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Updated: Feb 5, 2026

Silencing of BRCA2 to Identify Novel BRCA2-regulated Biological Functions in Cultured Human Cells
Published on: August 12, 2015
Ariella Weinberg-Shukron1, Mariana Rachmiel1, Paul Renbaum1
1From the Medical Genetics Institute, Shaare Zedek Medical Center (A.W.-S., P.R., O.L., S.Z., R.S., E.L.-L.), the Faculty of Medicine, Hebrew University of Jerusalem, Hadassah Medical School (A.W.-S., E.L.-L., D.Z.), the Department of Developmental Biology and Cancer Research, IMRIC (Institute for Medical Research, Israel-Canada), Faculty of Medicine, Hebrew University of Jerusalem (A.D., T.S., R.K., O.G.), the Department of Genetics, Alexander Silberman Institute of Life Sciences, Hebrew University of Jerusalem (A.B.-M., M.G.), and the Division of Pediatric Endocrinology, Hadassah Hebrew University Medical Center (D.Z.), Jerusalem, and the Pediatric Endocrinology Clinic, Assaf Harofeh Medical Center, Zerifin, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv (M.R.) - all in Israel; and the Division of Medical Genetics, Department of Medicine and the Department of Genome Sciences, University of Washington, Seattle (S.G., T.W., M.-C.K.).
Mutations in the BRCA2 gene cause ovarian dysgenesis by impairing DNA repair, leading to chromosomal instability. This highlights BRCA2
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