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STAT1 (基因名), Signal transducer and activator of transcription 1-alpha/beta (蛋白名), stat1_human.
产品名称:

Human STAT1/ Signal transducer and activator of transcription 1-alpha/beta Recombinant Protein
信号转换器和转录激活因子1- α / β

货号:

R1740h

商标:
EIAab®
监管等级:
别名:

Transcription factor ISGF-3 components p91/p84

序列号:
P42224
来源:
E.coli
种属:
Human
标签:
His
纯度:
>90% by SDS-PAGE
浓度:
Reconstitution Dependent
形态:
Liquid
内毒素水平:
Please contact protein@eiaab.com The technician for more information.
应用:
存储缓冲液:
50mM NaH2PO4, 500mM NaCl Buffer with 500mM Imidazole, 10%glycerol(PH8.0)
存储:
Store at -20°C. (Avoid repeated freezing and thawing.)
研究领域:
Cancer
Human STAT1 Protein
规格 & 价格: cart
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Human STAT1 Protein
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产品说明书
说明书: 下载说明书
MSDS: MSDS
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R&D 技术数据
更多信息,请参阅手册,或联系我们的技术支持: tech@eiaab.com.
基因位点
Cytogenetic band: 2q32.2 by HGNC 2q32.2 by Entrez Gene 2q32.2 by Ensembl
STAT1 Gene in genomic location: bands according to Ensembl, locations according to GeneLoc (and/or Entrez Gene and/or Ensembl if different)
基因位点
通用注释


亚单元:
Isoform alpha homodimerizes upon IFN-gamma induced phosphorylation. Heterodimer with STAT2 upon IFN-alpha/beta induced phosphorylation. The heterodimer STAT1:STAT2 forms the interferon-stimulated gene factor 3 complex (ISGF3) with IRF9. Interacts (phosphorylated at Ser 727) with PIAS1 (dimethylated on arginine); the interaction results in release of STAT1 from its target gene. Interacts with IFNAR1; the interaction requires the phosphorylation of IFNAR1 at 'Tyr-466'. Interacts with IFNAR2, NMI, PTK2/FAK1 and SRC. Interacts with ERBB4 (phosphorylated). 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. Interacts with HCV core protein; the interaction results in STAT1 degradation.


功能:
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.


亚细胞位置:
Cytoplasm Nucleus Translocated into the nucleus upon tyrosine phosphorylation and dimerization, in response to IFN-gamma and signaling by activated FGFR1, FGFR2, FGFR3 or FGFR4.


该产品尚未在任何出版物中被引用。

[1].
"Suppressor of cytokine signaling 1 inhibits IFN-gamma inflammatory signaling in human keratinocytes by sustaining ERK1/2 activation."

[2].
"Interferon beta augments tuberous sclerosis complex 2 (TSC2)-dependent inhibition of TSC2-null ELT3 and human lymphangioleiomyomatosis-derived cell proliferation."

[3].
"Inborn errors of interferon (IFN)-mediated immunity in humans: insights into the respective roles of IFN-alpha/beta, IFN-gamma, and IFN-lambda in host defense."

[4].
"The genetic heterogeneity of mendelian susceptibility to mycobacterial diseases."

[5].
"SOCS1 regulates the IFN but not NFkappaB pathway in TLR-stimulated human monocytes and macrophages."

[6].
"Phosphatase PTP1B negatively regulates MyD88- and TRIF-dependent proinflammatory cytokine and type I interferon production in TLR-triggered macrophages."

[7].
"Priming of peripheral monocytes with prolactin (PRL) sensitizes IFN-gamma-mediated indoleamine 2,3-dioxygenase (IDO) expression without affecting IFN-gamma signaling."

[8].
"STAT1 and STAT3 do not participate in FGF-mediated growth arrest in chondrocytes."

[9].
"Gene profiling analysis of ALVAC infected human monocyte derived dendritic cells."

[10].
"Interferon antagonist function of Japanese encephalitis virus NS4A and its interaction with DEAD-box RNA helicase DDX42."
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