Anti-TRPM4/FITC Conjugated抗体
产品名称： Anti-TRPM4/FITC Conjugated抗体
英文名称： Anti-TRPM4/FITC
产品编号： YB--9051R-FITC
产品价格： null
产品产地： 中国/美国
品牌商标： Ybscience
更新时间： 2023-08-17T10:24:20
使用范围： 科研使用
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Anti-TRPM4/FITC Conjugated抗体
| 产品编号 | YB-9051R-FITC |
| 英文名称 | Anti-TRPM4/FITC |
| 中文名称 | FITC标记的瞬时受体电位离子通道蛋白4抗体（M亚家族） |
| 别 名 | Long transient receptor potential channel 4; LTrpC-4; LTrpC4; Melastatin 4; Melastatin like 2 protein; Melastatin-4; Melastatin-like 2; Mls2s; PFHB1B; Transient receptor potential cation channel subfamily M member 4; Transient receptor potential cation channel, subfamily M, member 4; Trpm4; TRPM4_HUMAN; TRPM4B; 1110030C19Rik; AW047689; Calcium-activated non-selective cation channel 1; FLJ20041; hTRPM4. |
| 规格价格 | 50ug/1680元 购买 100ug/2980元 购买 大包装/询价 |
| 说 明 书 | 50ug 100ug |
| 研究领域 | 细胞生物 免疫学 神经生物学 信号转导 通道蛋白 |
| 抗体来源 | Rabbit |
| 克隆类型 | Polyclonal |
| 交叉反应 | Human, Mouse, Rat, |
| 产品应用 | Flow-Cyt=2ug/Test IF=1:50-200 not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. |
| 分 子 量 | 134kDa |
| 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 TRPM4 |
| 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: Calcium-activated non selective (CAN) cation channel that mediates membrane depolarization. While it is activated by increase in intracellular Ca(2+), it is impermeable to it. Mediates transport of monovalent cations (Na(+) > K(+) > Cs(+) > Li(+)), leading to depolarize the membrane. It thereby plays a central role in cadiomyocytes, neurons from entorhinal cortex, dorsal root and vomeronasal neurons, endocrine pancreas cells, kidney epithelial cells, cochlea hair cells etc. Participates in T-cell activation by modulating Ca(2+) oscillations after T lymphocyte activation, which is required for NFAT-dependent IL2 production. Involved in myogenic constriction of cerebral arteries. Controls insulin secretion in pancreatic beta-cells. May also be involved in pacemaking or could cause irregular electrical activity under conditions of Ca(2+) overload. Affects T-helper 1 (Th1) and T-helper 2 (Th2) cell motility and cytokine production through differential regulation of calcium signaling and NFATC1 localization. Enhances cell proliferation through up-regulation of the beta-catenin signaling pathway. Involvement in disease: Defects in TRPM4 are the cause of progressive familial heart block type 1B (PFHB1B) [MIM:604559]. It is a cardiac bundle branch disorder characterized by progressive alteration of cardiac conduction through the His-Purkinje system, with a pattern of a right bundle-branch block and/or left anterior hemiblock occurring individually or together. It leads to complete atrio-ventricular block causing syncope and sudden death. Function: Calcium-activated non selective (CAN) cation channel that mediates membrane depolarization. While it is activated by increase in intracellular Ca(2+), it is impermeable to it. Mediates transport of monovalent cations (Na(+) > K(+) > Cs(+) > Li(+)), leading to depolarize the membrane. It thereby plays a central role in cadiomyocytes, neurons from entorhinal cortex, dorsal root and vomeronasal neurons, endocrine pancreas cells, kidney epithelial cells, cochlea hair cells etc. Participates in T-cell activation by modulating Ca(2+) oscillations after T lymphocyte activation, which is required for NFAT-dependent IL2 production. Involved in myogenic constriction of cerebral arteries. Controls insulin secretion in pancreatic beta-cells. May also be involved in pacemaking or could cause irregular electrical activity under conditions of Ca(2+) overload. Affects T-helper 1 (Th1) and T-helper 2 (Th2) cell motility and cytokine production through differential regulation of calcium signaling and NFATC1 localization. Enhances cell proliferation through up-regulation of the beta-catenin signaling pathway. Subunit: Homomultimer. Subcellular Location: Endoplasmic reticulum. Golgi apparatus and Cell membrane. Endoplasmic reticulum. Golgi apparatus Tissue Specificity: Widely expressed with a high expression in intestine and prostate. In brain, it is both expressed in whole cerebral arteries and isolated vascular smooth muscle cells. Prominently expressed in Purkinje fibers. Expressed at higher levels in T-helper 2 (Th2) cells as compared to T-helper 1 (Th1) cells. Post-translational modifications: Phosphorylation by PKC leads to increase the sensitivity to Ca(2+). Sumoylated. Desumoylated by SENP1. DISEASE: Defects in TRPM4 are the cause of progressive familial heart block type 1B (PFHB1B) [MIM:604559]. It is a cardiac bundle branch disorder characterized by progressive alteration of cardiac conduction through the His-Purkinje system, with a pattern of a right bundle-branch block and/or left anterior hemiblock occurring individually or together. It leads to complete atrioventricular block causing syncope and sudden death. Similarity: Belongs to the transient receptor (TC 1.A.4) family. LTrpC subfamily. TRPM4 sub-subfamily. Database links: Entrez Gene: 54795 Human Entrez Gene: 68667 Mouse Entrez Gene: 171143 Rat Omim: 606936 Human SwissProt: Q8TD43 Human SwissProt: Q7TN37 Mouse SwissProt: Q9ESQ5 Rat Unigene: 467101 Human Unigene: 439890 Mouse Unigene: 205004 Rat Important Note: This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |