Abstract
1Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States of America, 2University ofPittsburgh Cancer Institute, Hillman Cancer Center, Pittsburgh, Pennsylvania, United States of America, 3Department of Human Genetics, University of PittsburghGraduate School of Public Health, Pittsburgh, Pennsylvania, United States of America
Highlights
In this issue of PLOS Genetics, Sweasy and colleagues conducted a detailed analysis of the POLB germline–coding SNP rs3136797 [22]
To determine whether the P242R mutation affected genome stability in human or mouse cells, the wild-type (WT) or P242R protein was produced in human normal mammary epithelial cells (MCF10A) and in mouse embryonic fibroblasts (MEFs)
The cells were treated with methyl methanesulfonate (MMS) to induce DNA damage repaired by polymerase ß (Polß) [5]
Summary
In this issue of PLOS Genetics, Sweasy and colleagues conducted a detailed analysis of the POLB germline–coding SNP rs3136797 [22]. Cancerspecific mutations in Polß (e.g., Y265C) induced an increase in mutant frequency [23,24] that could explain the increase in chromosome alterations seen with P242R. Cells producing the P242R protein were found to have the same mutant frequency as those expressing WT Polß.
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
