mFPR2 Transgenic and Knockout Mouse Models for Alzheimer's and Other Inflammatory Diseases
Posted Jun 15 2010 5:00pm
Description of Invention: Human Formyl Peptide-Like Receptor 1 (hFPLR1) has been implicated in host defense for disease processes including Alzheimer's disease, infection, and other inflammatory diseases. hFPLR1 and its mouse homologue Formyl Peptide Receptor 2 (mFPR2) are G-protein coupled receptors that are expressed at high levels on phagocytic leukocytes, mediating leukocyte chemotaxis and activation in response to a number of pathogen- and host-derived peptides. Activation of hFPRL1/mFPR2 by lipoxin A4 may play a role in preventing and resolving inflammation. Also, hFPRL1/mFPR2 has been shown to mediate the chemotactic activity of amyloid beta 1-42, a key pathogenic peptide in Alzheimer's disease.
Available for licensing are mice expressing the mFPR2 transgene on either the FVB or C58BL background, as well as mFPR2 knockout mice on the C57BL background. These mice are anticipated to be highly useful in the study of a wide variety of inflammatory, infectious, immunologic and neurodegenerative diseases.
Drug development model for Alzheimer's disease and other inflammatory diseases
Tool to probe the role of hFPRL1/mFPR2 in host responses in a variety of disease processes, including inflammatory, infectious, immunologic, and neurodegenerative disease
Research Tool -- patent protection is not being pursued for this technology
K Chen, Y Le, Y Liu, W Gong, G Ying, J Huang, T Yoshimura, L Tessarollo, JM Wang. Cutting Edge: A Critical Role for the G Protein-Coupled Receptor mFPR2 in Airway Inflammation and Immune Responses. J Immunol. 2010 Mar 3. Epub ahead of print. [ PubMed: 20200280 ]
K Chen, P Iribarren, J Hu, J Chen, W Gong, EH Cho, S Lockett, NM Dunlop, and JM Wang. Activation of Toll-like receptor 2 on microglia promotes cell uptake of Alzheimer disease-associated amyloid beta peptide. J Biol Chem. 2006 Feb 10;281(6):3651-3659. [ PubMed: 16339765 ]
H Yazawa, ZX Yu, Takeda, Y Le, W Gong, VJ Ferrans, JJ Oppenheim, CC Li, and JM Wang. Beta amyloid peptide (Abeta42) is internalized via the G-protein-coupled receptor FPRL1 and forms fibrillar aggregates in macrophages. FASEB J. 2001 Nov;15(13):2454-2462. [ PubMed: 11689470 ]
YH Cui, Y Le, W Gong, P Proost, J Van Damme, WJ Murphy, and JM Wang. Bacterial lipopolysaccharide selectively up-regulates the function of the chemotactic peptide receptor formyl peptide receptor 2 in murine microglial cells. J Immunol. 2002 Jan 1;168(1):434-442. [ PubMed: 11751990 ]
Licensing Status: This technology is available as a research tool under a Biological Materials License.
Collaborative Research Opportunity: The National Cancer Institute - Frederick, Laboratory of Molecular Immunoregulation, is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize mFPR2 Transgenic and Knockout Mouse Models for Alzheimer's and Other Inflammatory Diseases. Please contact John D. Hewes, Ph.D. at 301-435-3121 or firstname.lastname@example.org for more information.
Portfolios: Devices/Instrumentation Devices/Instrumentation - Research Tools and Materials Animal Model
For Additional Information Please Contact: Tara Kirby Ph.D. NIH Office of Technology Transfer 6011 Executive Blvd. Suite 325, Rockville, MD 20852 United States Email: email@example.com Phone: 301-435-4426 Fax: 301-402-0220