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Anti-phospho-STAT1 (Ser 727) Antibody, clone 12C5 is a Mouse Monoclonal Antibody for detection of phospho-STAT1 (Ser 727) also known as signal transducer & activator of transcription 1 & has been tested in ELISA & WB.
More>>Anti-phospho-STAT1 (Ser 727) Antibody, clone 12C5 is a Mouse Monoclonal Antibody for detection of phospho-STAT1 (Ser 727) also known as signal transducer & activator of transcription 1 & has been tested in ELISA & WB. Less<<
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Anti-phospho-STAT1 (Ser 727) Antibody, clone 12C5 is a Mouse Monoclonal Antibody for detection of phospho-STAT1 (Ser 727) also known as signal transducer & activator of transcription 1 & has been tested in ELISA & WB.
Key Applications
ELISA
Western Blotting
Biological Information
Immunogen
KLH-conjugated synthetic peptide encompassing the surrounding amino acids of Serine727 on phosphorylated STAT1
Clone
12C5
Host
Mouse
Specificity
Recognizes phosphorylated domain of STAT1 on Serine727
The protein encoded by this gene is a member of the STAT protein family. In response to cytokines and growth factors, STAT family members are phosphorylated by the receptor associated kinases, and then form homo- or heterodimers that translocate to the cell nucleus where they act as transcription activators. This protein can be activated by various ligands including interferon-alpha, interferon-gamma, EGF, PDGF and IL6. This protein mediates the expression of a variety of genes, which is thought to be important for cell viability in response to different cell stimuli and pathogens. Two alternatively spliced transcript variants encoding distinct isoforms have been described.
Gene Symbol
STAT1
ISGF-3
STAT91
DKFZp686B04100
Modifications
Phosphorylation
Purification Method
Subsequent thiophilic adsorption and size exclusion chromatography
FUNCTION: SwissProt: P42224 # Signal transducer and activator of transcription that mediates signaling by interferons (IFNs). Following type I IFN (IFN-alpha and IFN-beta) 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 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. SIZE: 750 amino acids; 87335 Da SUBUNIT: Isoform alpha homodimerizes upon IFN-gamma induced phosphorylation. Heterodimer with STAT2 upon IFN-alpha/beta induced phosphorylation. Interacts with NMI. Interacts with Sendai virus C', C, Y1 and Y2 proteins, Nipah virus P, V and W proteins, and rabies virus phosphoprotein preventing activation of ISRE and GAS promoter (By similarity). Interaction with HCV core protein results in STAT1 degradation. SUBCELLULAR LOCATION: Cytoplasm. Nucleus. Note=Translocated into the nucleus upon activation by IFN-alpha/beta. PTM: Phosphorylated on tyrosine residues in response to IFN-alpha, IFN-gamma, PDGF and EGF. Serine phosphorylation is also required for maximal transcriptional activity in IFN-gamma transduction (lacking in beta form). DISEASE: SwissProt: P42224 # Defects in STAT1 are the cause of STAT1 deficiency [MIM:600555]. Patients generally suffer from mycobacterial or viral diseases. In the case of complete deficiency, patients can die of viral disease. & Defects in STAT1 are a cause of mendelian susceptibility to mycobacterial disease (MSMD) [MIM:209950]; also known as familial disseminated atypical mycobacterial infection. This rare condition confers predisposition to illness caused by moderately virulent mycobacterial species, such as Bacillus Calmette-Guerin (BCG) vaccine and environmental non-tuberculous mycobacteria, and by the more virulent Mycobacterium tuberculosis. Other microorganisms rarely cause severe clinical disease in individuals with susceptibility to mycobacterial infections, with the exception of Salmonella which infects less than 50% of these individuals. The pathogenic mechanism underlying MSMD is the impairment of interferon-gamma mediated immunity whose severity determines the clinical outcome. Some patients die of overwhelming mycobacterial disease with lepromatous-like lesions in early childhood, whereas others develop, later in life, disseminated but curable infections with tuberculoid granulomas. MSMD is a genetically heterogeneous disease with autosomal recessive, autosomal dominant or X-linked inheritance. SIMILARITY: SwissProt: P42224 ## Belongs to the transcription factor STAT family. & Contains 1 SH2 domain.
Molecular Weight
92 kDa
Physicochemical Information
Dimensions
Materials Information
Toxicological Information
Safety Information according to GHS
Safety Information
Product Usage Statements
Quality Assurance
Routinely evaluated by immunoblot.
Usage Statement
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
Storage and Shipping Information
Storage Conditions
2 years at -20°C from date of shipment. Avoid repeated freeze/thaw cycles, which may damage IgG and affect product performance.
Prostacyclin receptor induces STAT1 and STAT3 phosphorylations in human erythroleukemia cells: a mechanism requiring PTX-insensitive G proteins, ERK and JNK Lo, Rico K H, et al Cell Signal, 18:307-17 (2006)
2005
VEGF receptors on chronic lymphocytic leukemia (CLL) B cells interact with STAT 1 and 3: implication for apoptosis resistance. Lee, Y K, et al. Leukemia, 19: 513-23 (2005)
2004
We have previously shown that chronic lymphocytic leukemia (CLL) B cells secrete vascular endothelial growth factor (VEGF) in vitro, have constitutively active VEGF receptors R1 and R2, and respond to exogenous VEGF by specifically upregulating Mcl-1 and XIAP in association with decreased cell death. We found that epigallocatechin (EGCG) decreases VEGF receptor phosphorylation and induces apoptosis in CLL B cells. The mechanism(s) by which VEGF receptor activation increases Mcl-1 and XIAP and promotes survival remains unknown. To further define the signaling pathway mediating VEGF induction of antiapoptotic proteins in CLL B-cells, we investigated downstream effects of VEGF-VEGF receptor binding on the STAT signaling pathway. We find that CLL B cells abundantly express cytoplasmic serine phosphorylated (p)-STAT-1 and p-STAT-3, VEGF-R1/2 are physically associated with p-STAT-1 and p-STAT-3, and p-STAT-3 (but not p-STAT-1) is found in the CLL nucleus. VEGF receptor ligation selectively induces activation and perinuclear translocation of STAT 3 through receptor-mediated endocytosis. The inhibition of VEGF receptor activation with either tyrosine kinase inhibitors or VEGF neutralizing antibodies inhibit VEGF receptor phosphorylation, decrease p-STAT-3 (serine 727), Mcl-1, and induces cell death in CLL B cells. Thus, a VEGF-VEGF receptor pathway in CLL B cells can be linked to activation of STAT proteins that are able to enhance their apoptotic resistance.
Differential effects of lipoprotein lipase on tumor necrosis factor-alpha and interferon-gamma-mediated gene expression in human endothelial cells Kota, Rama S, et al J Biol Chem, 280:31076-84 (2005)
2004
Roles of phosphatidylinositol 3-kinase in interferon-gamma-dependent phosphorylation of STAT1 on serine 727 and activation of gene expression Nguyen, H, et al J Biol Chem, 276:33361-8 (2001)
2001
