Endoglin/CD105: Proteins and Enzymes
Endoglin (CD105) is a transmembrane type III receptor for TGF-beta superfamily ligands and plays an important role in smooth muscle differentiation, angiogenesis, and neovascularization. It is highly expressed on proliferating vascular endothelial cells, chondrocytes, and syncytiotrophoblasts of term placenta. Human Endoglin haploinsufficiency can a cause the vascular disorder, hereditary hemorrhagic telangiectasia type I. Elevated levels of anti-angiogenic soluble Endoglin contribute to pathogenicity in preeclampsia. Endoglin associates with the receptors TGF-beta RII, Activin RIIA or RIIB, BMPR-IA/ALK-3, or BMPR-IB/ALK6 and enhance binding of Activin A, BMP-2, -7, -9, TGF-beta 1, or TGF-beta 3. Endoglin can either enhance or inhibit signaling through these receptor complexes.
8 results for "Endoglin/CD105 Proteins and Enzymes" in Products
8 results for "Endoglin/CD105 Proteins and Enzymes" in Products
Endoglin/CD105: Proteins and Enzymes
Endoglin (CD105) is a transmembrane type III receptor for TGF-beta superfamily ligands and plays an important role in smooth muscle differentiation, angiogenesis, and neovascularization. It is highly expressed on proliferating vascular endothelial cells, chondrocytes, and syncytiotrophoblasts of term placenta. Human Endoglin haploinsufficiency can a cause the vascular disorder, hereditary hemorrhagic telangiectasia type I. Elevated levels of anti-angiogenic soluble Endoglin contribute to pathogenicity in preeclampsia. Endoglin associates with the receptors TGF-beta RII, Activin RIIA or RIIB, BMPR-IA/ALK-3, or BMPR-IB/ALK6 and enhance binding of Activin A, BMP-2, -7, -9, TGF-beta 1, or TGF-beta 3. Endoglin can either enhance or inhibit signaling through these receptor complexes.
Source: | NS0 |
Accession #: | NP_001010968 |
Applications: | BA |
Source: | CHO |
Accession #: | P17813 |
Applications: | BA |
Source: | NS0 |
Accession #: | Q8K100 |
Applications: | BA |
Source: | NS0 |
Accession #: | Q5T9C0 |
Applications: | BA |
Source: | CHO |
Accession #: | P37176 |
Applications: | BA |
Applications: | AC |
Applications: | AC |
Applications: | AC |