FITC标记的肿瘤坏死因子受体超家族成员EDAR抗体
产品名称： FITC标记的肿瘤坏死因子受体超家族成员EDAR抗体
英文名称： Anti-EDAR/FITC
产品编号： HZ-13050R-FITC
产品价格： null
产品产地： 中国/上海
品牌商标： HZbscience
更新时间： 2023-08-17T10:24:20
使用范围： ICC=1:50-200 IF=1:50-200
上海沪震实业有限公司
- 联系人 : 鲍丽雯
- 地址 : 上海市闵行区闵北路88弄1-30号第22幢AQ136室
- 邮编 : 200612
- 所在区域 : 上海
- 电话 : 139****0749 点击查看
- 传真 : 点击查看
- 邮箱 : www.shzbio.net
- 二维码 : 点击查看
Rabbit Anti-EDAR/FITC Conjugated antibody
FITC标记的肿瘤坏死因子受体超家族成员EDAR抗体
| 英文名称 | Anti-EDAR/FITC |
| 中文名称 | FITC标记的肿瘤坏死因子受体超家族成员EDAR抗体 |
| 别 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. |
| 规格价格 | 100ul/2980元 购买 大包装/询价 |
| 说 明 书 | 100ul |
| 研究领域 | 肿瘤 细胞生物 生长因子和激素 表观遗传学 |
| 抗体来源 | Rabbit |
| 克隆类型 | Polyclonal |
| 交叉反应 | Human, Mouse, Rat, Dog, Rabbit, |
| 产品应用 | 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 |
| 细胞定位 | 细胞膜 |
| 性 状 | Lyophilized or Liquid |
| 浓 度 | 1mg/ml |
| 免 疫 原 | KLH conjugated synthetic peptide derived from human EDAR |
| 亚 型 | IgG |
| 纯化方法 | affinity purified by Protein A |
| 储 存 液 | 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol. |
| 保存条件 | 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. |
| 产品介绍 | 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 Entrez Gene: 365581 Rat 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 |
肿瘤坏死因子受体（TNFR）超家族代表了越来越多的I型跨膜糖蛋白家族，涉及多种细胞功能，包括增殖、分化和程序性细胞死亡。这些蛋白质在细胞外配体结合域和细胞内死亡域与富含半胱氨酸的重复序列具有同源性。TNFR超家族的成员通过蛋白质-蛋白质相互作用传递信号，这些信号可导致促进细胞死亡的caspase和Jun激酶途径或导致细胞存活的NNFκB途径的激活。外胚层发育不良受体（EDAR）促进所有这三个途径，并介导外胚层分化。EDAR由downless基因编码，在外胚层发育不良综合征中突变，其特征是头发、牙齿和汗腺发育受损。外胚层粘连蛋白A（EDA）是由Tabby基因编码的II型膜蛋白，产生许多剪接变异体，其中最长的EDA-A1是EDAR的配体。EDA A2与EDA A1不同，其缺失的是两个氨基酸，仅结合X连锁的胞外凝血素A2受体（XEDAR）。EDAR和XEDAR都显示出与TROY的同源性。