This purified ABfinity™ recombinant rabbit anti-STAT4 monoclonal antibody reacts with human, mouse, and rat STAT4. STAT4 is encoded by the 6775 gene, also known as signal transducer and activator of transcription 4, SLEB11. Anti-STAT4 monoclonal antibody is used in western blotting, ELISA, flow cytometry, immunofluorescence, and immunohistochemistry applications.

Antibody Specifications:

• Applications: Validated applications for anti-STAT4 monoclonal antibody are western blotting, ELISA, flow cytometry, immunofluorescence, and immunohistochemistry.
• Host Species and Isotype: The host species and isotype of the antibody is rabbit IgG.
• Clone ID of Monoclonal Antibody (mAb): The anti-STAT4 monoclonal antibody clone is 2H9L5.
• Reactivity: Reacts with human, mouse, and rat STAT4.
• Product Size: Rabbit anti-STAT4 monoclonal antibody is available in a 100 µg size.

Signal transducer and activator of transcription 4 (STAT4) was originally identified using degenerate primers complementary to sequences encoding conserved regions of other STAT proteins. The STAT4 protein is most similar to STAT 1 (52%) and STAT3 (47%). Functionally, STAT4 is similar to other STAT family members in that it can be tyrosine phosphorylated by Jak1 or Jak2. STAT4 forms homodimers and heterodimers with related STAT family members. Tyrosine phosphorylated STAT4 can bind the IFN-γ activated site (GAS). Serine phosphorylation of STAT is also required for maximal transcriptional activity. STAT4 expression is restricted to the thymus, spleen and testis. Until recently the cytokine(s) responsible for activation of STAT4 had not been identified. STAT4 is now known to be activated by the cytokine interleukin-12 (IL-12). IL-12 is required for the T-cell independent induction of IFN-γ which is a key step in the initial suppression of bacterial and parasitic infections. In addition, IL-12 is required for the development of a Th1 response which is necessary for effective host defense against intracellular pathogens. Perhaps not surprisingly, STAT4-deficient mice display impaired IL-12 development of Th1 cells and enhanced development of Th2 cells. A recent study in mouse has shown that in response to viral infection IFN-a/b activation of STAT4 is required for IFN-γ production.