EDAR Protein, Mouse, Recombinant (hFc)

Catalog No. TMPJ-01370

Ectodysplasin A receptor (EDAR) is a type I transmembrane protein of the TNF-α receptor superfamily which plays a key role in ectodermal differentiation. EDAR was encoded by the mouse downless gene and defective in human dominant and recessive forms of autosomal hypohidrotic ectodermal dysplasia (EDA) syndrome. The extracellular domain of EDAR contains 14 cysteine residues, six of which approximate the TNFRSF cysteine-rich region, the cytoplasmic domain contains a region with homology to the death domains found in other TNFRSF members. EDAR has been suggested to be an early and important promoter of placode development in all ectodermal organs, such as uch as hair follicles, teeth and sweat glands. EDA-A1, the A1 isoform of EDA, is the EDAR ligand. EDA and EDA are implicated in appendage development by the cloning of a gene underlying hypohidrotic ectodermal dysplasia (HED) in mouse and human. HED is characterized by agenesis or malformation of ectoderm-derived appendages, such as teeth, sweat glands and hair follicles, while the skin itself develops normally.

EDAR Protein, Mouse, Recombinant (hFc)

Catalog No. TMPJ-01370

Pack Size	Price	Availability
10 μg	$116	7-10 days
50 μg	$310	7-10 days
500 μg	$1,900	7-10 days
1 mg	$2,730	7-10 days

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Product Information

Biological Activity	Activity has not been tested. It is theoretically active, but we cannot guarantee it. If you require protein activity, we recommend choosing the eukaryotic expression version first.
Description	Ectodysplasin A receptor (EDAR) is a type I transmembrane protein of the TNF-α receptor superfamily which plays a key role in ectodermal differentiation. EDAR was encoded by the mouse downless gene and defective in human dominant and recessive forms of autosomal hypohidrotic ectodermal dysplasia (EDA) syndrome. The extracellular domain of EDAR contains 14 cysteine residues, six of which approximate the TNFRSF cysteine-rich region, the cytoplasmic domain contains a region with homology to the death domains found in other TNFRSF members. EDAR has been suggested to be an early and important promoter of placode development in all ectodermal organs, such as uch as hair follicles, teeth and sweat glands. EDA-A1, the A1 isoform of EDA, is the EDAR ligand. EDA and EDA are implicated in appendage development by the cloning of a gene underlying hypohidrotic ectodermal dysplasia (HED) in mouse and human. HED is characterized by agenesis or malformation of ectoderm-derived appendages, such as teeth, sweat glands and hair follicles, while the skin itself develops normally.
Species	Mouse
Expression System	HEK293 Cells
Tag	C-hFc
Accession Number	Q9R187
Synonyms	Tumor necrosis factor receptor superfamily member EDAR,Ectodysplasin-A receptor,Ectodermal dysplasia receptor,Downless,Anhidrotic ectodysplasin receptor 1
Amino Acid	Glu27-Ile189
Construction	Glu27-Ile189
Protein Purity	Greater than 95% as determined by reducing SDS-PAGE. (QC verified)
Molecular Weight	58-88 KDa (reducing condition)
Endotoxin	< 0.1 ng/µg (1 EU/µg) as determined by LAL test.
Formulation	Lyophilized from a solution filtered through a 0.22 μm filter, containing PBS, pH 7.4.
Reconstitution	Reconstitute the lyophilized protein in distilled water. The product concentration should not be less than 100 μg/ml. Before opening, centrifuge the tube to collect powder at the bottom. After adding the reconstitution buffer, avoid vortexing or pipetting for mixing.
Stability & Storage	Lyophilized powders can be stably stored for over 12 months, while liquid products can be stored for 6-12 months at -80°C. For reconstituted protein solutions, the solution can be stored at -20°C to -80°C for at least 3 months. Please avoid multiple freeze-thaw cycles and store products in aliquots.
Shipping	In general, Lyophilized powders are shipping with blue ice. Solutions are shipping with dry ice.
Research Background	Ectodysplasin A receptor (EDAR) is a type I transmembrane protein of the TNF-α receptor superfamily which plays a key role in ectodermal differentiation. EDAR was encoded by the mouse downless gene and defective in human dominant and recessive forms of autosomal hypohidrotic ectodermal dysplasia (EDA) syndrome. The extracellular domain of EDAR contains 14 cysteine residues, six of which approximate the TNFRSF cysteine-rich region, the cytoplasmic domain contains a region with homology to the death domains found in other TNFRSF members. EDAR has been suggested to be an early and important promoter of placode development in all ectodermal organs, such as uch as hair follicles, teeth and sweat glands. EDA-A1, the A1 isoform of EDA, is the EDAR ligand. EDA and EDA are implicated in appendage development by the cloning of a gene underlying hypohidrotic ectodermal dysplasia (HED) in mouse and human. HED is characterized by agenesis or malformation of ectoderm-derived appendages, such as teeth, sweat glands and hair follicles, while the skin itself develops normally.

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