The goals of Core A are to provide cellular and molecular assays in support of all projects. The technologies and methods employed include flow and image cytometry;genetic analyses, cell and tissue culture support and development of common reagents. This Core and its personnel have had a long and productive history of application of specialized cell and molecular assays to the study of Werner Syndrome. These notably include flow and image cytometric assays of cell cycle, survival, DNA damage and telomere status, reagents and assays for Immunologic probes and gene silencing, as well as cell culture support for the broad variety of in vitro assays that is encompassed by this work. Both the characterization of WRN RecQ protein activities and the consequences of these activities on cellular phenotypes thus rely on the use of cell and molecular assays that are used in com man by all of the Projects within this P01 renewal application. The implementation, enhancement and where needed, development of these assays is a service will be most effectively and efficiently performed by this specialized Core in order to optimize their use by the P01 Projects.

Public Health Relevance

Both the characterization of WRN RecQ protein activities and the consequences of these activities on cellular phenotypes rely on the use of Core A cell and molecular assays that are used in common by all of the Projects within this Program Project.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Research Program Projects (P01)
Project #
5P01CA077852-15
Application #
8494586
Study Section
Special Emphasis Panel (ZCA1-GRB-S)
Project Start
Project End
Budget Start
2013-07-01
Budget End
2014-06-30
Support Year
15
Fiscal Year
2013
Total Cost
$185,813
Indirect Cost
$71,026
Name
University of Washington
Department
Type
DUNS #
605799469
City
Seattle
State
WA
Country
United States
Zip Code
98195
Reid-Bayliss, Kate S; Loeb, Lawrence A (2017) Accurate RNA consensus sequencing for high-fidelity detection of transcriptional mutagenesis-induced epimutations. Proc Natl Acad Sci U S A 114:9415-9420
Kamath-Loeb, Ashwini S; Zavala-van Rankin, Diego G; Flores-Morales, Jeny et al. (2017) Homozygosity for the WRN Helicase-Inactivating Variant, R834C, does not confer a Werner syndrome clinical phenotype. Sci Rep 7:44081
Oshima, Junko; Sidorova, Julia M; Monnat Jr, Raymond J (2017) Werner syndrome: Clinical features, pathogenesis and potential therapeutic interventions. Ageing Res Rev 33:105-114
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Poole, William; Leinonen, Kalle; Shmulevich, Ilya et al. (2017) Multiscale mutation clustering algorithm identifies pan-cancer mutational clusters associated with pathway-level changes in gene expression. PLoS Comput Biol 13:e1005347
Fu, Wenqing; Ligabue, Alessio; Rogers, Kai J et al. (2017) Human RECQ Helicase Pathogenic Variants, Population Variation and ""Missing"" Diseases. Hum Mutat 38:193-203
Beckman, Robert A; Loeb, Lawrence A (2017) Evolutionary dynamics and significance of multiple subclonal mutations in cancer. DNA Repair (Amst) 56:7-15
Fox, Edward J; Salk, Jesse J; Loeb, Lawrence A (2016) Exploring the implications of distinct mutational signatures and mutation rates in aging and cancer. Genome Med 8:30
Tokita, Mari; Kennedy, Scott R; Risques, Rosa Ana et al. (2016) Werner syndrome through the lens of tissue and tumour genomics. Sci Rep 6:32038
Reid-Bayliss, Kate S; Arron, Sarah T; Loeb, Lawrence A et al. (2016) Why Cockayne syndrome patients do not get cancer despite their DNA repair deficiency. Proc Natl Acad Sci U S A 113:10151-6

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