Recombinant Rat TNFRSF11A Protein (Fc tag) 200µg

NA

NA

C-Fc

61 KDa

47.1 kDa

TNFRSF11A

Met1-Pro213

HEK293 Cells

recombinants

Rattus norvegicus

Recombinants or rec. proteins

> 80 % as determined by SDS-PAGE

Lyophilized from sterile PBS, pH 7.4

< 1.0 EU per μg of the protein as determined by the LAL method

Samples are stable for up to twelve months from date of receipt at -70℃.Store it under sterile conditions at -20℃ to -80℃. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.

In general, recombinant proteins are provided as lyophilized powder which are shipped at ambient temperature.Bulk packages of recombinant proteins are provided as frozen liquid. They are shipped out with blue ice unless customers require otherwise.

Rats are used to make rat monoclonal anti mouse antibodies. There are less rat- than mouse clones however. Rats genes from rodents of the genus Rattus norvegicus are often studied in vivo as a model of human genes in Sprague-Dawley or Wistar rats.

TNFRSF11A is a member of the TNF-receptor superfamily. In mouse, it is also known as CD265. TNFRSF11A contains 4 TNFR-Cys repeats and is widely expressed with high levels in skeletal muscle, thymus, liver, colon, small intestine and adrenal gland. It is an essential mediator for osteoclast and lymph node development. TNFRSF11A and its ligand are important regulators of the interaction between T cells and dendritic cells. It can interact with various TRAF family proteins, through which this receptor induces the activation of NF-kappa B and MAPK8/JNK. Defects in TNFRSF11A can cause familial expansile osteolysis (FEO). FEO is a rare autosomal dominant bone disorder characterized by focal areas of increased bone remodeling. Defects in TNFRSF11A also can cause Paget disease of bone type 2 (PDB2). PDB2 is a bone-remodeling disorder with clinical similarities to FEO. Defects in TNFRSF11A are the cause of osteopetrosis autosomal recessive type 7 which characterized by abnormally dense bone, due to defective resorption of immature bone.