ITN0303
ITN0303
- Catalog: ITN0303
- Gene/Protein: EDAR DL
- Product Description: Immunotag™ EDAR Polyclonal Antibody
385.0000
Price in reward points: 385
| Antibody Specification | |
| Datasheet | 
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| Target Protein | EDAR |
| Clonality | Polyclonal |
| Storage/Stability | -20°C/1 year |
| Application | WB,ELISA |
| Recommended Dilution | WB 1:500-2000 ELISA 1:5000-20000 |
| Concentration | 1 mg/ml |
| Reactive Species | Human,Mouse |
| Host Species | Rabbit |
| Immunogen | Synthesized peptide derived from human protein . at AA range: 50-130 |
| Specificity | EDAR Polyclonal Antibody detects endogenous levels of protein. |
| Purification | The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen |
| Form | Liquid in PBS containing 50% glycerol, and 0.02% sodium azide. |
| Gene Name | EDAR DL |
| Accession No. | Q9UNE0 Q9R187 |
| Description | ectodysplasin A receptor(EDAR) Homo sapiens 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], |
| Cell Pathway/ Category | Cytokine-cytokine receptor interaction, |
| Protein Expression | Fetal heart,Liver,Rectum tumor,Skin, |
| Subcellular Localization | plasma membrane,integral component of membrane,apical part of cell, |
| Protein 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.,function:Receptor for EDA isoform A1, but not for EDA isoform A2. Mediates the activation of NF-kappa-B and JNK. May promote caspase-independent cell death.,polymorphism:Genetic variation in EDAR is associated with hair morphology type 1 (HRM1) [MIM:612630]; also called variation in hair thickness. Besides skin color and facial features, hair morphology is one of the most distinctive traits among human populations, and classical classification of human population is based on such visible traits.,similarity:Contains 1 death domain.,similarity:Contains 3 TNFR-Cys repeats.,subunit:Binds to EDARADD. Associates with TRAF1, TRAF2, TRAF3 and NIK.,tissue specificity:Detected in fetal kidney, lung, skin and cultured neonatal epidermal keratinocytes. Not detected in lymphoblast and fibroblast cell lines., |
| Usage | For Research Use Only! Not for diagnostic or therapeutic procedures. |
| Material Safety Data Sheet | |
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