The Systems Biology and Bioinformatics Core will support the Program Subprojects and Cores in data management and analysis. We will achieve this by providing statistical sen/ices, bioinformatics collaboration and data management across the entirety of the program project. Merging biostatistical expertise at the Mayo Clinic and bioinformatics expertise at the Buck Institute for Research on Aging Bioinformatics Core, together we represent a significant resource for participant investigators. We will achieve this goal through three service-based aims. First, we will provide bioinformatics collaboration through pathway analysis, network modeling and comparative genomic analysis of tissue specific effects in mice and humans. Second, we will provide data management sen/ices with the goal of integration and cross project analyses. Finally, we will provide biostatistical analysis to ensure that each experiment within the program project is sufficiently powered and the resulting analysis is quantitatively sound. Together this represents a comprehensive approach to providing quantitative methodologies to the project.
Modern biomedical research is largely data driven. This Core will provide access to and analysis of public and project generated data as it relates to aging and cellular senescence. To do this, we will combine biostatistics, data management and bioinformatic analysis to enable generation and testing of new hypotheses.
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|Campisi, Judith; Robert, Ladislas (2014) Cell senescence: role in aging and age-related diseases. Interdiscip Top Gerontol 39:45-61|
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|Campisi, Judith (2014) Cell biology: The beginning of the end. Nature 505:35-6|
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|Tchkonia, Tamara; Thomou, Thomas; Zhu, Yi et al. (2013) Mechanisms and metabolic implications of regional differences among fat depots. Cell Metab 17:644-56|
|Kirkland, James L (2013) Translating advances from the basic biology of aging into clinical application. Exp Gerontol 48:1-5|
|Baker, Darren J; Weaver, Robbyn L; van Deursen, Jan M (2013) p21 both attenuates and drives senescence and aging in BubR1 progeroid mice. Cell Rep 3:1164-74|
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