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STAT1 Antibody

Mouse Monoclonal Antibody (Mab)

     
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  • 1 - STAT1 Antibody AW5195
    Western blot analysis of lysates from Hela,MCF-7 cell line (from left to right), using STAT1 Antibody(Cat. #AW5195). AW5195 was diluted at 1:1000 at each lane. A goat anti-mouse IgG H&L(HRP) at 1:10000 dilution was used as the secondary antibody.Lysates at 20ug per lane.
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Product info
Application
  • Applications Legend:
  • E=ELISA
  • WB=Western Blotting
  • IHC=Immunohistochemistry
  • IHC-P=Immunohistochemistry (Paraffin)
  • IP=Immunoprecipitation
  • IF=Immunofluorescence
  • IC=Immunochemistry
  • ICC=Immunocytochemistry
  • FC=Flow Cytometry
  • DB=Dot Blot
WB
Primary Accession P42224
Reactivity Human
Host Mouse
Clonality Monoclonal
Isotype IgG1
Clone Names 1141CT26.2.1
Calculated MW H=87 KDa
Additional info
Gene ID 6772
Other Names STAT1;Signal transducer and activator of transcription 1-alpha/beta; Signal transducer and activator of transcription 1-alpha/beta; Transcription factor ISGF-3 components p91/p84
Target/Specificity Purified His-tagged STAT1 protein was used to produced this monoclonal antibody.
Dilution WB~~1:1000
Format Purified monoclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein G column, followed by dialysis against PBS.
StorageMaintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.
PrecautionsSTAT1 Antibody is for research use only and not for use in diagnostic or therapeutic procedures.
Protein Information
Name STAT1
Function Signal transducer and transcription activator that mediates cellular responses to interferons (IFNs), cytokine KITLG/SCF and other cytokines and other growth factors. Following type I IFN (IFN-alpha and IFN-beta) binding to cell surface receptors, signaling via protein kinases leads to activation of Jak kinases (TYK2 and JAK1) and to tyrosine phosphorylation of STAT1 and STAT2. The phosphorylated STATs dimerize and associate with ISGF3G/IRF-9 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 IFN- stimulated genes (ISG), which drive the cell in an antiviral state. In response to type II IFN (IFN-gamma), STAT1 is tyrosine- and serine-phosphorylated. It then forms a homodimer termed IFN- gamma-activated factor (GAF), migrates into the nucleus and binds to the IFN gamma activated sequence (GAS) to drive the expression of the target genes, inducing a cellular antiviral state. Becomes activated in response to KITLG/SCF and KIT signaling. May mediate cellular responses to activated FGFR1, FGFR2, FGFR3 and FGFR4.
Cellular Location Cytoplasm. Nucleus. Note=Translocated into the nucleus upon tyrosine phosphorylation and dimerization, in response to IFN-gamma and signaling by activated FGFR1, FGFR2, FGFR3 or FGFR4
Research Areas

BACKGROUND

Signal transducer and transcription activator that mediates cellular responses to interferons (IFNs), cytokine KITLG/SCF and other cytokines and growth factors. Following type I IFN (IFN-alpha and IFN-beta) binding to cell surface receptors, signaling via protein kinases leads to activation of Jak kinases (TYK2 and JAK1) and to tyrosine phosphorylation of STAT1 and STAT2. The phosphorylated STATs dimerize, associate with ISGF3G/IRF-9 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 response to type II IFN (IFN-gamma), STAT1 is tyrosine-and serine-phosphorylated. It then forms a homodimer termed IFN-gamma-activated factor (GAF), migrates into the nucleus and binds to the IFN gamma activated sequence (GAS) to drive the expression of the target genes, inducing a cellular antiviral state. Becomes activated in response to KITLG/SCF and KIT signaling. May mediate cellular responses to activated FGFR1, FGFR2, FGFR3 and FGFR4.

REFERENCES

Kristensen I., et al. Submitted (NOV-2009) to the EMBL/GenBank/DDBJ databases.
Schindler C., et al. Proc. Natl. Acad. Sci. U.S.A. 89:7836-7839(1992).
Ota T., et al. Nat. Genet. 36:40-45(2004).
Bechtel S., et al. BMC Genomics 8:399-399(2007).
Kalnine N., et al. Submitted (MAY-2003) to the EMBL/GenBank/DDBJ databases.

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