Specific Ablation of STAT3(beta) Distorts the Pattern of STAT3-Responsive Gene Expression and Impairs Recovery from Endotoxic Shock

Stat3 is one of seven mammalian signal transducer and activator of transcription molecules that are activated by the Janus Kinases in response to cytokines. Although originally identified as an acute-phase response factor activated by interleukin (IL)-6, Stat3 is now known to be activated in response to many other cytokines. Alternative splicing produces two Stat3 isoforms in mammals; Stat3-alpha and Stat3-beta, which exhibit overlapping but distinct biological properties. Targeted deletion of Stat3 (both isoforms) in mice results in early embryonic lethality. Recently, scientists at Johns Hopkins generated mice that are selectively unable to synthesize the Stat3-beta isoform. These mice are viable but exhibit diminished recovery from endotoxic shock and hyperresponsiveness of some endotoxin-inducible genes in liver. Description (Set) Proposed Use (Set) Stat3-beta deficient mice provide a model for studying effects of dysregulated systemic inflammation on development of chronic diseases such as atherosclerosis and autoimmune syndromes. The mice also provide a potential system for the testing of antiinflammatory agents that target the Stat3 pathway.

Inventor(s): Desiderio, Stephen V.

Type of Offer: Licensing



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