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. 2009 Jul 22;284(39):26631–26645. doi: 10.1074/jbc.M109.034405

FIGURE 1.

FIGURE 1.

hLigI mutations and polymorphisms between different 46BR.1G1 derivatives. Upper, human hLigI protein schematic outlining various functional motifs including the PCNA-interacting protein box (PIP box) that mediates the interaction with PCNA. Ser-51, -66, -76, and -91 are the amino acid positions phosphorylated during the cell cycle (50–53). Lower, sequencing results. Broken arrow, intronic primers (46BR-F and 46BR-R) were used to check the Arg-771 to Trp 46BR mutation at genomic hLigI sequence (16). Solid arrows, a set of four pairs of exonic primers were used to check possible polymorphisms in cloned wild type hLigI cDNAs used to stably supplement 46BR.1G1 cells (18). The 8–9-amino acid mutation in the 46BRLigIm/m;wt-PCNA cell line that abolish binding to PCNA was also confirmed (18).