Replisome component that maintains genome stability by protecting stalled or damaged replication forks. After the induction of replication stress, required for the stabilization of stalled replication forks, the efficient activation of the intra-S-phase and G/2M cell-cycle checkpoints and the maintenance of genome stability. Component of the replisome complex composed of at least DONSON, MCM2, MCM7, PCNA and TICRR; interaction at least with PCNA occurs during DNA replication. Localizes at DNA replication sites. Experimental confirmation may be lacking for some isoforms. Expressed in the brain, with higher levels in prenatal compared to adult brain. Expressed during embryonic development. At Carnegie stage 22 (about 7.5 weeks gestation), expressed in numerous tissues, including brain, heart, lung, gastrointestinal tract, kidney, hind limb and forelimb digits. Similar expression is observed at 9 weeks of gestation. In the brain of a 9-week old fetus, prominently expressed in the neocortex subventricular zone and in the cortical plate and also detected in the ganglionic eminences. At 12 weeks of gestation, expression in the fetal brain is prominent in the basal ganglia and the ventricular and subventricular zones and cortical plate of the neocortex, mesencephalon, and rhombencephalon. At 15 and 16 weeks, highly expressed in the ventricular and subventricular zones, respectively. Highly expressed in the ganglionic eminence of 15 week-old brain and subplate of 16 week-old brain. At 20 weeks of gestation, expressed in the ventricular and subventricular zones, intermediate zone, and cortical plate of the neocortex. At 21 weeks of gestation, expressed in the neocortex with highest levels in the cortical plate. Expression is cell-cycle dependent with highest levels during S phase. The disease is caused by variants affecting the gene represented in this entry. This extremely rare syndrome is caused by an intronic mutation that leads to the retention of intron 6, probably resulting in non-sense mediated mRNA decay. This isoform has also been detected in healthy tissues, but at much lower levels than in MIMIS samples. The disease is caused by variants affecting the gene represented in this entry. May be produced at very low levels due to a premature stop codon in the mRNA, leading to nonsense-mediated mRNA decay. May be produced at very low levels due to a premature stop codon in the mRNA, leading to nonsense-mediated mRNA decay. Belongs to the DONSON family.