IFNAR KNOCKOUT MOUSE
|
UCLA Technology Available For Licensing |
INNOVATION:
Researchers at UCLA have developed a C57Bl/6 based mouse model which lacks expression of a receptor for Type I Interferon (IFNAR). The animal lacks expression of the Type I receptor on all cells which has been shown to be the case genetically, biochemically and systemically in pathogen infection models. This is the first IFNAR KO mouse to be available on the C57Bl/6 background which is of most value to immunologists.
Related Papers (Selected)
- O'Connell RM, Saha SK, Vaidya SA, Bruhn KW, Miranda GA, Zarnegar B, Perry AK, Nguyen BO, Lane TF, Taniguchi T, Miller JF, Cheng G. Type I interferon production enhances susceptibility to Listeria monocytogenes infection. J Exp Med. 2004 Aug 16;200(4):437-45. [more]
- Guo B, Chang EY, Cheng G. The type I IFN induction pathway constrains Th17-mediated autoimmune inflammation in mice. J Clin Invest. 2008 May;118(5):1680-90. [more]
- Chow EK, O'Connell RM, Schilling S, Wang XF, Fu XY, Cheng G. TLR agonists regulate PDGF-B production and cell proliferation through TGF-beta/type I IFN crosstalk. EMBO J. 2005 Dec 7;24(23):4071-81. [more]
Reference: UCLA Case No. 2009-214
For additional technical details and current licensing
availability,
please contact the following UCLA office:
UCLA Office of Intellectual Property
11000 Kinross Avenue, Suite #200
Los Angeles, CA 90095
Tel: 310-794-0558 Fax: 310-794-0638
email: ncd@research.ucla.edu
|
NCD URL: http://www.research.ucla.edu/tech/ucla09-214.htm
|
UCLA Technologies Available for
Licensing
http://www.research.ucla.edu/oipa/industry
Copyright © 2008 The Regents of the
University of California.
keywords: mouse model, knockout, IFNAR, Type I Interferon, immunology, C57Bl/6
uclancd ucla latest inventions technology top ten 10 technologies intellectual property patents technology transfer invention business card