Key features and details
- Rabbit polyclonal to STAT1 alpha
- Suitable for: IHC-P, ICC/IF, WB
- Reacts with: Mouse, Rat, Human
- Isotype: IgG
製品名Anti-STAT1 alpha antibody
STAT1 alpha 一次抗体 製品一覧
製品の詳細Rabbit polyclonal to STAT1 alpha
アプリケーション適用あり: IHC-P, ICC/IF, WBmore details
種交差性交差種: Mouse, Rat, Human
Synthetic peptide corresponding to Human STAT1 alpha aa 712-750. The sequences differ from the murine corresponding sequences by four amino acids.
- HeLa whole cell lysate, Jurkat whole cell lysate or A431 whole cell. lysate.
特記事項JAK activated transcription.
保存方法Shipped at 4°C. Upon delivery aliquot and store at -20°C or -80°C. Avoid repeated freeze / thaw cycles.
バッファーPreservative: 0.02% Sodium azide
Concentration information loading...
Our Abpromise guarantee covers the use of ab2071 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|IHC-P||Use a concentration of 2.5 µg/ml.|
|ICC/IF||Use a concentration of 10 µg/ml.|
|WB||1/1000 - 1/2000. Detects a band of approximately 200 kDa (predicted molecular weight: 100 kDa).|
機能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.
関連疾患Note=STAT1 deficiency results in impaired immune response leading to severe mycobacterial and 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.
配列類似性Belongs to the transcription factor STAT family.
Contains 1 SH2 domain.
翻訳後修飾Phosphorylated on tyrosine and serine residues in response to IFN-alpha, IFN-gamma, PDGF and EGF. Phosphorylation on Tyr-701 (lacking in beta form) by JAK promotes dimerization and subsequent translocation to the nucleus. Phosphorylation on Ser-727 by several kinases including MAPK14, ERK1/2 and CAMKII on IFN-gamma stimulation, regulates STAT1 transcriptional activity. Phosphorylation on Ser-727 promotes sumoylation though increasing interaction with PIAS. Phosphorylation on Ser-727 by PKCdelta induces apoptosis in response to DNA-damaging agents.
Sumoylated by SUMO1, SUMO2 and SUMO3. Sumoylation is enhanced by IFN-gamma-induced phosphorylation on Ser-727, and by interaction with PIAS proteins. Enhances the transactivation activity.
細胞内局在Cytoplasm. Nucleus. Translocated into the nucleus in response to IFN-gamma-induced tyrosine phosphorylation and dimerization.
- Information by UniProt
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Immunofluorescence of STAT1 in human colon tissue with ab2071 at 20 μg/mL.
All lanes : Anti-STAT1 alpha antibody (ab2071) at 0.5 µg/ml
Lane 1 : Mouse skin
Lane 2 : Mouse skeletal muscle
Lane 3 : Mouse bladder
Lane 4 : Mouse lung
Lysates/proteins at 15 µg per lane.
All lanes : Goat anti-rabbit IgG HRP conjugate at 1/10000 dilution
Predicted band size: 100 kDa
Immunohistochemistry of STAT1 in human colon tissue with ab2071 at 2.5 μg/ml.
Anti-STAT1 alpha antibody (ab2071) at 1 µg/ml + YB2/0 at 15 µg
Goat anti-rabbit IgG HRP conjugate at 1/10000 dilution
Predicted band size: 100 kDa
All lanes : Anti-STAT1 alpha antibody (ab2071) at 1 µg/ml
Lane 1 : HeLa whole cell lysate
Lane 2 : Jurkat whole cell lysate
Lane 3 : A431 whole cell lysate
Lane 4 : K562 whole cell lysate
Lane 5 : NIH3T3 whole cell lysate
Predicted band size: 100 kDa
Observed band size: 91 kDa why is the actual band size different from the predicted?
Immunocytochemistry of STAT1a in HeLa cells with STAT1a antibody at 10 µg/ml.
ab2071 は 5 報の論文で使用されています。
- Yang J et al. IL-1ß increases the expression of inflammatory factors in synovial fluid-derived fibroblast-like synoviocytes via activation of the NF-?B-mediated ERK-STAT1 signaling pathway. Mol Med Rep 20:4993-5001 (2019). PubMed: 31638264
- Matthes F et al. Inhibition of the MID1 protein complex: a novel approach targeting APP protein synthesis. Cell Death Discov 4:4 (2018). PubMed: 29531801
- Ip JPK et al. Major Vault Protein, a Candidate Gene in 16p11.2 Microdeletion Syndrome, Is Required for the Homeostatic Regulation of Visual Cortical Plasticity. J Neurosci 38:3890-3900 (2018). PubMed: 29540554
- Nagakura I et al. STAT1 Regulates the Homeostatic Component of Visual Cortical Plasticity via an AMPA Receptor-Mediated Mechanism. J Neurosci 34:10256-63 (2014). Mouse . PubMed: 25080587
- Carlos TS et al. Parainfluenza virus 5 genomes are located in viral cytoplasmic bodies whilst the virus dismantles the interferon-induced antiviral state of cells. J Gen Virol 90:2147-56 (2009). ICC/IF ; Human . PubMed: 19458173