Recombinant Human Endoglin/CD105 Protein (His&Trx Tag) | PKSH032379

Recombinant Human Endoglin/CD105 Protein (His&Trx Tag) | PKSH032379 | Gentaur US, UK & Europe Disrtribition

Synonyms: Endoglin; END; CD105; ENG;HHT1;ORW1

Active Protein: N/A

Activity: Recombinant Human Endoglin is produced by our E.coli expression system and the target gene encoding Glu26-Gln176 is expressed with a Trx, 6His tag at the N-terminus.

Protein Construction: Recombinant Human Endoglin is produced by our E.coli expression system and the target gene encoding Glu26-Gln176 is expressed with a Trx, 6His tag at the N-terminus.

Fusion Tag: N-Trx & His

Species: Human

Expressed Host: E.coli

Shipping: This product is provided as liquid. It is shipped at frozen temperature with blue ice/gel packs. Upon receipt, store it immediately at<-20°C.

Purity: > 95 % as determined by reducing SDS-PAGE.

Endotoxin: < 1.0 EU per µg as determined by the LAL method.

Stability and Storage: Store at < -20°C, stable for 6 months. Please minimize freeze-thaw cycles.

Molecular Mass: 33.6 kDa

Formulation: Supplied as a 0.2 μm filtered solution of 20mM PB，150mM NaCl, pH7.4.

Reconstitution: Not Applicable

Background: Endoglin is a single-pass type I membrane protein which restricted to endothelial cells in all tissues except bone marrow. Endoglin as major glycoprotein of vascular endothelium, it has been found on endothelial cells, activated macrophages, fibroblasts, and smooth muscle cells. Furthermore, Homodimer forms a heteromeric complex with the signaling receptors for transforming growth factor-beta: TGFBR1 and/or TGFBR2. It may have an important role in the binding of endothelial cells to integrins and/or other RGD receptors. Defects in ENG are the cause of hereditary hemorrhagic telangiectasia type 1 (HHT1), which is an autosomal dominant multisystemic vascular dysplasia, characterized by recurrent epistaxis, muco-cutaneous telangiectases, gastro-intestinal hemorrhage, and pulmonary (PAVM), cerebral (CAVM) and hepatic arteriovenous malformations.

Research Area: N/A