| 產(chǎn)品編號 | bs-13050R-PE |
| 英文名稱1 | Rabbit Anti-EDAR/PE Conjugated antibody |
| 中文名稱 | PE標(biāo)記的腫瘤壞死因子受體超家族成員EDAR抗體 |
| 別 名 | Anhidrotic ectodysplasin receptor 1; DL; Downless (mouse) homolog; Downless homolog; Downless mouse homolog of; Ectodermal dysplasia receptor; Ectodysplasin 1 anhidrotic receptor; Ectodysplasin A receptor; Ectodysplasin-A receptor; ED 1R; ED 3; ED 5; ED1R; ED3; ED5; EDA 1R; EDA 3; EDA A1 receptor; EDA A1R; EDA-A1 receptor; EDA1R; EDA3; Edar; EDAR_HUMAN; HRM1; Tumor necrosis factor receptor superfamily member EDAR. |
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Journal
PMID
IF
Application
[IF=3.54] Sisto et al. Downstream activation of NF-κB in the EDA-A1/EDAR signalling in Sj?gren's syndrome and its regulation by the ubiquitin-editing enzyme A20. (2016) Clin.Exp.Immunol. FCM ; Human.
[IF=3.04] Sisto, Margherita, et al. "Downstream activation of NF‐κB in the EDA‐A1/EDAR signalling in Sj?grens syndrome and its regulation by the ubiquitin‐editing enzyme A20." Clinical & Experimental Immunology (2016). Human.
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| 規(guī)格價(jià)格 | 100ul/2980元 購買 大包裝/詢價(jià) |
| 說 明 書 | 100ul |
| 研究領(lǐng)域 | 腫瘤 細(xì)胞生物 生長因子和激素 表觀遺傳學(xué) |
| 抗體來源 | Rabbit |
| 克隆類型 | Polyclonal |
| 交叉反應(yīng) | (predicted: Human, Mouse, Rat, Dog, Rabbit, ) |
| 產(chǎn)品應(yīng)用 | ICC=1:50-200 IF=1:50-200
not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. |
| 分 子 量 | 46kDa |
| 細(xì)胞定位 | 細(xì)胞膜 |
| 性 狀 | Lyophilized or Liquid |
| 濃 度 | 1mg/ml |
| 免 疫 原 | KLH conjugated synthetic peptide derived from human EDAR |
| 亞 型 | IgG |
| 純化方法 | affinity purified by Protein A |
| 儲 存 液 | 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol. |
| 保存條件 | Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. 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. |
| 產(chǎn)品介紹 |
background: 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. 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. Subunit: Binds to EDARADD. Associates with TRAF1, TRAF2, TRAF3 and NIK. Subcellular Location: Membrane; Single-pass type I membrane protein (Probable). Tissue Specificity: Detected in fetal kidney, lung, skin and cultured neonatal epidermal keratinocytes. Not detected in lymphoblast and fibroblast cell lines. 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. Similarity: Contains 1 death domain. Contains 3 TNFR-Cys repeats. Database links: Entrez Gene: 10913 Human Entrez Gene: 13608 Mouse Omim: 604095 Human SwissProt: Q9UNE0 Human SwissProt: Q9R187 Mouse Unigene: 171971 Human Unigene: 174523 Mouse Unigene: 133578 Rat Important Note: This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
