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Details for Product No. ABIN968467

CD105 (Endoglin / TGF-Beta1/3 Receptor) (AA 24-144) antibody

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Synonyms CD105, AI528660, AI662476, S-endoglin, END, HHT1, ORW1
»Alternatives AA 24-144
»Alternatives Human
»Alternatives Mouse
Clonality (Clone) Monoclonal ()
»Alternatives Un-conjugated
»Alternatives Western Blotting (WB), Immunofluorescence (IF)
Pubmed 4 references available
Catalog no. ABIN968467
Quantity 50 µg
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Immunogen Human S-Endoglin
Clone G52C7-1
Isotype IgG1, kappa
Characteristics 1. Since applications vary, each investigator should titrate the reagent to obtain optimal results.
2. Please refer to us for technical protocols.
3. Source of all serum proteins is from USDA inspected abattoirs located in the United States.
4. Caution: Sodium azide yields highly toxic hydrazoic acid under acidic conditions. Dilute azide compounds in running water before discarding to avoid accumulation of potentially explosive deposits in plumbing.
Purification Purified from tissue culture supernatant or ascites by affinity chromatography.
Purity Purified
Alternative Name CD105
Background Endoglin (CD105), a major glycoprotein of human vascular endothelium, is a type I integral membrane protein with a large extracellular region, a hydrophobic transmembrane region, and a short cytoplasmic tail. It also contains an RGD tripeptide that may be important for cellular adhesion. There are two forms of endoglin (S-endoglin and L-endoglin) that differ in the length of their cytoplasmic tails. However, the isoforms may have similar functional activity. When overexpressed in fibroblasts, both form disulfide-linked homodimers via their extracellular domains. Endoglin binds TGF-beta1 and TGF-beta3 by associating with TGF-beta type II receptor and binds BMP-7 by associating with activin type II receptor. Thus, endoglin is an accessory protein of multiple TGF-beta superfamily kinase receptor complexes. Loss of function mutations in the human endoglin gene cause hereditary hemorrhagic telangiectasia, which is characterized by vascular malformations. Deletion of endoglin in mice leads to death due to defective vascular development. Thus, endoglin is an endothelial specific cell surface protein that may regulate angiogenesis through interactions with TGF-beta superfamily kinase receptors. This antibody is routinely tested by western blot analysis.
Synonyms: Endoglin
Molecular Weight 95 kDa
Research Area Stem Cells, CD Antigens, Surface Receptors of Immune Cells

Related Products: ABIN968536, ABIN967389

Restrictions For Research Use only
Format Liquid
Concentration 250 µg/ml
Buffer Aqueous buffered solution containing BSA, glycerol.
Preservative Sodium azide
Storage -20 °C
Product cited in: Gougos, Letarte: "Primary structure of endoglin, an RGD-containing glycoprotein of human endothelial cells." in: The Journal of biological chemistry, Vol. 265, Issue 15, pp. 8361-4, 1990 (PubMed).

Bellón, Corbí, Lastres et al.: "Identification and expression of two forms of the human transforming growth factor-beta-binding protein endoglin with distinct cytoplasmic regions." in: European journal of immunology, Vol. 23, Issue 9, pp. 2340-5, 1993 (PubMed).

Barbara, Wrana, Letarte: "Endoglin is an accessory protein that interacts with the signaling receptor complex of multiple members of the transforming growth factor-beta superfamily." in: The Journal of biological chemistry, Vol. 274, Issue 2, pp. 584-94, 1999 (PubMed).

Li, Sorensen, Brooke et al.: "Defective angiogenesis in mice lacking endoglin." in: Science (New York, N.Y.), Vol. 284, Issue 5419, pp. 1534-7, 1999 (PubMed).

Alternatives for antigen "CD105 (Endoglin / TGF-Beta1/3 Receptor)", type "Antibodies"
Hosts (148), (121), (46), (3), (2)
Reactivities (232), (101), (37), (29), (23), (13), (13), (6), (1)
Applications (198), (179), (72), (64), (56), (45), (29), (27), (18), (16), (15), (9), (8), (7), (4), (4), (1)
Conjugates (29), (26), (24), (8), (4), (3), (3), (3), (3), (3), (3), (3), (3), (3), (2), (2), (2), (2), (1), (1), (1), (1), (1)
Epitopes (9), (5), (4), (3), (3), (3), (3), (2), (2), (2), (2), (2), (2), (2), (2), (2), (1), (1), (1), (1), (1)