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MOUSE ANTI-STAT4 100 UG

 
包装:
运保温度: -20°C
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描述:

Details
Tested species reactivity Mouse , Rat , Human
Host / Isotype Mouse / IgG2a, kappa
Class Monoclonal
Type Antibody
Clone ST4-5D6
Immunogen A synthetic peptide derived form the C terminus of murine STAT4.
Conjugate Unconjugated
Form Liquid
Concentration 0.5 mg/ml
Purification Protein A
Storage buffer PBS, pH 7.4
Preservative 0.1% sodium azide
Storage Conditions -20°C
Tested Applications Dilution *
ELISA (ELISA) 0.1-1.0 ug/ml
Gel Shift (GS) 1-5 ug/ml
Immunoprecipitation (IP) 5 ug
Western Blot (WB) 1-3 ug/ml

* Suggested working dilutions are given as a guide only. It is recommended that the user titrate the product for use in their own experiment using appropriate negative and positive controls.

 

Background/Target Information

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-gamma 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-gamma 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-g production.

 


注意事项:

For Research Use Only. Not for use in diagnostic procedures.
 


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