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EDAR Polyclonal Antibody
EDAR Polyclonal Antibody
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EDAR Polyclonal Antibody
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经销商客户: ¥214.5
实验室客户: ¥292.5
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Target:EDAR

Fields:Cytokine-cytokine receptor interaction;NF-kappa B signaling pathway

Gene Name:EDAR DL

Protein Name:Tumor necrosis factor receptor superfamily member EDAR (Anhidrotic ectodysplasin receptor 1) (Downless homolog) (EDA-A1 receptor) (Ectodermal dysplasia receptor) (Ectodysplasin-A receptor)

Human Gene Id:10913

Human Swiss Prot No:Q9UNE0

Mouse Swiss Prot No:Q9R187

Immunogen:Synthesized peptide derived from human protein . at AA range: 50-130

Specificity:EDAR Polyclonal Antibody detects endogenous levels of protein.

Formulation:Liquid in PBS containing 50% glycerol, and 0.02% sodium azide.

Source:Polyclonal, Rabbit,IgG

Dilution:WB 1:500-2000 ELISA 1:5000-20000

Purification:The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.

Concentration:1 mg/ml

Storage Stability:-15°C to -25°C/1 year(Do not lower than -25°C)

Observed Band(KD):49kD

Background: This gene encodes a member of the tumor necrosis factor receptor family. The encoded transmembrane protein is a receptor for the soluble ligand ectodysplasin A, and can activate the nuclear factor-kappaB, JNK, and caspase-independent cell death pathways. It is required for the development of hair, teeth, and other ectodermal derivatives. Mutations in this gene result in autosomal dominant and recessive forms of hypohidrotic ectodermal dysplasia. [provided by RefSeq, Jul 2008],

Function:developmental stage:Found in craniofacial tissues from embryonic day 42-53. Expressed in fetal skin 11 and 15 weeks after gestation.,disease:Defects in EDAR are a cause of ectodermal dysplasia anhidrotic (EDA) [MIM:224900]; also known ectodermal dysplasia hypohidrotic autosomal recessive (HED). Ectodermal dysplasia defines a heterogeneous group of disorders due to abnormal development of two or more ectodermal structures. EDA is characterized by sparse hair (atrichosis or hypotrichosis), abnormal or missing teeth and the inability to sweat due to the absence of sweat glands.,disease:Defects in EDAR are the cause of ectodermal dysplasia type 3 (ED3) [MIM:129490]; also known as ectodermal dysplasia hypohidrotic autosomal dominant or EDA3. ED3 is an autosomal dominant condition characterized by hypotrichosis, abnormal or missing teeth, and hypohidrosis due to the absence of sweat glands.,fu

Subcellular Location:Membrane ; Single-pass type I membrane protein .

Expression:Detected in fetal kidney, lung, skin and cultured neonatal epidermal keratinocytes. Not detected in lymphoblast and fibroblast cell lines.

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