• Species Reactivity

  Mouse

• Specificity

  Detects mouse Endoglin/CD105 in ELISAs and Western blots. In Western blots, this antibody does not cross-react with recombinant human Endoglin.

• Source

  Monoclonal Rat IgG    _2A Clone # 209721

• Purification

  Protein A or G purified from hybridoma culture supernatant

• Immunogen

  Mouse myeloma cell line NS0-derived recombinant mouse Endoglin/CD105    
  Glu27-Gly581    
  Accession # Q8K100

• Formulation

  Lyophilized from a 0.2 μm filtered solution in PBS with Trehalose. *Small pack size (SP) is supplied as a 0.2 µm filtered solution in PBS.

• Label

  Unconjugated

Applications

• Recommended    
  Concentration

  Sample

• Western Blot

  1 µg/mL

  Recombinant Mouse Endoglin/CD105 Fc Chimera (Catalog # )    
  under non-reducing conditions only

• 
  

• Mouse Endoglin/CD105 Sandwich Immunoassay

  Reagent    

• ELISA Capture (Matched Antibody Pair)

  2-8 µg/mL 

  Mouse Endoglin/CD105 Antibody (Catalog # )

• ELISA Detection (Matched Antibody Pair)

  0.1-0.4 µg/mL 

  Mouse Endoglin/CD105 Biotinylated Antibody (Catalog # )

• ELISA Standard

   

  Recombinant Mouse Endoglin/CD105 Fc Chimera Protein, CF (Catalog # )

• 
  

Please Note: Optimal dilutions should be determined by each laboratory for each application.  are available in the Technical Information section on our website.

Preparation and Storage

• Reconstitution

  Reconstitute at 0.5 mg/mL in sterile PBS.

• Shipping

  The product is shipped at ambient temperature. Upon receipt, store it immediately at the temperature recommended below. *Small pack size (SP) is shipped with polar packs. Upon receipt, store it immediately at -20 to -70 °C

• Stability & Storage

  Use a manual defrost freezer and avoid repeated freeze-thaw cycles.    

• 12 months from date of receipt, -20 to -70 °C as supplied.

• 1 month, 2 to 8 °C under sterile conditions after reconstitution.

• 6 months, -20 to -70 °C under sterile conditions after reconstitution.

Background: Endoglin/CD105

Endoglin (CD105) is a 90 kDa type I transmembrane glycoprotein of the zona pellucida (ZP) family of proteins (1-3). Endoglin and betaglycan/T beta RIII are type III receptors for TGF‑ beta superfamily ligands, sharing 71% amino acid (aa) identity within the transmembrane (TM) and cytoplasmic domains. Endoglin is highly expressed on proliferating vascular endothelial cells, chondrocytes, and syncytiotrophoblasts of term placenta, with lower amounts on hematopoietic, mesenchymal and neural crest stem cells, activated monocytes, and lymphoid and myeloid leukemic cells (2-5). Mouse Endoglin cDNA encodes 653 aa including a 26 aa signal sequence, a 555 aa extracellular domain (ECD) with an orphan domain and a two-part ZP domain, a TM domain and a 47 aa cytoplasmic domain (1-3). A mouse isoform with a 35 aa cytoplasmic domain (S-endoglin) can oppose effects of long (L) Endoglin (6, 7). The mouse Endoglin ECD shares 69%, 84%, 62%, 63%, and 66% aa identity with human, rat, bovine, porcine, and canine Endoglin, respectively. Endoglin homodimers interact with TGF-beta 1 and TGF-beta 3 (but not TGF-beta 2), but only after binding T beta RII (8). Similarly, they interact with activin-A and BMP-7 via activin type IIA or B receptors, and with BMP-2 via BMPR-IA/ALK-3 or BMPR-IB/ALK-6 (9). BMP-9, however, is reported to bind Endoglin directly (10). Endoglin modifies ligand-induced signaling in multiple ways. For example, expression of Endoglin can inhibit TGF-beta 1 signals but enhance BMP-7 signals in the same myoblast cell line (11). In endothelial cells, Endoglin inhibits T beta RI/ALK5, but enhances ALK-1-mediated activation (12). Deletion of mouse Endoglin causes lethal vascular and cardiovascular defects, and human Endoglin haploinsufficiency can a cause the vascular disorder, hereditary hemorrhagic telangiectasia type I (13, 14). These abnormalities confirm the essential function of Endoglin in differentiation of smooth muscle, angiogenesis, and neovascularization (2-4, 12-14). In preeclampsia of pregnancy, high levels of proteolytically generated soluble Endoglin and VEGF R1 (sFlt-1), along with low placental growth factor (PlGF), are pathogenic due to anti-angiogenic activity (15).

• References:

1. Ge, A.Z. and E.C. Butcher (1994) Gene 138:201.

2. ten Dijke, P. et al. (2008) Angiogenesis 11:79.

3. Bernabeu, C. et al. (2007) J. Cell. Biochem. 102:1375.

4. Mancini, M.L. et al. (2007) Dev. Biol. 308:520.

5. Moody, J.L. et al. (2007) Stem Cells 25:2809.

6. Velasco, S. et al. (2008) J. Cell Sci. 121:913.

7. Perez-Gomez, E. et al. (2005) Oncogene 24:4450.

8. Cheifetz, S, et al. (1992) J. Biol. Chem. 267:19027.

9. Barbara, N.P. et al. (1999) J. Biol. Chem. 274:584.

10. Scharpfenecker, M. et al. (2007) J. Cell Sci. 120:964.

11. Scherner, O. et al. (2007) J. Biol. Chem. 282:13934.

12. Pece-Barbara, N. et al. (2005) J. Biol. Chem. 280:27800.

13. Arthur, H.M. et al. (2000) Dev. Biol. 217:42.

14. Lebrin, F. and C.L. Mummery (2008) Trends Cardiovasc. Med. 18:25.    

15. Venkatesha, S. et al. (2006) Nat. Med. 12:642.

• Entrez Gene IDs:

  2022 (Human); 13805 (Mouse); 497010 (Rat)

• Alternate Names:

  CD105 antigen; CD105; Endoglin; ENDOsler-Rendu-Weber syndrome 1; ENG; HHT1FLJ41744; ORW; ORW1