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Researchers create mouse lacking key inflammation gene
September 07, 2006Will likely lead to new treatments for inflammatory disorders
(Boston) - In a paper published yesterday in The Proceedings of the National Academy of Science (PNAS), researchers from Boston University School of Dental Medicine generated a mouse model exhibiting reduced inflammation.
The Boston University researchers found that the transcription factor LITAF (Lipopolysaccharide [LPS]-Induced TNF-Alpha Factor) controls inflammation through a completely different pathway than the better known and studied NF-kB transcriptional regulator.
Drugs regulating TNF-alpha through the better-known NF-kB pathway such as Remicade, Embrel, and Humira represent a multibillion market. The LITAF transcription factor offers a new approach to treating inflammatory disorders along with other immunological conditions. Researchers are offering this in vivo model for sale to spearhead discovery of drugs against inflammatory disorders such as arthritis and Crohn's disease.
In the study, Boston University researchers created a mouse lacking the gene that encodes for the LITAF protein. They found that several cytokines were induced at lower levels in the LITAF-deficient mice compared with the levels observed in the LITAF-positive control mice. Specifically, the deficient mice were more resistant to LPS-induced lethality.
"The generation of the macrophage-specific LITAF-deficient animals opens new opportunities for assessing the role of LITAF in inflammation in hopes of designing anti-LITAF drugs for major inflammatory diseases," says Dr. Salomon Amar of Boston University, the lead author of the paper. Amar discovered the LITAF transcription factor in 1999.
Researchers, who have applied to patent the mouse, are now working on whether other molecules work in synergy with LITAF.
Boston University
Drugs regulating TNF-alpha through the better-known NF-kB pathway such as Remicade, Embrel, and Humira represent a multibillion market. The LITAF transcription factor offers a new approach to treating inflammatory disorders along with other immunological conditions. Researchers are offering this in vivo model for sale to spearhead discovery of drugs against inflammatory disorders such as arthritis and Crohn's disease.
In the study, Boston University researchers created a mouse lacking the gene that encodes for the LITAF protein. They found that several cytokines were induced at lower levels in the LITAF-deficient mice compared with the levels observed in the LITAF-positive control mice. Specifically, the deficient mice were more resistant to LPS-induced lethality.
"The generation of the macrophage-specific LITAF-deficient animals opens new opportunities for assessing the role of LITAF in inflammation in hopes of designing anti-LITAF drugs for major inflammatory diseases," says Dr. Salomon Amar of Boston University, the lead author of the paper. Amar discovered the LITAF transcription factor in 1999.
Researchers, who have applied to patent the mouse, are now working on whether other molecules work in synergy with LITAF.
Boston University
Papers published online on 8 February by the Nature Research Journals
NATURE GENETICS(http://www.nature.com/naturegenetics) [1] Risk of heart attack and stroke tied to inflammation gene DOI: 10.1038/ng1311 (http://dx.doi.org/10.1038/ng1311) In the March issue of Nature Genetics, Kari Stefansson and colleagues report the identification of the first gene associated with a higher risk of both heart attacks and strokes, the diseases that result in the death of most people in developed countries. Since the genetic markers they studied are associated with just a twofold increased risk of incurring a heart attack, this work is just the first step toward the goal of unravelling the complex interplay of genes with significant environmental factors such as diet and e
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