184–8. (October 2001). doi:10.1038/ng1001-184. PMID11586299.
“The gene mutated in ataxia-ocular apraxia 1 encodes the new HIT/Zn-finger protein aprataxin”. Nature Genetics29 (2): 189–93. (October 2001). doi:10.1038/ng1001-189. PMID11586300.
“Defective DNA single-strand break repair in spinocerebellar ataxia with axonal neuropathy-1”. Nature434 (7029): 108–13. (March 2005). doi:10.1038/nature03314. PMID15744309.