- ¥2980
- LMAI Bio
- LM-4892R-FITC
- 中国/美国/欧洲
- 2025年07月12日
- IF=1:50-200
- Human, Mouse, Rat,
- Human, Mouse, Rat,
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- 详细信息
- 文献和实验
- 技术资料
- 供应商：
上海联迈生物工程有限公司
- 库存：
大量
- 靶点：
详见说明书
- 级别：
1
- 目录编号：
LM-4892R-FITC
- 克隆性：
多克隆
- 抗原来源：
Rabbit
- 保质期：
1年
- 抗体英文名：
Anti-Apolipoprotein E/FITC
- 抗体名：
Anti-Apolipoprotein E/FITC
- 标记物：
FITC标记
- 宿主：
Human, Mouse, Rat,
- 适应物种：
Human, Mouse, Rat,
- 免疫原：
详见说明书
- 亚型：
IGg
- 形态：
粉末、液体、冻干粉
- 应用范围：
IF=1:50-200
- 浓度：
1mg/ml
- 保存条件：
-20 °C
- 规格：
100ul
FITC标记的载脂蛋白E抗体
| 英文名称 | Anti-Apolipoprotein E/FITC |
| 中文名称 | FITC标记的载脂蛋白E抗体 |
| 别 名 | Apo E2; APOE; Apolipoprotein E precursor; AD2; Alzheimer disease 2; Apo E; ApoE; APOEA; ApolipoproteinE; Apoprotein; MGC1571; Apo E2; ApoE2; APOE 2; Apolipoprotein E2; LDLCQ5; LPG; AD2; Alzheimer disease 2; Apo E; Apo-E; ApoE; APOE_HUMAN; APOEA; Apolipoprotein E; Apolipoprotein E3; ApolipoproteinE; Apoprotein; MGC1571. |
| 规格价格 | 100ul/2980元 购买 大包装/询价 |
| 说 明 书 | 100ul |
| 研究领域 | 肿瘤 心血管 细胞生物 神经生物学 信号转导 细胞凋亡 转录调节因子 合成与降解 Alzheimer's |
| 抗体来源 | Rabbit |
| 克隆类型 | Polyclonal |
| 交叉反应 | Human, Mouse, Rat, |
| 产品应用 | IF=1:50-200 not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. |
| 分 子 量 | 38kDa |
| 性 状 | Lyophilized or Liquid |
| 浓 度 | 1mg/ml |
| 免 疫 原 | KLH conjugated synthetic peptide derived from human APOE/Apo E2 |
| 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: Apolipoprotein E, a main apoprotein of the chylomicron, binds to a specific receptor on liver cells and peripheral cells and is essential for the normal catabolism of triglyceride-rich lipoprotein constituents. ApoE exists in three major isoforms; E2, E3, and E4, which differ from one another by a single amino-acid substitution. Compared with E3 and E4, E2 exhibits the lowest receptor binding affinity. Defects in ApoE are a cause of hyperlipoproteinemia type III due to increased plasma cholesterol and triglycerides levels which are the consequence of impaired clearance of chylomicron and VLDL remnants. Function: Mediates the binding, internalization, and catabolism of lipoprotein particles. It can serve as a ligand for the LDL (apo B/E) receptor and for the specific apo-E receptor (chylomicron remnant) of hepatic tissues. Subcellular Location: Secreted. Tissue Specificity: Occurs in all lipoprotein fractions in plasma. It constitutes 10-20% of very low density lipoproteins (VLDL) and 1-2% of high density lipoproteins (HDL). APOE is produced in most organs. Significant quantities are produced in liver, brain, spleen, lung, adrenal, ovary, kidney and muscle. Post-translational modifications: Synthesized with the sialic acid attached by O-glycosidic linkage and is subsequently desialylated in plasma. O-glycosylated with core 1 or possibly core 8 glycans. Thr-307 is a minor glycosylation site compared to Ser-308. Glycated in plasma VLDL of normal subjects, and of hyperglycemic diabetic patients at a higher level (2-3 fold). Phosphorylation sites are present in the extracellular medium. DISEASE: Defects in APOE are a cause of hyperlipoproteinemia type 3 (HLPP3) [MIM:107741]; also known as familial dysbetalipoproteinemia. Individuals with HLPP3 are clinically characterized by xanthomas, yellowish lipid deposits in the palmar crease, or less specific on tendons and on elbows. The disorder rarely manifests before the third decade in men. In women, it is usually expressed only after the