Cynomolgus EDAR Protein (Cytokine)

Ectodysplasin A receptor Protein Datasheet

EDAR Protein Product Information

• Synonym: EDAR
• Protein Construction: A DNA sequence encoding the cynomolgus EDAR (Met1-Ala187) was expressed, fused with the Fc region of human IgG1 at the C-terminus.
• Source: Cynomolgus
• Expression Host: Human Cells

EDAR Protein QC Testing

• Purity: > 95 % as determined by SDS-PAGE
• Endotoxin: < 1.0 EU per μg of the protein as determined by the LAL method
• Stability: Samples are stable for up to twelve months from date of receipt at -70℃
• Predicted N terminal: Glu 27
• Molecular Mass: The recombinant cynomolgus EDAR is a disulfide-linked homodimer. The reduced monomer comprises 404 amino acids and has a calculated molecular mass of 44.6 KDa.The apparent molecular mass of the protein is approximately 60-64 KDa respectively in SDS-PAGE.
• Formulation: Lyophilized from sterile PBS, pH 7.4.
  1. Normally 5 % - 8 % trehalose and mannitol are added as protectants before lyophilization. Specific concentrations are included in the hardcopy of COA.
  2. Please contact us for any concerns or special requirements.
• SDS-PAGE: EDAR protein

EDAR Protein Usage Guide

• Storage: Store it under sterile conditions at -70℃. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.
• Reconstitution: A hardcopy of COA with reconstitution instruction is sent along with the products. Please refer to it for detailed information.

EDAR Protein Description

Tumor necrosis factor receptor superfamily member EDAR, also known as Anhidrotic ectodysplasin receptor 1, Ectodysplasin-A receptor, Ectodermal dysplasia receptor, Downless homolog, EDAR and DL, is a single-pass type I membrane protein which contains one death domain and three TNFR-Cys repeats. EDAR / DL is a receptor for EDA isoform A1, but not for EDA isoform A2. It mediates the activation of NF-kappa-B and JNK and may promote caspase-independent cell death. EDAR / DL is detected in fetal kidney, lung, skin and cultured neonatal epidermal keratinocytes. It is not detected in lymphoblast and fibroblast cell lines. Defects in EDAR are a cause of ectodermal dysplasia anhidrotic which is characterized by sparse hair (atrichosis or hypotrichosis), abnormal or missing teeth and the inability to sweat due to the absence of sweat glands. Defects in EDAR are also the cause of ectodermal dysplasia type 3 (ED3) which is an autosomal dominant condition characterized by hypotrichosis, abnormal or missing teeth, and hypohidrosis due to the absence of sweat glands.

References

1. Koppinen P. et al., 2001, Exp Cell Res. 269 (2): 180-92.
2. Fessing MY. et al., 2006, Am J Pathol. 169 (6): 2075-84.
3. Drew CF. et al., 2007, Dev Biol. 305 (1): 232-45.
4. Fujimoto A.et al., 2008, Hum Mol Genet. 17: 835-43.
5. Kimura R. et al., 2009, Am J Hum Genet. 85 (4): 528-35.