Involved in DNA single-strand break repair by mediating the assembly of DNA break repair protein complexes (By similarity). Probably during DNA repair, negatively regulates ADP-ribose levels by modulating ADP-ribosyltransferase PARP1 activity (PubMed:28002403). Homodimer. Interacts with polynucleotide kinase (PNK), DNA polymerase-beta (POLB) and DNA ligase III (LIG3). Interacts with APTX and APLF. Interacts with APEX1; the interaction is induced by SIRT1 and increases with the acetylated form of APEX1 (By similarity). Moves from the nucleoli to the global nuclear chromatin upon DNA damage. Phosphorylation of Ser-371 causes dimer dissociation. Phosphorylation by CK2 promotes interaction with APTX and APLF (By similarity). Sumoylated. Embryonic lethal. Conditional knockout in brain causes cerebellar histopathology including increased apoptosis of cerebellar granule neurons, reduced numbers of cerebellar interneurons and decreased electrophysiological spike activity in Purkinje cells. Mutant mice exhibit cerebellar ataxia and elevated levels of ADP-ribose in cerebellum. Double knockout with PARP1 restores the normal interneuron density and ADP-ribose levels, reducing cerebellar ataxia in comparison to the single XRCC1 knockout mice.