TRADD Recombinant Rabbit mAb (一抗) - WB,ICC/IF,IP | Bioss

Rrmab?兔单抗
2026-03-02~2026-04-30,KXJ2603
TRADD Recombinant Rabbit mAb (一抗) - WB,ICC/IF,IP | Bioss
货号:bsm-61653R
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概述

产品编号
bsm-61653R
产品类型
重组兔单抗
英文名称
TRADD Recombinant Rabbit mAb
中文名称
肿瘤坏死因子受体1相关死亡域蛋白重组兔单抗
英文别名
Hs.89862; 9130005N23Rik; TRADD_HUMAN; TRADD; TNFR1-associated DEATH domain protein; TNFRSF1A-associated via death domain; TRADD_MOUSE;
抗体来源
Rabbit
免疫原
A synthesized peptide derived from human TRADD: 210-312
亚型
IgG
性状
Liquid
纯化方法
affinity purified by Protein A
克隆类型
Recombinant
克隆号
2C10
理论分子量
34 kDa
检测分子量
35 kDa
储存液
10mM phosphate buffered saline(pH 7.4) with 150mM sodium chloride, 0.05% BSA, 0.02% Proclin300 and 50% glycerol.
SWISS
Gene ID
保存条件
Store at 4℃ for short term. Store at -20℃ for long term. Avoid repeated freeze/thaw cycles.
注意事项
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
产品介绍
TRADD在凋亡信号传导中起重要作用,近年来多用于研究其在肿瘤中的作用,探讨TRADD在促细胞凋亡和促细胞存活的机制如何控制,将有利于我们了解肿瘤发病机理。
背景资料
Adapter molecule for TNFRSF1A/TNFR1 that specifically associates with the cytoplasmic domain of activated TNFRSF1A/TNFR1 mediating its interaction with FADD.Overexpression of TRADD leads to two major TNF-induced responses, apoptosis and activation of NF-kappa-B.
肿瘤坏死因子受体1相关死亡域蛋白重组兔单抗-bsm-61653R

产品应用

应用已检合格种属预测种属推荐稀释比例
WBHumanMouse, Rat1:500-2000
ICC/IFHuman, Mouse, Rat1:50-200
IPHuman, Mouse, Rat1:20-50

交叉反应

交叉反应: Human (predicted: Mouse, Rat)

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靶标

基因名
TRADD
蛋白名
Tumor necrosis factor receptor type 1-associated DEATH domain protein
亚基
Interacts with TRIP12. Heterodimer with TNFRSF1A/TNFR1. Interacts with DAB2IP, FADD, HIPK2, KRT14, KRT16, KRT17, KRT18, RIPK1, SQSTM1, TRAF1, TRAF2 and TRPC4AP.
亚细胞定位
Cytoplasm > cytoskeleton.
组织特异性
Found in all examined tissues.
相似性
Contains 1 death domain.
功能
Adapter molecule for TNFRSF1A/TNFR1 that specifically associates with the cytoplasmic domain of activated TNFRSF1A/TNFR1 mediating its interaction with FADD. Overexpression of TRADD leads to two major TNF-induced responses, apoptosis and activation of NF-kappa-B.

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