Technology ID
TAB-4873
Genetically Modified Traf3ip2-/- Mice as a Valuable Resource for Exploring IL-17 Signaling in Autoimmune, Inflammatory Diseases, and Beyond
E-Numbers
E-051-2014-0
Lead Inventor
Siebenlist (Estate), Ulrich
Lead IC
NIAID
ICs
NIAID
Applications
Therapeutics
Research Materials
Therapeutic Areas
Rare/Neglected Diseases
Oncology
Immunology
Development Stages
Pre-clinical (in vivo)
Research Products
Animal Models
Traf3ip2-/- C57/BL6 mice are a genetically modified mouse model in which the Traf3ip2 gene, responsible for encoding the CIKS adaptor protein essential for IL-17 cytokine signaling, has been disrupted. These mice offer a robust platform for research in autoimmune and inflammatory diseases, as well as potential applications in cancer studies. By eliminating IL-17 signaling and cross-interactions with other pathways, they provide a unique opportunity for drug discovery and proof-of-principle studies, shedding light on disease mechanisms and therapeutic development.
Commercial Applications
Traf3ip2-/- C57/BL6 mice find utility in research on autoimmune and inflammatory diseases, cancer studies, and drug development targeting IL-17 signaling pathways. These genetically engineered mice offer a valuable platform for gaining insights into disease mechanisms and testing novel therapeutic interventions. Their versatility makes them an essential resource for diverse biomedical research endeavors.
Competitive Advantages
Traf3ip2-/- C57/BL6 mice provide researchers with a focused and efficient tool for investigating IL-17 signaling pathways and related diseases. By eliminating CIKS adaptor protein expression, these mice streamline research efforts, enabling targeted drug discovery, proof-of-principle studies, and a deeper understanding of autoimmune, inflammatory, and potentially cancer-related conditions.
Licensing Contact: