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Endoglin/CD105   Protein, Antibody, ELISA Kit, cDNA Clone

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Expression host: Human Cells  
10149-H02H-50
10149-H02H-20
50 µg 
20 µg 
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Expression host: Human Cells  
10149-H08H-50
10149-H08H-20
50 µg 
20 µg 
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Description: Active  
Expression host: Human Cells  
50407-M08H-50
50407-M08H-20
50407-M08H-100
50 µg 
20 µg 
100 µg 
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Endoglin/CD105  Related Area

Endoglin/CD105  Related Pathways

Endoglin/CD105  Related Protein, Antibody, cDNA Gene, and ELISA Kits

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Endoglin/CD105  Summary & Protein Information

Endoglin/CD105  Background

Gene Summary: ENG gene encodes a homodimeric transmembrane protein which is a major glycoprotein of the vascular endothelium. This protein is a component of the transforming growth factor beta receptor complex and it binds TGFB1 and TGFB3 with high affinity. Mutations in ENG gene cause hereditary hemorrhagic telangiectasia, also known as Osler-Rendu-Weber syndrome 1, an autosomal dominant multisystemic vascular dysplasia. Alternatively spliced transcript variants encoding different isoforms have been found for ENG gene. [provided by RefSeq, Sep 2008]
General information above from NCBI
Subunit structure: Homodimer that forms a heteromeric complex with the signaling receptors for transforming growth factor-beta: TGFBR1 and/or TGFBR2. It is able to bind TGF-beta 1, and 3 efficiently and TGF-beta 2 less efficiently. Interacts with TCTEX1D4. Interacts with ARRB2. Interacts with GDF2. {ECO:0000269|PubMed:16982625, ECO:0000269|PubMed:17540773, ECO:0000269|PubMed:21737454, ECO:0000269|PubMed:22347366}.
Subcellular location: Membrane; Single-pass type I membrane protein.
Tissue specificity: Endoglin is restricted to endothelial cells in all tissues except bone marrow.
Involvement in disease: DISEASE: Telangiectasia, hereditary hemorrhagic, 1 (HHT1) [MIM:187300]: A multisystemic vascular dysplasia leading to dilation of permanent blood vessels and arteriovenous malformations of skin, mucosa, and viscera. The disease is characterized by recurrent epistaxis and gastro-intestinal hemorrhage. Visceral involvement includes arteriovenous malformations of the lung, liver, and brain. {ECO:0000269|PubMed:10545596, ECO:0000269|PubMed:10625079, ECO:0000269|PubMed:10982033, ECO:0000269|PubMed:15024723, ECO:0000269|PubMed:15712270, ECO:0000269|PubMed:16525724, ECO:0000269|PubMed:16752392, ECO:0000269|PubMed:20414677, ECO:0000269|PubMed:9157574, ECO:0000269|PubMed:9245986, ECO:0000269|PubMed:9554745}. Note=The disease is caused by mutations affecting the gene represented in this entry.

Endoglin, also known as CD105, is a type I  homodimeric transmembrane glycoprotein with a large, disulfide-linked, extracellular region and a short, constitutively phosphorylated cytoplasmic tail. Endoglin contains an RGD tripeptide which is a key recognition structure in cellular adhesion,,suggesting a critical role for endoglin in the binding of endothelial cells to integrins and/or other RGD receptors. Endoglin is highly expressed on vascular endothelial cells, chondrocytes, and syncytiotrophoblasts of term placenta. It is also found on activated monocytes, mesenchymal stem cells and leukemic cells of lymphoid and myeloid lineages. As an accessory receptor for the TGF-β superfamily ligands, endoglin binds TGF-β1 and TGF-β3 with high affinity not by itself but by associating with TGF-β type I I receptor (TβRII) and activates the downstream signal pathways. In addition, in human umbilical vein endothelial cells, ALK-1 is also a receptor kinase for endoglin threonine phosphorylation, and mutations in either of the two genes result in the autosomal-dominant vascular dysplasia, hereditary hemorrhagic telangiectasia (HHT). Endoglin has been regarded as a powerful biomarker of neovascularization, and is associated with several solid tumor types.

Endoglin/CD105  Alternative Name

Endoglin/CD105  Related Studies

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