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瞬时受体电位离子通道蛋白4抗体

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产物名称: 瞬时受体电位离子通道蛋白4抗体
产物型号: TRPM4
产物展商: 单克隆抗体/多克隆抗体
产物文档: 无相关文档

简单介绍

瞬时受体电位离子通道蛋白4抗体应用于IHC、WB、 IF、IP、ELISA等科研实验,按理化性质和生物学功能IgM、IgG、IgA、IgE、IgD五类。按抗体的来源,可将其分为天然抗体和**抗体。瞬时受体电位离子通道蛋白4抗体生产每个流程都执行严格的检测标准,保证蛋白抗原产物质量,质量稳定,实验效果明显。


瞬时受体电位离子通道蛋白4抗体  的详细介绍

瞬时受体电位离子通道蛋白4抗体

规格:1尘驳/1尘濒

英文名: TRPM4

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 subfa

分子量: 134kDa

储存液:0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glyce

克隆类型:笔辞濒测肠濒辞苍补濒

亚型:滨驳骋

纯化方法:affinity purified by Protein A

**原:KLH conjugated synthetic peptide derived from human TRPM4

交叉反应:Human, Mouse, Rat,

细胞定位:细胞浆 细胞膜

瞬时受体电位离子通道蛋白4抗体产物介绍: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 瞬时受体电位离子通道蛋白4抗体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瞬时受体电位离子通道蛋白4抗体 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.

瞬时受体电位离子通道蛋白4抗体产物应用:WB=1:100-500 ELISA=1:500-1000 IHC-P=1:100-500 IHC-F=1:100-500 IF=1:50-200 (石蜡切片需做抗原修复) not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user.

研究领域:细胞生物  **学  神经生物学  信号转导  通道蛋白  

储存条件: Store at -20 °C for one year. Avoid repeated freeze/thaw cycles.

来源: Rabbit

外观: Lyophilized or Liquid


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