EDA-A1, Soluble (human) (rec.)

Ectodysplasin-A; Ectodermal Dysplasia Protein

0.1mg/ml after reconstitution.

32160000

<0.1EU/µg purified protein (LAL test; Lonza).

liquid

Lyophilized. Contains PBS.

After reconstitution, prepare aliquots and store at -20°C.Avoid freeze/thaw cycles.Centrifuge lyophilized vial before opening and reconstitution.PBS containing at least 0.1% BSA should be used for further dilutions.

Protein. The extracellular domain of human EDA-A1 (aa 240-391) is fused at the N-terminus to a FLAG®-tag. Source: E. coli. Endotoxin content: <0.1EU/µg purified protein (LAL test; Lonza). Lyophilized. Contains PBS. Binds to human and mouse EDAR (ectodysplasin-A1 receptor). Purity: >95% (SDS-PAGE). The TNF family ligand ectodysplasin A (EDA) and its receptor EDAR are required for proper development of skin appendages such as hair, teeth, and eccrine sweat glands. Loss of function mutations in the Eda gene cause X-linked hypohidrotic ectodermal dysplasia (XLHED), a condition that can be ameliorated in mice and dogs by timely administration of recombinant EDA. The Eda gene on the X chromosome is transcribed as multiple splice variants, only two of which code for the receptor-binding C-terminal TNF homology domain. These two variants code for 391- and 389-amino acid-long proteins called EDA1 and EDA2. EDA1 binds EDAR, whereas EDA2 binds to another receptor, XEDAR. The biology of EDA2 and XEDAR is distinct from that of EDA1. Indeed, XEDAR-deficient mice have no obvious ectodermal dysplasia phenotype, whereas mice deficient in EDA, EDAR, or the signaling adaptor protein EDARADD all display virtually indistinguishable ectodermal dysplasia phenotypes, indicating the predominance of the EDA1-EDAR axis in the development of skin-derived appendages.

~19kDa (SDS-PAGE)

Q92838

Plastic Vial

The TNF family ligand ectodysplasin A (EDA) and its receptor EDAR are required for proper development of skin appendages such as hair, teeth, and eccrine sweat glands. Loss of function mutations in the Eda gene cause X-linked hypohidrotic ectodermal dysplasia (XLHED), a condition that can be ameliorated in mice and dogs by timely administration of recombinant EDA. The Eda gene on the X chromosome is transcribed as multiple splice variants, only two of which code for the receptor-binding C-terminal TNF homology domain. These two variants code for 391- and 389-amino acid-long proteins called EDA1 and EDA2. EDA1 binds EDAR, whereas EDA2 binds to another receptor, XEDAR. The biology of EDA2 and XEDAR is distinct from that of EDA1. Indeed, XEDAR-deficient mice have no obvious ectodermal dysplasia phenotype, whereas mice deficient in EDA, EDAR, or the signaling adaptor protein EDARADD all display virtually indistinguishable ectodermal dysplasia phenotypes, indicating the predominance of the EDA1-EDAR axis in the development of skin-derived appendages.

>95% (SDS-PAGE)

The extracellular domain of human EDA-A1 (aa 240-391) is fused at the N-terminus to a FLAG®-tag.

E. coli

Binds to human and mouse EDAR (ectodysplasin-A1 receptor).

FLAG

Non-hazardous

Other Proteins

12352202

Stable for at least 6 months after receipt when stored at -20°C. Working aliquots are stable for up to 3 months when stored at -20°C.