特异性
ADAP/SLAP-130/Fyb
免疫原
对应于小鼠Fyn 结合蛋白氨基酸755-768的合成肽(ADAP/SLAP-130/Fyb)。
应用
抗-ADAP/SLAP-130/Fyb抗体是针对ADAP/SLAP-130/Fyb的抗体,用于WB & IP。
研究子类别
免疫信号传导
激酶&磷酸酶
免疫信号传导
激酶&磷酸酶
研究类别
信号传导
信号传导
质量
通过免疫印迹对RAW 264.7巨噬细胞的RIPA裂解液进行了常规评估
目标描述
130kDa
外形
0.1M Tris-甘氨酸,pH 7.4,0.15M NaCl,0.05%叠氮化钠,然后添加甘油至30%
形式:纯化
纯化蛋白A
储存及稳定性
在-20°C下可保存2年
法律信息
UPSTATE is a registered trademark of Merck KGaA, Darmstadt, Germany
免责声明
除非我们的产品目录或产品附带的其他公司文档另有说明,否则我们的产品仅供研究使用,不得用于任何其他目的,包括但不限于未经授权的商业用途、体外诊断用途、离体或体内治疗用途或任何类型的消费或应用于人类或动物。
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储存分类代码
10 - Combustible liquids
WGK
WGK 1
Signaling by Fyn-ADAP via the Carma1-Bcl-10-MAP3K7 signalosome exclusively regulates inflammatory cytokine production in NK cells.
Nature Immunology null
Proceedings of the National Academy of Sciences of the United States of America, 98(20), 11527-11532 (2001-09-13)
Aggregation of the high-affinity IgE receptor (FcepsilonRI) on mast cells activates a tyrosine phosphorylation cascade that is required for adhesion and degranulation events leading to the release of histamine and other inflammatory mediators. The full range of intracellular mediators that
The Journal of biological chemistry, 275(7), 5143-5152 (2000-02-15)
T cell antigen receptor (TCR) engagement results in protein-tyrosine kinase activation which initiates signaling cascades leading to induction of the interleukin-2 gene. Previous studies identified two substrates of the TCR-induced protein-tyrosine kinases, SH2 domain-containing leukocyte specific protein of 76 kDa
Journal of immunology (Baltimore, Md. : 1950), 164(3), 1143-1147 (2000-01-21)
The role of integrin-mediated signaling events in T cell function remains incompletely characterized. We report here that alpha4beta1 integrin stimulation of H9 T cells and normal human T cell blasts results in rapid and transient tyrosine phosphorylation of the adapter
Communications biology, 4(1), 905-905 (2021-07-24)
Natural Killer (NK) cell dysfunction is associated with poorer clinical outcome in cancer patients. What regulates NK cell dysfunction in tumor microenvironment is not well understood. Here, we demonstrate that the human tumor-derived NKG2D ligand soluble MIC (sMIC) reprograms NK
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