癌症的基本特征包括细胞增殖、血管生成、迁移、凋亡逃避机制和细胞永生等。找到癌症发生过程中这些通路的关键标记物和对应的抗体用于检测至关重要。
为您推荐一个泛素化位点预测神器——泛素化分析工具，可以为您的蛋白的泛素化位点作出预测和评分。
细胞自噬受体图形绘图工具为你的蛋白的细胞受体结合位点作出预测和评分，识别结合到自噬通路中的蛋白是非常重要的，便于让我们理解自噬在正常生理、病理过程中的作用，如发育、细胞分化、神经退化性疾病、压力条件下、感染和癌症。
EDAR Polyclonal Antibody
Purified Rabbit Polyclonal Antibody (Pab)
- 产品详情
- 实验流程
Application 
| IHC-P, IHC-F, IF, ICC, E |
|---|---|
| Primary Accession | Q9UNE0 |
| Reactivity | Rat, Dog |
| Host | Rabbit |
| Clonality | Polyclonal |
| Calculated MW | 48582 Da |
| Physical State | Liquid |
| Immunogen | KLH conjugated synthetic peptide derived from human EDAR |
| Epitope Specificity | 141-230/448 |
| Isotype | IgG |
| Purity | affinity purified by Protein A |
| Buffer | 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol. |
| SUBCELLULAR LOCATION | Membrane; Single-pass type I membrane protein (Probable). |
| SIMILARITY | Contains 1 death domain. Contains 3 TNFR-Cys repeats. |
| SUBUNIT | Binds to EDARADD. Associates with TRAF1, TRAF2, TRAF3 and NIK. |
| 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. 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. |
| Important Note | This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
| Background Descriptions | The tumor necrosis factor receptor (TNFR) superfamily represents a growing family of type I transmembrane glycoproteins that are involved in various cellular functions, including proliferation, differentiation and programmed cell death. These proteins share homology for cysteine-rich repeats in the extracellular ligand binding domain and an intracellular death domain. Members of the TNFR superfamily transmit signals through protein-protein interactions, and these signals can lead to the activation of either the caspase and Jun kinase pathways, which promote cell death, or the NFκB pathway, which results in cell survival. The ectodermal dysplasia receptor (EDAR) promotes all three of these pathways and mediates ectodermal differentiation. EDAR is encoded by the downless gene and is mutated in ectodermal dysplasia syndromes, which are characterized by impaired hair, teeth and sweat gland development. Ectodysplasin A (EDA) is a type II membrane protein that is encoded by the Tabby gene and produces many splice variants, the longest of which, EDA-A1, serves as the ligand for EDAR. EDA-A2, which differs from EDA-A1 by the deletion of two amino acids, binds only the X-linked ectodysplasin-A2 receptor (XEDAR). Both EDAR and XEDAR exhibit homology with TROY. |
| Gene ID | 10913 |
|---|---|
| Other Names | Tumor necrosis factor receptor superfamily member EDAR, Anhidrotic ectodysplasin receptor 1, Downless homolog, EDA-A1 receptor, Ectodermal dysplasia receptor, Ectodysplasin-A receptor, EDAR, DL |
| Target/Specificity | Detected in fetal kidney, lung, skin and cultured neonatal epidermal keratinocytes. Not detected in lymphoblast and fibroblast cell lines. |
| Dilution | IHC-P=1:100-500,IHC-F=1:100-500,ICC=1:100-500,IF=1:100-500,ELISA=1:5000-10000 |
| Format | 0.01M TBS(pH7.4) with 1% BSA, 0.09% (W/V) sodium azide and 50% Glyce |
| Storage | Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C. |
| Name | EDAR |
|---|---|
| Synonyms | DL |
| 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. |
| Cellular Location | Membrane; Single-pass type I membrane protein |
| Tissue Location | Detected in fetal kidney, lung, skin and cultured neonatal epidermal keratinocytes. Not detected in lymphoblast and fibroblast cell lines |
Research Areas
For Research Use Only. Not For Use In Diagnostic Procedures.
Application Protocols
Provided below are standard protocols that you may find useful for product applications.
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