Anti-Apolipoprotein A I抗体[12C8] (ab17278)
Key features and details
- Mouse monoclonal [12C8] to Apolipoprotein A I
- Suitable for: ELISA, WB, IHC-P
- Reacts with: Human
- Isotype: IgG1
选择批间可重复性更高的重组抗体
- 研究可靠 —— 各批次间结果一致且可重复
- 长期批量供应 —— 采用重组技术,可实现快速生产
- 首次实验即可成功 —— 经过大量验证确认了特异性
- 符合伦理标准 —— 产品不含动物成分
概述
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产品名称
Anti-Apolipoprotein A I抗体[12C8]
参阅全部 Apolipoprotein A I 一抗 -
描述
小鼠单克隆抗体[12C8] to Apolipoprotein A I -
宿主
Mouse -
特异性
No cross reactivity is seen with human apolipoprotein B. -
经测试应用
适用于: ELISA, WB, IHC-Pmore details -
种属反应性
与反应: Human -
免疫原
Full length native Apolipoprotein A1, isolated from human plasma.
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常规说明
The Life Science industry has been in the grips of a reproducibility crisis for a number of years. Abcam is leading the way in addressing this with our range of recombinant monoclonal antibodies and knockout edited cell lines for gold-standard validation. Please check that this product meets your needs before purchasing.
If you have any questions, special requirements or concerns, please send us an inquiry and/or contact our Support team ahead of purchase. Recommended alternatives for this product can be found below, along with publications, customer reviews and Q&As
性能
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形式
Liquid -
存放说明
Shipped at 4°C. Store at +4°C short term (1-2 weeks). Store at -20°C long term. -
存储溶液
pH: 7.40
Preservative: 0.097% Sodium azide
Constituents: 0.0268% PBS, 2.9% Sodium chloride -
Concentration information loading...
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纯度
Protein G purified -
克隆
单克隆 -
克隆编号
12C8 -
同种型
IgG1 -
轻链类型
kappa -
研究领域
相关产品
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Compatible Secondaries
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Isotype control
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Recombinant Protein
应用
The Abpromise guarantee
Abpromise™承诺保证使用ab17278于以下的经测试应用
“应用说明”部分 下显示的仅为推荐的起始稀释度;实际最佳的稀释度/浓度应由使用者检定。
应用 | Ab评论 | 说明 |
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ELISA |
Use at an assay dependent concentration.
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WB |
Use at an assay dependent concentration. Predicted molecular weight: 24 kDa.
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IHC-P |
Use a concentration of 2 µg/ml. Perform heat mediated antigen retrieval before commencing with IHC staining protocol.
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说明 |
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ELISA
Use at an assay dependent concentration. |
WB
Use at an assay dependent concentration. Predicted molecular weight: 24 kDa. |
IHC-P
Use a concentration of 2 µg/ml. Perform heat mediated antigen retrieval before commencing with IHC staining protocol. |
靶标
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功能
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. -
组织特异性
Major protein of plasma HDL, also found in chylomicrons. Synthesized in the liver and small intestine. -
疾病相关
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.
Defects in APOA1 are the cause of amyloid polyneuropathy-nephropathy Iowa type (AMYLIOWA) [MIM:107680]; 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. -
序列相似性
Belongs to the apolipoprotein A1/A4/E family. -
翻译后修饰
Palmitoylated.
Phosphorylation sites are present in the extracelllular medium. -
细胞定位
Secreted. - Information by UniProt
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数据库链接
- Entrez Gene: 335 Human
- Omim: 107680 Human
- SwissProt: P02647 Human
- Unigene: 93194 Human
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别名
- Apo-AI antibody
- ApoA I antibody
- ApoA-I antibody
see all
图片
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All lanes : Anti-Apolipoprotein A I antibody [12C8] (ab17278) at 5 µg/ml
Lane 1 : Human ovary tissue lysate - total protein (ab30222)
Lane 2 : Lung (Human) Tissue Lysate
Lysates/proteins at 10 µg per lane.
Secondary
Lane 1 : Goat polyclonal to Mouse IgG - H&L - Pre-Adsorbed (HRP) at 1/3000 dilution
Lane 2 : Goat polyclonal to Mouse IgG - H&L - Pre-Adsorbed (HRP) at 1/3000 dilution
Predicted band size: 24 kDa
Observed band size: 25 kDa why is the actual band size different from the predicted?
Additional bands at: 260 kDa, 45 kDa, 55 kDa, 75 kDa. We are unsure as to the identity of these extra bands. -
Ab17278 staining human normal skeletal muscle. Staining is localised to the cytoplasm.
Left panel: with primary antibody at 2 ug/ml. Right panel: isotype control.
Sections were stained using an automated system DAKO Autostainer Plus , at room temperature. Sections were rehydrated and antigen retrieved with the Dako 3-in-1 AR buffer EDTA pH 9.0 in a DAKO PT Link. Slides were peroxidase blocked in 3% H2O2 in methanol for 10 minutes. They were then blocked with Dako Protein block for 10 minutes (containing casein 0.25% in PBS), then incubated with primary antibody for 20 minutes, and detected with Dako Envision Flex amplification kit for 30 minutes. Colorimetric detection was completed with diaminobenzidine for 5 minutes. Slides were counterstained with Haematoxylin and coverslipped under DePeX. Please note that for manual staining we recommend to optimize the primary antibody concentration and incubation time (overnight incubation), and amplification may be required.
数据表及文件
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SDS download
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Datasheet download
文献 (9)
ab17278 被引用在 9 文献中.
- Gori A et al. Membrane-binding peptides for extracellular vesicles on-chip analysis. J Extracell Vesicles 9:1751428 (2020). PubMed: 32363015
- Garg PK et al. Cholesterol mass efflux capacity and risk of peripheral artery disease: The Multi-Ethnic Study of Atherosclerosis. Atherosclerosis 297:81-86 (2020). PubMed: 32097805
- Zocco D et al. Isolation of extracellular vesicles improves the detection of mutant DNA from plasma of metastatic melanoma patients. Sci Rep 10:15745 (2020). PubMed: 32978468
- Cortelazzo A et al. Expression and oxidative modifications of plasma proteins in autism spectrum disorders: Interplay between inflammatory response and lipid peroxidation. Proteomics Clin Appl 10:1103-1112 (2016). PubMed: 27246309
- Amjadi F et al. Apolipoprotein A1 as a novel anti-implantation biomarker in polycystic ovary syndrome: A case-control study. J Res Med Sci 20:1039-45 (2015). WB, IHC . PubMed: 26941806
- Johnson LA et al. Diabetic atherosclerosis in APOE*4 mice: synergy between lipoprotein metabolism and vascular inflammation. J Lipid Res 54:386-96 (2013). Mouse . PubMed: 23204275
- Yvan-Charvet L et al. Cholesterol efflux potential and antiinflammatory properties of high-density lipoprotein after treatment with niacin or anacetrapib. Arterioscler Thromb Vasc Biol 30:1430-8 (2010). PubMed: 20448206
- Yvan-Charvet L et al. Inhibition of cholesteryl ester transfer protein by torcetrapib modestly increases macrophage cholesterol efflux to HDL. Arterioscler Thromb Vasc Biol 27:1132-8 (2007). PubMed: 17322101
- Matsuura F et al. HDL from CETP-deficient subjects shows enhanced ability to promote cholesterol efflux from macrophages in an apoE- and ABCG1-dependent pathway. J Clin Invest 116:1435-42 (2006). PubMed: 16670775