In the past, a substantial part of preclinical data in rheumatic diseases has come from studying using rodent models. Cutting edge experiments are now performed using elegant manipulation of the mouse genome with the creation of transgenics and knockouts. As an integral part of the UCSD RDCC, we propose to develop a Core facility that would facilitate the preparation of the desired strains of mice not commercially available for researchers. The Core will perform three main functions: 1) an animal genetics backcross service, in which we will establish a facility dedicated to the rigorous tasks of breeding backcrosses and testing for specific traits; 2) an animal genetics mouse strain service which will maintain small numbers of immunodeficient mice as well as strains that are commonly requested for backcrossing in our barrier facility.; and 3) an animal genetics consultation service which will assist researchers in making novel transgenics or knockouts by coordinating with the Transgenics and Gene Targeting Core. This Core will be able to offer marker assisted back crossing if requested. In addition, the Core will provide advice and references to assist investigators in planning experiments with genetically manipulated mice in murine models of rheumatic diseases. As a centralized facility, the Core may be able to avoid duplication of effort and will be able to suggest the most cost- effective means of creating mice for specific projects.

National Institute of Health (NIH)
National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS)
Center Core Grants (P30)
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Special Emphasis Panel (ZAR1)
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University of California San Diego
La Jolla
United States
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Silverman, Gregg J (2011) Regulatory natural autoantibodies to apoptotic cells: pallbearers and protectors. Arthritis Rheum 63:597-602
Silverman, Gregg J (2010) Regulatory natural autoantibodies to apoptotic cells: Pallbearers and protectors. Arthritis Rheum :
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Rosengren, Sanna; Mueller, James L; Anderson, Justin P et al. (2007) Monocytes from familial cold autoinflammatory syndrome patients are activated by mild hypothermia. J Allergy Clin Immunol 119:991-6

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