| 产品编号 | bs-0849R-Gold |
| 英文名称1 | Rabbit Anti-APOA1/Gold Conjugated antibody |
| 中文名称 | 胶体金标记的载脂蛋白A1抗体 |
| 别 名 | Apo-AI; ApoA I; ApoA-I; APOA1_HUMAN; Apolipoprotein A-I(1-242); Apolipoprotein A1; Apolipoprotein A 1; Apolipoprotein AI; Apolipoprotein A I; Brp14; Ltw1; Lvtw1; Sep1; Sep2. |
| 规格价格 | 100ul/2980元 购买 大包装/询价 |
| 说 明 书 | 100ul（10nm 15nm 35nm） |
| 研究领域 | 心血管 免疫学 糖尿病 脂蛋白 |
| 抗体来源 | Rabbit |
| 克隆类型 | Polyclonal |
| 交叉反应 | Human, Mouse, Rat, Chicken, (predicted: Pig, Cow, ) |
| 产品应用 | IEM=1:20-200 ICA=1:20-200 ChIP=1:20-200
not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. |
| 分 子 量 | 28kDa |
| 性 状 | Lyophilized or Liquid |
| 浓 度 | 0.4mg/ml |
| 免 疫 原 | KLH conjugated synthetic peptide derived from human APOA1 |
| 亚 型 | IgG |
| 纯化方法 | affinity purified by Protein A |
| 储 存 液 | 0.02M TBS(pH8.2) with 1% BSA, 0.03% Proclin300. |
| 保存条件 | Store at 2-8 ºC for 3-6 months. Avoid repeated freeze/thaw cycles. |
| 产品介绍 |
background: This gene encodes apolipoprotein A-I, which is the major protein component of high density lipoprotein (HDL) in plasma. The protein promotes cholesterol efflux from tissues to the liver for excretion, and it is a cofactor for lecithin cholesterolacyltransferase (LCAT) which is responsible for the formation of most plasma cholesteryl esters. This gene is closely linked with two other apolipoprotein genes on chromosome 11. Defects in this gene are associated with HDL deficiencies, including Tangier disease, and with systemic non-neuropathic amyloidosis. [provided by RefSeq, Jul 2008] Function: Participates in the reverse transport of cholesterol from tissues to the liver for excretion by promoting cholesterol efflux from tissues and by acting as a cofactor for the lecithin cholesterol acyltransferase (LCAT). As part of the SPAP complex, activates spermatozoa motility. Subunit: Interacts with APOA1BP and CLU. Component of a sperm activating protein complex (SPAP), consisting of APOA1, an immunoglobulin heavy chain, an immunoglobulin light chain and albumin. Interacts with NDRG1. Subcellular Location: Secreted. Tissue Specificity: Major protein of plasma HDL, also found in chylomicrons. Synthesized in the liver and small intestine. The oxidized form at Met-110 and Met-136 is increased in individuals with increased risk for coronary artery disease, such as in carrier of the eNOSa/b genotype and exposure to cigarette smoking. It is also present in increased levels in aortic lesions relative to native ApoA-I and increased levels are seen with increasing severity of disease. Post-translational modifications: Palmitoylated. Met-110 and Met-136 are oxidized to methionine sulfoxides. Phosphorylation sites are present in the extracelllular medium. DISEASE: Defects in APOA1 are a cause of high density lipoprotein deficiency type 2 (HDLD2) [MIM:604091]; also known as familial hypoalphalipoproteinemia (FHA). Inheritance is autosomal dominant. Defects in APOA1 are a cause of the low HDL levels observed in high density lipoprotein deficiency type 1 (HDLD1) [MIM:205400]; also known as analphalipoproteinemia or Tangier disease (TGD). HDLD1 is a recessive disorder characterized by the absence of plasma HDL, accumulation of cholesteryl esters, premature coronary artery disease, hepatosplenomegaly, recurrent peripheral neuropathy and progressive muscle wasting and weakness. In HDLD1 patients, ApoA-I fails to associate with HDL probably because of the faulty conversion of pro-ApoA-I molecules into mature chains, either due to a defect in the converting enzyme activity or a specific structural defect in Tangier ApoA-I. Note=A mutation in APOA1 is the cause of amyloid polyneuropathy-nephropathy Iowa type (AMYLIOWA); also known as amyloidosis van Allen type or familial amyloid polyneuropathy type III. AMYLIOWA is a hereditary generalized amyloidosis due to deposition of amyloid mainly constituted by apolipoprotein A1. The clinical picture is dominated by neuropathy in the early stages of the disease and nephropathy late in the course. Death is due in most cases to renal amyloidosis. Severe peptic ulcer disease can occurr in some and hearing loss is frequent. Cataracts is present in several, but vitreous opacities are not observed. Defects in APOA1 are a cause of amyloidosis type 8 (AMYL8) [MIM:105200]; also known as systemic non-neuropathic amyloidosis or Ostertag-type amyloidosis. AMYL8 is a hereditary generalized amyloidosis due to deposition of apolipoprotein A1, fibrinogen and lysozyme amyloids. Viscera are particularly affected. There is no involvement of the nervous system. Clinical features include renal amyloidosis resulting in nephrotic syndrome, arterial hypertension, hepatosplenomegaly, cholestasis, petechial skin rash. Similarity: Belongs to the apolipoprotein A1/A4/E family. Database links: Entrez Gene: 335 Human Omim: 107680 Human SwissProt: P02647 Human Unigene: 93194 Human Important Note: This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
| 1、抗体溶解方法 | |
| 2、抗体修复方式 | |
| 3、常用试剂的配制 | |
| 4、免疫组化操作步骤 | |
| 5、免疫组化问题解答 | |
| 6、Western Blotting 操作步骤 | |
| 7、Western Blotting 问题解答 | |
| 8、关于肽链的设计 | |
| 9、多肽的溶解与保存 | |
| 10、酶标抗体效价测定程序 | |
