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Model animals non-responsive to mycobacterial-origin lipoprotein/lipopeptide achieved

Foreign code F110005239
File No. B02-02WO
Posted date Aug 29, 2011
Country United States of America
Application number 51766302
Gazette No. 20060059579
Gazette No. 7329795
Date of filing Dec 10, 2002
Gazette Date Mar 16, 2006
Gazette Date Feb 12, 2008
International application number JP2002012908
International publication number WO2003105578
Date of international filing Dec 10, 2002
Date of international publication Dec 24, 2003
Priority data
  • P2002-173254 (Jun 13, 2002) JP
  • 2002WO-JP12908 (Dec 10, 2002) WO
Title Model animals non-responsive to mycobacterial-origin lipoprotein/lipopeptide achieved
Abstract (US7329795)
The present invention is to provide TLR1 knockout mice specifically recognizing mycobacterial lipoproteins/lipopeptides, being useful to clarify the role of TLR1 in vivo, or a method for screening substances promoting or suppressing the response to mycobacterial lipoproteins/lipopeptides by using the same.
TLR1 genes are separated from murine genomic library, the genomic part containing the intracellular and transmembrane domain of the TLR1 gene is replaced with a neomycin resistant gene, HSV-tk gene being gene encoding thymidine kinase into 3' end is introduced, ES cell clones having double resistance to G418 and Gancyclovir are screened, and ES cell clones are injected into the blastocyst of C57BL/6 mice, to generate TLR1 knockout mice through the germline.
Scope of claims [claim1]
1. A transgenic mouse whose genome comprises a homozygous inactivation of the Toll-like Receptor 1 (TLR1) gene;
said TLR1 gene encoding a polypeptide that recognizes triacylated mycobacterial lipoproteins;
wherein peritoneal macrophages of the mouse, also comprising a homozygous inactivation of the TLR1 gene, exhibit decreased responsiveness to triacylated mycobacterial lipoproteins.
[claim2]
2. A method for screening substances that promote or suppres a response to triacylated mycobacterial lipoproteins comprising contacting peritoneal macrophages isolated from the transgenic TLR-1 inactivated mouse of claim 1, which exhibits a decreased responsiveness to triacylated mycobacterial lipoproteins, with a substance, contacting peritoneal macrophages isolated from a wild-type control mouse with said substance, and comparing the response between the TLR-1 inactivated peritoneal macrophages and the control macrophages, wherein an increase in said responsiveness in comparison to the control is indicative of a substance that promotes a response to a mycobacterial lipoprotein/lipopeptide in a TLR-1 independent manner and wherein a greater decrease in responsiveness to a mycobacterial lipoprotein/lipopeptide in comparison to a wild-type control mouse is indicative of a substance that inhibits a response to a mycobacterial lipoprotein/lipopeptide in a TLR-1 independent manner.
  • Inventor, and Inventor/Applicant
  • AKIRA SHIZUO
  • JAPAN SCIENCE AND TECHNOLOGY AGENCY
IPC(International Patent Classification)
Reference ( R and D project ) SORST Selected in Fiscal 2000
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