FITC标记的β淀粉样肽/Aβ42抗体
2017-5-2
英文名称Anti-beta-Amyloid 1-42(CT)/FITC
中文名称:FITC标记的β淀粉样肽/Aβ42抗体
别 名beta Amyloid(1-42); beta Amyloid 1-42; beta-Amyloid 1-42; Amyloid 1-42; beta-Amyloid 42; A4; AAA; ABETA; ABPP; AD1; Alzheimers Disease Amyloid Protein; Amyloid B; Amyloid Beta A4 Protein Precursor; Amyloid Beta; Amyloid of Aging and Alzheimer Disease; APP; APPI; B Amyloid; Beta APP; Cerebral Vascular Amyloid Peptide; CTFgamma; CVAP; PN II; PN2; PreA4; Protease nexin II; A beta; A4_HUMAN.
规格:100ul
说 明 书100ul
研究领域细胞生物 免疫学 神经生物学
抗体来源Rabbit
克隆类型Polyclonal
交叉反应 Human, Mouse, Rat, Dog, Pig, Cow, Horse, Rabbit,
产品应用Flow-Cyt=1:50-200 IF=1:50-200
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量4.3kDa
性 状Lyophilized or Liquid
浓 度1mg/ml
免 疫 原KLH conjugated synthetic peptide derived from human beta-Amyloid(35-42)
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:
The cerebral and vascular plaques associated with Alzheimer's disease are mainly composed of Amyloid beta peptides. beta Amyloid is derived from cleavage of the Amyloid precursor protein and varies in length from 39 to 43 amino acids. beta Amyloid [1-40], beta Amyloid [1-42], and beta Amyloid [1-43] peptides result from cleavage of Amyloid precursor protein after residues 40, 42, and 43, respectively. The cleavage takes place by gamma-secretase during the last Amyloid precursor protein processing step. beta Amyloid [1-40], beta Amyloid [1-42], and beta Amyloid [1-43] peptides are major constituents of the plaques and tangles that occur in Alzheimer's disease. beta Amyloid antibodies and peptides have been developed as tools for elucidating the biology of Alzheimer's disease
Function:
Functions as a cell surface receptor and performs physiological functions on the surface of neurons relevant to neurite growth, neuronal adhesion and axonogenesis. 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. Acts as a kinesin I membrane receptor, mediating the axonal transport of beta-secretase and presenilin 1. 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.
Beta-amyloid 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. Beta-amyloid 42 is a more effective reductant than beta-amyloid 40. Beta-amyloid peptides bind to lipoproteins and apolipoproteins E and J in the CSF and to HDL particles in plasma, inhibiting metal-catalyzed oxidation of lipoproteins. Beta-APP42 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.
Appicans elicit adhesion of neural cells to the extracellular matrix and may regulate neurite outgrowth in the brai.
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).
中文名称:FITC标记的β淀粉样肽/Aβ42抗体
别 名beta Amyloid(1-42); beta Amyloid 1-42; beta-Amyloid 1-42; Amyloid 1-42; beta-Amyloid 42; A4; AAA; ABETA; ABPP; AD1; Alzheimers Disease Amyloid Protein; Amyloid B; Amyloid Beta A4 Protein Precursor; Amyloid Beta; Amyloid of Aging and Alzheimer Disease; APP; APPI; B Amyloid; Beta APP; Cerebral Vascular Amyloid Peptide; CTFgamma; CVAP; PN II; PN2; PreA4; Protease nexin II; A beta; A4_HUMAN.
详细介绍：
规格:100ul
说 明 书100ul
研究领域细胞生物 免疫学 神经生物学
抗体来源Rabbit
克隆类型Polyclonal
交叉反应 Human, Mouse, Rat, Dog, Pig, Cow, Horse, Rabbit,
产品应用Flow-Cyt=1:50-200 IF=1:50-200
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量4.3kDa
性 状Lyophilized or Liquid
浓 度1mg/ml
免 疫 原KLH conjugated synthetic peptide derived from human beta-Amyloid(35-42)
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.
相关资料：
产品介绍background:
The cerebral and vascular plaques associated with Alzheimer's disease are mainly composed of Amyloid beta peptides. beta Amyloid is derived from cleavage of the Amyloid precursor protein and varies in length from 39 to 43 amino acids. beta Amyloid [1-40], beta Amyloid [1-42], and beta Amyloid [1-43] peptides result from cleavage of Amyloid precursor protein after residues 40, 42, and 43, respectively. The cleavage takes place by gamma-secretase during the last Amyloid precursor protein processing step. beta Amyloid [1-40], beta Amyloid [1-42], and beta Amyloid [1-43] peptides are major constituents of the plaques and tangles that occur in Alzheimer's disease. beta Amyloid antibodies and peptides have been developed as tools for elucidating the biology of Alzheimer's disease
Function:
Functions as a cell surface receptor and performs physiological functions on the surface of neurons relevant to neurite growth, neuronal adhesion and axonogenesis. 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. Acts as a kinesin I membrane receptor, mediating the axonal transport of beta-secretase and presenilin 1. 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.
Beta-amyloid 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. Beta-amyloid 42 is a more effective reductant than beta-amyloid 40. Beta-amyloid peptides bind to lipoproteins and apolipoproteins E and J in the CSF and to HDL particles in plasma, inhibiting metal-catalyzed oxidation of lipoproteins. Beta-APP42 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.
Appicans elicit adhesion of neural cells to the extracellular matrix and may regulate neurite outgrowth in the brai.
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).
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