AdipoGen Life Sciences

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

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Product Details
Synonyms Ectodysplasin-A; Ectodermal Dysplasia Protein
Product Type Protein
Properties
Source/Host HEK 293 cells
Sequence

The extracellular domain of human EDA-A1 (aa 245-391) is fused at the N-terminus to a FLAG®-tag.

Crossreactivity Human
Mouse
Specificity Binds to human and mouse EDAR (ectodysplasin-A1 receptor).
MW ~19kDa (SDS-PAGE) (non-glycosylated form) and ~24 kDa (glycosylated form)
Purity ≥95% (SDS-PAGE)
Endotoxin Content <0.01EU/μg purified protein (LAL test; Lonza).
Concentration 0.1mg/ml after reconstitution.
Reconstitution Reconstitute with 100μl sterile water.
Accession Number Q92838
Formulation Lyophilized. Contains PBS.
Other Product Data

Uni-Prot link Q92838: EDA-A1 (human)

Shipping and Handling
Shipping BLUE ICE
Short Term Storage +4°C
Long Term Storage -20°C
Handling Advice 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.
Use/Stability 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.
Documents
Product Specification Sheet
Datasheet Download PDF
Description

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.

Product References
  1. Biological activity of Ectodysplasin A is conditioned by its collagen and heparan sulfate proteoglycan-binding domains: L.K. Swee, et al.; J. Biol. Chem. 284, 27567 (2009)
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