Figure 1.
Effect of RAD51C point mutations on the interaction with XRCC3 and RAD51B.
(A) Yeast two-hybrid assays were performed with XRCC3 in the DNA-binding domain vector and either wild-type or site-specifically mutated RAD51C in the activating domain vector. (B) Yeast two-hybrid assays were performed with RAD51B in the DNA-binding domain vector and the RAD51C variants in the activating domain vector. Results from liquid ONPG assays are the average of 5–7 different transformants performed in triplicate, with the standard error of the mean. * : P<0.05 and ** :P≤0.001 using the student T-test.
Figure 2.
Immunoblots of RAD51C in the yeast strains used for the two-hybrid analysis
. The upper panel shows the immunoblot blot analysis of the yeast strains containing human XRCC3 and RAD51C while the lower panel shows the same immunoblots from the yeast strains used in the RAD51B and RAD51C analysis. The RAD51C-Gal4 fusion peptides were identified using an anti-Gal4 monoclonal antibody. The same lysates were probed with an antibody against β-actin as a control for equal loading of protein.
Figure 3.
Pedigrees of cases carrying the R214C and G153D mutations.
(A) R214C: African-American proband diagnosed with stage IIA, ER/PR positive, Her2/Neu positive, infiltrating ductal carcinoma of the breast at age 42 years. (B) G153D: Non-Hispanic Caucasian proband diagnosed with breast cancer at age 60 years and with stage IV, serous carcinoma of the ovary at age 79 years.
Table 1.
Characteristics of tested individual in family.
Table 2.
Variants identified through sequencing.