The Administrative Core provides administrative services to the three projects and two other cores of this program project. The program project proposal brings together the unique talents of several groups to perform an integrative and interdisciplinary analysis of the mechanism by which p66Shc-deficiency extends lifespan, across several levels of biological organization, and utilizing analyses of many different types that generate data in multiple formats. The Administrative Core is central to the synergistic interaction of the projects and cores, and in fact has demonstrated the facilitation of research transactions between these groups since the proposal's original submission. As a result of this synergistic interaction, the program has generated multiple new hypotheses for She function. Through this coordination over the last 4.5 years, the research conducted by the program project has demonstrated that Shcs control adiposity, metabolism, insulin signaling, and stress resistance, and the Administrative Core has facilitated the publication of >64 manuscripts from our laboratories.
The Specific Aims of this core are: to 1) provide an organizational structure to expedite and coordinate research and promote interactions among investigators;2) monitor and regularly review the quality of research and prepare progress reports;3) manage the fiscal components of the program project;4) facilitate publications, presentations, and the dissemination of research results;5) organize annual meetings by project members and an external review committee;and 6) coordinate and monitor data and resource sharing. Central to how these Aims will be achieved, Core A will organize and manage the monthly teleconference, the weekly lab meetings, the annual External Advisory Committee meeting, and the web-based server for data interchange between the seven units.
Obesity and diabetes are consequences of the Western high-fat diet, and these consequences contribute massively to unhealthy aging. The Administrative Core will coordinate the scientific efforts of a multilaboratory study to identify the mechanism of anti-adiposity, insulin sensitization, stress resistance and improved longevity ilinder caloric restriction and high-fat diets in She knockout mice, and facilitate the discovery and distribution of nutritional and pharmacological interventions to improve human healthy aging.
|Roberts, Megan N; Wallace, Marita A; Tomilov, Alexey A et al. (2018) A Ketogenic Diet Extends Longevity and Healthspan in Adult Mice. Cell Metab 27:1156|
|Penna, Elisa; Espino, Javier; De Stefani, Diego et al. (2018) The MCU complex in cell death. Cell Calcium 69:73-80|
|Pallafacchina, Giorgia; Zanin, Sofia; Rizzuto, Rosario (2018) Recent advances in the molecular mechanism of mitochondrial calcium uptake. F1000Res 7:|
|Jasoliya, Mittal J; McMackin, Marissa Z; Henderson, Chelsea K et al. (2017) Frataxin deficiency impairs mitochondrial biogenesis in cells, mice and humans. Hum Mol Genet 26:2627-2633|
|Song, Lanying; Yu, Alfred; Murray, Karl et al. (2017) Bipolar cell reduction precedes retinal ganglion neuron loss in a complex 1 knockout mouse model. Brain Res 1657:232-244|
|Roberts, Megan N; Wallace, Marita A; Tomilov, Alexey A et al. (2017) A Ketogenic Diet Extends Longevity and Healthspan in Adult Mice. Cell Metab 26:539-546.e5|
|Taylor, Sandra L; Ruhaak, L Renee; Weiss, Robert H et al. (2017) Multivariate two-part statistics for analysis of correlated mass spectrometry data from multiple biological specimens. Bioinformatics 33:17-25|
|Hayashi, Genki; Jasoliya, Mittal; Sahdeo, Sunil et al. (2017) Dimethyl fumarate mediates Nrf2-dependent mitochondrial biogenesis in mice and humans. Hum Mol Genet 26:2864-2873|
|Wright, Lauren E; Vecellio Reane, Denis; Milan, Gabriella et al. (2017) Increased mitochondrial calcium uniporter in adipocytes underlies mitochondrial alterations associated with insulin resistance. Am J Physiol Endocrinol Metab 313:E641-E650|
|Baldassini, W A; Ramsey, J J; Hagopian, K et al. (2017) The influence of Shc proteins and high-fat diet on energy metabolism of mice. Cell Biochem Funct 35:527-537|
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