Tumor Necrosis Factor Receptor Superfamily Member 1A (TNFRSF1A) Reagents

Tumor necrosis factor receptor superfamily member 1A

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.

Familial hibernian fever (FHF); Multiple sclerosis 5 (MS5)

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.; [Isoform 4]: Secreted. Note=Lacks a Golgi-retention motif, is not membrane bound and therefore is secreted.

Apoptosis, Signal Transduction

CD120a; FPF; MGC19588; p55; p55-R; p60; TBP1; TBPI; TNF R; TNF R55; TNF-R1; TNF-RI; TNFAR; TNFR-I; TNFR1; TNFR55; TNFR60; TNFRI; TNFRSF1a; TNR1A_HUMAN; Tumor necrosis factor receptor 1; Tumor necrosis factor receptor superfamily, member 1A; Tumor necrosis factor receptor type 1; Tumor necrosis factor receptor type I; Tumor necrosis factor-binding protein 1

This gene encodes a member of the TNF receptor superfamily of proteins. The encoded receptor is found in membrane-bound and soluble forms that interact with membrane-bound and soluble forms, respectively, of its ligand, tumor necrosis factor alpha. Binding of membrane-bound tumor necrosis factor alpha to the membrane-bound receptor induces receptor trimerization and activation, which plays a role in cell survival, apoptosis, and inflammation. Proteolytic processing of the encoded receptor results in release of the soluble form of the receptor, which can interact with free tumor necrosis factor alpha to inhibit inflammation. Mutations in this gene underlie tumor necrosis factor receptor-associated periodic syndrome (TRAPS), characterized by fever, abdominal pain and other features. Mutations in this gene may also be associated with multiple sclerosis in human patients.