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Anti-STAT2 (MOUSE) Monoclonal Antibody
Stat2 Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
| Host | Mouse |
|---|---|
| Conjugate | Unconjugated |
| Target Species | Mouse |
| Reactivity | Human |
| Clonality | Monoclonal |
Application 
| WB, IHC, E, I, LCI |
| Application Note | This Protein-A purified antibody has been tested for use in ELISA, immunohistochemistry, and western blotting. Specific conditions for reactivity should be optimized by the end user. Expect a band approximately 113 kDa in size corresponding to STAT2 protein by western blotting in the appropriate cell lysate or extract. |
| Physical State | Liquid (sterile filtered) |
| Buffer | 0.02 M Potassium Phosphate, 0.15 M Sodium Chloride, pH 7.2 |
| Immunogen | This monoclonal antibody was produced by repeated immunizations with a synthetic peptide corresponding to residues near the carboxy terminus of mouse STAT2 protein. |
| Preservative | 0.01% (w/v) Sodium Azide |
| Other Names | 6773 |
|---|---|
| Purity | This Protein-A purified antibody is directed against human STAT2 protein. A BLAST analysis was used to suggest cross-reactivity with STAT2 protein from human, rat (73%) and mouse (76%), sources based on homology with the immunizing sequence. Reactivity against homologues from other sources is not known. |
| Storage Condition | Store vial at -20° C prior to opening. Aliquot contents and freeze at -20° C or below for extended storage. Avoid cycles of freezing and thawing. Centrifuge product if not completely clear after standing at room temperature. This product is stable for several weeks at 4° C as an undiluted liquid. Dilute only prior to immediate use. |
| Precautions Note | This product is for research use only and is not intended for therapeutic or diagnostic applications. |
| Name | Stat2 |
|---|---|
| Function | Signal transducer and activator of transcription that mediates signaling by type I interferons (IFN-alpha and IFN-beta). Following type I IFN binding to cell surface receptors, Jak kinases (TYK2 and JAK1) are activated, leading to tyrosine phosphorylation of STAT1 and STAT2. The phosphorylated STATs dimerize, associate with IRF9/ISGF3G to form a complex termed ISGF3 transcription factor, that enters the nucleus. ISGF3 binds to the IFN stimulated response element (ISRE) to activate the transcription of interferon stimulated genes, which drive the cell in an antiviral state. In addition, also has a negative feedback regulatory role in the type I interferon signaling by recruiting USP18 to the type I IFN receptor subunit IFNAR2 thereby mitigating the response to type I IFNs. Acts as a regulator of mitochondrial fission by modulating the phosphorylation of DNM1L at 'Ser-616' and 'Ser-637' which activate and inactivate the GTPase activity of DNM1L respectively. |
| Cellular Location | Cytoplasm {ECO:0000250|UniProtKB:P52630}. Nucleus {ECO:0000250|UniProtKB:P52630}. Note=Translocated into the nucleus upon activation by IFN-alpha/beta. {ECO:0000250|UniProtKB:P52630} |
| Tissue Location | Found in the brain, lung, heart, spleen, liver, kidney, muscle and the testis |
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Provided below are standard protocols that you may find useful for product applications.
Background
STAT2 is a member of the STAT family of transcription factors. Unlike other STATs, STAT2 is unique as it can only be activated by interferons (IFNs). STAT2 is a critical component in mediating many IFN-stimulated biological activities including antiproliferation and antiviral responses. Upon IFN treatment, STAT1 and STAT2 become tyrosine phosphorylated, assemble as heterodimers that bind IRF9 to form the ISGF3 complex. This complex translocates to the nucleus, binds to promoters of IFN-stimulated genes and mediates gene transcription. Consequently, mutations in STAT2 or loss of STAT2 expression leads to impairment in IFN signal transduction and gene activation. IFN-alpha is an approved drug for the treatment of several forms of cancer. Yet only a subset of patients who receive IFN-alpha therapy benefit from the treatment. Given that STAT2 is activated by IFNs, it is important to define if the reduced or lack of antitumor effects seen in cancer patients on IFN therapy is due to in defects in STAT2 function. Our goal is to identify regions/motifs within the structural domains of STAT2 that not only are essential for the tyrosine phosphorylation of STAT2, but also regulate the antitumor effects of IFN-alpha. Collectively, the results of our studies will emphasize the physiological role of STAT2 in cancer. From a clinical viewpoint, cancer patients who may benefit the most from receiving IFN-alpha therapy can be selected based on their STAT2 function.
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