TNF-R1 Polyclonal Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application ![]()
| WB, IHC-P |
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Primary Accession | P19438 |
Reactivity | Human, Mouse, Rat |
Host | Rabbit |
Clonality | Polyclonal |
Calculated MW | 50495 Da |
Gene ID | 7132 |
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Other Names | TNFRSF1A; TNFAR; TNFR1; 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; CD antigen CD120a |
Dilution | WB~~WB 1:500-2000 Immunohistochemistry: 1/100 - 1/300. ELISA: 1/20000. Not yet tested in other applications. |
Format | Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.09% (W/V) sodium azide. |
Storage Conditions | -20℃ |
Name | TNFRSF1A |
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Synonyms | TNFAR, TNFR1 |
Function | Receptor for TNFSF2/TNF-alpha and homotrimeric TNFSF1/lymphotoxin-alpha. The adapter molecule FADD recruits caspase-8 to the activated receptor. The resulting death-inducing signaling complex (DISC) performs caspase-8 proteolytic activation which initiates the subsequent cascade of caspases (aspartate-specific cysteine proteases) mediating apoptosis. Contributes to the induction of non-cytocidal TNF effects including anti-viral state and activation of the acid sphingomyelinase. |
Cellular Location | Cell membrane; Single-pass type I membrane protein Golgi apparatus membrane; Single-pass type I membrane protein. Secreted. Note=A secreted form is produced through proteolytic processing |
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Provided below are standard protocols that you may find useful for product applications.
Background
Receptor for TNFSF2/TNF-alpha and homotrimeric TNFSF1/lymphotoxin-alpha. The adapter molecule FADD recruits caspase-8 to the activated receptor. The resulting death-inducing signaling complex (DISC) performs caspase-8 proteolytic activation which initiates the subsequent cascade of caspases (aspartate- specific cysteine proteases) mediating apoptosis. Contributes to the induction of non-cytocidal TNF effects including anti-viral state and activation of the acid sphingomyelinase.
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