The proposed Nathan Shock Center on Aging as a four-fold purpose: (1) To enhance the quality of research in the basic biology of aging, (2) to facilitate coordination of research on aging, (3) to create a regional/national resource and (4) to create an environment for faculty growth in aging research. The creation of an environment for faculty growth by the Research Development Core also will enhance the quality of research in the basic biology of aging. The creation of an environment for faculty growth by the Research Development Core also will enhance the quality of research in the basic biology of aging. A major focus of the Research Development will be to promote the integration of the technologies offered by the Core so to develop research in the cellular and molecular basis of cell senescence and death in selected model systems. Research programs utilizing the Cores will be able to discover aging- related genes, localize their gene products, describe their phenotype and determine the function of the gene products. This integration will be created by a series of activities: (1) Rigorous selection of applications for the support of Pilot Projects, (2) rigorous selection of faculty with approved Pilot Projects for limited salary support, (3) a formal program of mentoring junior faculty and others new to th4e biology of aging by senior faculty (4) creation of a seminar course in the biology of aging and (5) mounting a program of guest speakers and retreats for prevention of findings on the biology of aging. The selection of applications for support of Pilot Projects and the selection of faculty for limited salary support will be by a committee of senior faculty. All these activities are designed to create an interactive and collegial but rigorous environment in which the intellectual ferment would lead to recruitment of new faculty to research in the cell and molecular biology of aging and provide them with outstanding facilities to support the production of high quality research by outstanding faculty.

Agency
National Institute of Health (NIH)
Institute
National Institute on Aging (NIA)
Type
Center Core Grants (P30)
Project #
5P30AG018254-02
Application #
6468882
Study Section
Special Emphasis Panel (ZAG1)
Project Start
2001-07-01
Project End
2002-06-30
Budget Start
Budget End
Support Year
2
Fiscal Year
2001
Total Cost
$130,001
Indirect Cost
Name
University of Rochester
Department
Type
DUNS #
208469486
City
Rochester
State
NY
Country
United States
Zip Code
14627
Cox, Christopher; Matheson, Matthew (2014) A comparison of the generalized gamma and exponentiated Weibull distributions. Stat Med 33:3772-80
Kravets, Anatoliy; Qin, Hong; Ahmad, Ausaf et al. (2010) Widespread occurrence of dosage compensation in Candida albicans. PLoS One 5:e10856
Qin, Hong; Lu, Meng; Goldfarb, David S (2008) Genomic instability is associated with natural life span variation in Saccharomyces cerevisiae. PLoS One 3:e2670
Welle, Stephen; Tawil, Rabi; Thornton, Charles A (2008) Sex-related differences in gene expression in human skeletal muscle. PLoS One 3:e1385
Wu, Qiuqian; Kim, Kyung-Ok; Sampson, Erik R et al. (2008) Induction of an osteoarthritis-like phenotype and degradation of phosphorylated Smad3 by Smurf2 in transgenic mice. Arthritis Rheum 58:3132-44
Burris, Clark A; de Silva, Suresh; Narrow, Wade C et al. (2008) Hexamethylene bisacetamide leads to reduced helper virus-free HSV-1 amplicon expression titers via suppression of ICP0. J Gene Med 10:152-64
Lim, Kuei-Cheng; Tyler, Carolyn M; Lim, Seung T et al. (2007) Proteolytic processing of proNGF is necessary for mature NGF regulated secretion from neurons. Biochem Biophys Res Commun 361:599-604
Baudry, E; Desmadril, M; Werren, J H (2006) Rapid adaptive evolution of the tumor suppressor gene Pten in an insect lineage. J Mol Evol 62:738-44
Kannanayakal, Theresa J; Tao, Haiyang; Vandre, Dale D et al. (2006) Casein kinase-1 isoforms differentially associate with neurofibrillary and granulovacuolar degeneration lesions. Acta Neuropathol 111:413-21
Polakos, Noelle K; Cornejo, Judith C; Murray, Debbie A et al. (2006) Kupffer cell-dependent hepatitis occurs during influenza infection. Am J Pathol 168:1169-78; quiz 1404-5

Showing the most recent 10 out of 32 publications