menopause. The vast majority of the patients are homozygous for APOE*2 alleles. More severe cases of HLPP3 have also been observed in individuals heterozygous for rare APOE variants. The influence of APOE on lipid levels is often suggested to have major implications for the risk of coronary artery disease (CAD). Individuals carrying the common APOE*4 variant are at higher risk of CAD. Genetic variations in APOE are associated with Alzheimer disease type 2 (AD2) [MIM:104310]. It is a late-onset neurodegenerative disorder characterized by progressive dementia, loss of cognitive abilities, and deposition of fibrillar amyloid proteins as intraneuronal neurofibrillary tangles, extracellular amyloid plaques and vascular amyloid deposits. The major constituent of these plaques is the neurotoxic amyloid-beta-APP 40-42 peptide (s), derived proteolytically from the transmembrane precursor protein APP by sequential secretase processing. The cytotoxic C-terminal fragments (CTFs) and the caspase-cleaved products such as C31 derived from APP, are also implicated in neuronal death. Note=The APOE*4 allele is genetically associated with the common late onset familial and sporadic forms of Alzheimer disease. Risk for AD increased from 20% to 90% and mean age at onset decreased from 84 to 68 years with increasing number of APOE*4 alleles in 42 families with late onset AD. Thus APOE*4 gene dose is a major risk factor for late onset AD and, in these families, homozygosity for APOE*4 was virtually sufficient to cause AD by age 80. The mechanism by which APOE*4 participates in pathogenesis is not known. [DISEASE] Defects in APOE are a cause of sea-blue histiocyte disease (SBHD) [MIM:269600]; also known as sea-blue histiocytosis. This disorder is characterized by splenomegaly, mild thrombocytopenia and, in the bone marrow, numerous histiocytes containing cytoplasmic granules which stain bright blue with the usual hematologic stains. The syndrome is the consequence of an inherited metabolic defect analogous to Gaucher disease and other sphingolipidoses. [DISEASE] Defects in APOE are a cause of lipoprotein glomerulopathy (LPG) [MIM:611771]. LPG is an uncommon kidney disease characterized by proteinuria, progressive kidney failure, and distinctive lipoprotein thrombi in glomerular capillaries. It mainly affects people of Japanese and Chinese origin. The disorder has rarely been described in Caucasians. Similarity: Belongs to the apolipoprotein A1/A4/E family. Database links: Entrez Gene: 348 Human Entrez Gene: 11816 Mouse Omim: 107741 Human SwissProt: P02649 Human SwissProt: P08226 Mouse Unigene: 654439 Human Unigene: 305152 Mouse Important Note: This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. ApoE 是在肝脏中合成的极低密度脂蛋白的组分，也是在细胞间转运胆固醇的高密度脂蛋白的一种亚类. |
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文献和实验相关实验
当FITC在碱性溶液中与抗体蛋白反应时，主要是蛋白质上赖氨酸的r氨基与荧光素的硫碳胺键(thiocarbmide)结合，形成FITC-蛋白质结合物，即荧光抗体或荧光结合物。一个IgG分子中有86个赖氨酸残基，一般最多能结合15～20个，一个IgG分子可结合2～8个分子的FITC，其反应式如下FITC-N=C=S + N-H2-蛋白质 → FITC-NS-C-N-H2-蛋白质常用Marsshall(1958)法标记荧光抗体，也可以根据条件采用Chadwick等标记法或Clark
ml三蒸水中即成； 方法与步骤： 根据Marshall氏法高效价的抗人球蛋白兔免疫血清，分离球蛋白。 1. 用0.15 mol/L NaCl的盐水及0.15 mol/L pH9.0的NaHCO3-Na2CO3缓冲液稀释使每毫升内含抗体10mg，缓冲液为总量的10%； 2. 将以上溶液降温至4℃，按蛋白：荧光素=50—80mg：1mg的比例加入异硫氰酸荧光素，在0—4℃下电磁搅拌12—14h； 3.用半饱和硫酸铵将标记球蛋白
5. 过柱。取透析过夜的标记物，过葡萄糖凝胶G-25或G-50柱，分离出游离荧光素，收集标记的荧光抗体进行鉴定。
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FITC标记的载脂蛋白E抗体
¥2980
