Datasheet

生物描述

特异性	FADD Rabbit Recombinant mAb detects endogenous levels of total FADD.
背景	FAS-associated protein with death domain (FADD) is the key adaptor protein transmitting apoptotic signals mediated by the main death receptors (DRs). Besides being an essential instrument in cell death, FADD is also implicated in proliferation, cell cycle progression, tumor development, inflammation, innate immunity, and autophagy. Depending on the cell type, FADD protein can either be present in the cytoplasm as a constitutive minor pool or be exported from the nucleus to the cytoplasm, possibly through DRs engagement. Cytoplasmic FADD interacts with the death domain of death receptors and recruits procaspase-8 to induce apoptosis of the cell. In addition, FADD protein can be expressed in the cytoplasm, but contained within microvesicles shed from the plasma membrane. Rapid release of phosphatidylserine (PS) expressing-microvesicles in the extracellular compartment following adenosine receptor activation will lead to a lack of cytoplasmic FADD, and therefore may protect cells from apoptosis. Expression of FADD in the nucleus is implicated in survival mechanisms. Nuclear sequestration of the protein enabling FADD-procaspase-8 interaction in the cytoplasm could account for the anti-apoptotic function of nuclear FADD. Alternatively, FADD could act as a transcription factor that activates survival genes. Nuclear FADD, through MBD4 interaction, could either protect the cell from apoptosis or couple genome surveillance to cell death.

特异性

FADD Rabbit Recombinant mAb detects endogenous levels of total FADD.

背景

FAS-associated protein with death domain (FADD) is the key adaptor protein transmitting apoptotic signals mediated by the main death receptors (DRs). Besides being an essential instrument in cell death, FADD is also implicated in proliferation, cell cycle progression, tumor development, inflammation, innate immunity, and autophagy. Depending on the cell type, FADD protein can either be present in the cytoplasm as a constitutive minor pool or be exported from the nucleus to the cytoplasm, possibly through DRs engagement. Cytoplasmic FADD interacts with the death domain of death receptors and recruits procaspase-8 to induce apoptosis of the cell. In addition, FADD protein can be expressed in the cytoplasm, but contained within microvesicles shed from the plasma membrane. Rapid release of phosphatidylserine (PS) expressing-microvesicles in the extracellular compartment following adenosine receptor activation will lead to a lack of cytoplasmic FADD, and therefore may protect cells from apoptosis. Expression of FADD in the nucleus is implicated in survival mechanisms. Nuclear sequestration of the protein enabling FADD-procaspase-8 interaction in the cytoplasm could account for the anti-apoptotic function of nuclear FADD. Alternatively, FADD could act as a transcription factor that activates survival genes. Nuclear FADD, through MBD4 interaction, could either protect the cell from apoptosis or couple genome surveillance to cell death.

使用信息

抗体应用

wb,ELISA,ELISA

稀释比例

WB

1:1000

反应性

Human

MW (kDa)

28kDa

抗体类型

储存液配方

10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide.

储存条件
(自收到货起)

Store at –20°C.

文献参考

[1] Tourneur L, et al. Trends Immunol. 2010, 31(7):260-9.

Application Data

WB

Validated by Selleck