Amyloid Fibrils 抗体
适用: 人
WB, ELISA, IHC, DB, IP, IF/ICC
宿主: 兔
Polyclonal
unconjugated
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- 抗原
- Amyloid Fibrils
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适用
- 人
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宿主
- 兔
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克隆类型
- 多克隆
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标记
- 非结合性
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应用范围
- Western Blotting (WB), ELISA, Immunohistochemistry (IHC), Dot Blot (DB), Immunoprecipitation (IP), Immunofluorescence (fixed cells) (IF/ICC)
- 原理
- Anti-Amyloid Fibrils Rabbit Polyclonal Antibody
- 特异性
- This antibody recognizes epitopes common to many human amyloid fibrils and fibrillar oligomers but not prefibrillar oligomers or natively folded proteins. Predicted to recognize mouse and rat based on sequence homology.
- 交叉反应
- 人, 小鼠, 大鼠
- 免疫原
- Fibrils prepared from human Ab42 peptide.
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anti-Amyloid Fibrils antibody
适用: 人 WB, DB, IP, EIA, IHC (fro), IF 宿主: 兔 Polyclonal unconjugated
anti-Amyloid Fibrils antibody适用: 人 WB, ELISA, IHC, IP 宿主: 兔 Polyclonal unconjugated
anti-Amyloid Fibrils antibody适用: 人, 小鼠, 大鼠 WB, ELISA, IHC, DB, IP, ICC 宿主: 兔 Polyclonal unconjugated
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- 应用备注
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Immunoblotting: use at 1:1,000 dilution
.Dot blot: use at 1:1,000 dilution.
Immunohistochemistry: use at 1:1,000 dilution
ELISA: use at 1:1,000 dilution with amyloid fibril-containing samples on the solid phase.
These are recommended concentrations.
Enduser should determine optimal concentrations for their applications. - 限制
- 仅限研究用
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- 状态
- Liquid
- 溶解方式
- Dilute in PBS or medium that is identical to that used in the assay system.
- 浓度
- Lot specific
- 缓冲液
- PBS, pH 7.0, 0.09 % sodium azide and 50 % glycerol
- 储存液
- Sodium azide
- 注意事项
- This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
- 储存条件
- -20 °C
- 储存方法
- This product is stable for at least 1 year at -20°C. Freeze in multiple aliquots to avoid repeated freeze-thaw cycles.
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- 抗原
- Amyloid Fibrils
- 背景
- Amyloid-beta precursor protein,Functions as a cell surface receptor and performs physiological functions on the surface of neurons relevant to neurite growth, neuronal adhesion and axonogenesis. Interaction between APP molecules on neighboring cells promotes synaptogenesis (PubMed:25122912). Involved in cell mobility and transcription regulation through protein-protein interactions. Can promote transcription activation through binding to APBB1-KAT5 and inhibits Notch signaling through interaction with Numb. Couples to apoptosis-inducing pathways such as those mediated by G(o) and JIP. Inhibits G(o) alpha ATPase activity (By similarity). Acts as a kinesin I membrane receptor, mediating the axonal transport of beta-secretase and presenilin 1 (By similarity). By acting as a kinesin I membrane receptor, plays a role in axonal anterograde transport of cargo towards synapes in axons (PubMed:17062754, PubMed:23011729). Involved in copper homeostasis/oxidative stress through copper ion reduction. In vitro, copper-metallated APP induces neuronal death directly or is potentiated through Cu(2+)-mediated low-density lipoprotein oxidation. Can regulate neurite outgrowth through binding to components of the extracellular matrix such as heparin and collagen I and IV. The splice isoforms that contain the BPTI domain possess protease inhibitor activity. Induces a AGER-dependent pathway that involves activation of p38 MAPK, resulting in internalization of amyloid-beta peptide and leading to mitochondrial dysfunction in cultured cortical neurons. Provides Cu(2+) ions for GPC1 which are required for release of nitric oxide (NO) and subsequent degradation of the heparan sulfate chains on GPC1. {UniProtKB:P12023, PubMed:17062754, PubMed:23011729, PubMed:25122912}., Amyloid-beta peptides are lipophilic metal chelators with metal-reducing activity. Bind transient metals such as copper, zinc and iron. In vitro, can reduce Cu(2+) and Fe(3+) to Cu(+) and Fe(2+), respectively. Amyloid-beta protein 42 is a more effective reductant than amyloid-beta protein 40. Amyloid-beta peptides bind to lipoproteins and apolipoproteins E and J in the CSF and to HDL particles in plasma, inhibiting metal-catalyzed oxidation of lipoproteins. APP42-beta may activate mononuclear phagocytes in the brain and elicit inflammatory responses. Promotes both tau aggregation and TPK II-mediated phosphorylation. Interaction with overexpressed HADH2 leads to oxidative stress and neurotoxicity. Also binds GPC1 in lipid rafts., Appicans elicit adhesion of neural cells to the extracellular matrix and may regulate neurite outgrowth in the brain. {ECO:0000250}., The gamma-CTF peptides as well as the caspase-cleaved peptides, including C31, are potent enhancers of neuronal apoptosis., N-APP binds TNFRSF21 triggering caspase activation and degeneration of both neuronal cell bodies (via caspase-3) and axons (via caspase-6).,Amyloid monomeric proteins can oligomerize into destructive amyloid fibrils. Amyloidogenic conformations of non- disease related proteins can be created by partial protein misfolding or denaturation. Many degenerative diseases are known to be related to the accumulation of misfolded proteins as amyloid fibers. These include the amyloid-beta peptide plaques and tau neurofibrillary tangles in senile plaques of Alzheimer's symptomology, the deposition of alpha-synuclein in the Lewy bodies of Parkinson's disease, and accumulation of polyglutamine-containing aggregates in Huntington's disease.,Cell membrane, Membrane, Perikaryon, Cell projection, growth cone, Membrane, clathrin-coated pit, Early endosome, Cytoplasmic vesicle,APP, ABPP, APPI, Alzheimer disease amyloid A4 protein homolog, Alzheimer disease amyloid protein, Amyloid precursor protein, Amyloid-beta
- UniProt
- P05067
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