TNFR-S274 Antibody | 55-666

TNFR-S274 Antibody | 55-666 | Gentaur UK, US & Europe Distribution

Host: Rabbit

Reactivity: Human

Homology: N/A

Immunogen: This TNFR antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 252-281 amino acids from human TNFR.

Research Area: Cancer, Cell Cycle, Immunology, Signal Transduction,

Tested Application: WB, Flow

Application: For WB starting dilution is: 1:1000
For FACS starting dilution is: 1:10~50

Specificiy: N/A

Positive Control 1: N/A

Positive Control 2: N/A

Positive Control 3: N/A

Positive Control 4: N/A

Positive Control 5: N/A

Positive Control 6: N/A

Molecular Weight: 50 kDa

Validation: N/A

Isoform: N/A

Purification: This antibody is purified through a protein A column, followed by peptide affinity purification.

Clonality: Polyclonal

Clone: N/A

Isotype: Rabbit Ig

Conjugate: Unconjugated

Physical State: Liquid

Buffer: Supplied in PBS with 0.09% (W/V) sodium azide.

Concentration: batch dependent

Storage Condition: Store at 4˚C for three months and -20˚C, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.

Alternate Name: Tumor necrosis factor receptor superfamily member 1A, Tumor necrosis factor receptor 1, TNF-R1, Tumor necrosis factor receptor type I, TNF-RI, TNFR-I, p55, p60, CD120a, Tumor necrosis factor receptor superfamily member 1A, membrane form, Tumor necrosis factor-binding protein 1, TBPI, TNFRSF1A, TNFAR, TNFR1

User Note: Optimal dilutions for each application to be determined by the researcher.

BACKGROUND: The protein encoded by this gene is a member of the TNF-receptor superfamily. This protein is one of the major receptors for the tumor necrosis factor-alpha. This receptor can activate NF-kappaB, mediate apoptosis, and function as a regulator of inflammation. Antiapoptotic protein BCL2-associated athanogene 4 (BAG4/SODD) and adaptor proteins TRADD and TRAF2 have been shown to interact with this receptor, and thus play regulatory roles in the signal transduction mediated by the receptor. Germline mutations of the extracellular domains of this receptor were found to be associated with the autosomal dominant periodic fever syndrome. The impaired receptor clearance is thought to be a mechanism of the disease.