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> 抗原抗體、ELISA、WB > 一抗 > Monoclonal Antibodies > APP / Beta Amyloid Antibody (aa18-289, clone J4H9)品牌 |
Leading Biology | 貨號 |
APG03157G |
產(chǎn)品分類 |
Monoclonal Antibodies | 研究領(lǐng)域 |
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產(chǎn)品概述 |
We constantly strive to ensure we provide our customers with the best antibodies. As a result of this work we offer this antibody in purified format.
We are in the process of updating our datasheets. If you have any questions regarding this update, please feel free to contact our technical support team.
This product is a high quality APP / Beta Amyloid antibody (aa18-289, clone J4H9).
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分子量 |
87kDa
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細(xì)胞定位 |
Antigen Cellular Localization:
Membrane; Single-pass type I membrane protein. Membrane, clathrin-coated pit. Note=Cell surface protein that rapidly becomes internalized via clathrin-coated pits. During maturation, the immature APP (N-glycosylated in the endoplasmic reticulum) moves to the Golgi complex where complete maturation occurs (O-glycosylated and sulfated). After alpha-secretase cleavage, soluble APP is released into the extracellular space and the C-terminal is internalized to endosomes and lysosomes. Some APP accumulates in secretory transport vesicles leaving the late Golgi compartment and returns to the cell surface. Gamma-CTF(59) peptide is located to both the cytoplasm and nuclei of neurons. It can be translocated to the nucleus through association with APBB1 (Fe65). Beta-APP42 associates with FRPL1 at the cell surface and the complex is then rapidly internalized. APP sorts to the basolateral surface in epithelial cells. During neuronal differentiation, the Thr-743 phosphorylated form is located mainly in growth cones, moderately in neurites and sparingly in the cell body. Casein kinase phosphorylation can occur either at the cell surface or within a post-Golgi compartment. Associates with GPC1 in perinuclear compartments. Colocalizes with SORL1 in a vesicular pattern in cytoplasm and perinuclear regions
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宿主 |
Mouse
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種屬反應(yīng)性 |
Human
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克隆號 |
J4H9
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通用名 |
A4, AD1
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基因ID |
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UniProt ID |
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功能 |
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 (By similarity). 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. 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. 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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總結(jié) |
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 (By similarity). 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. 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. 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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形式 |
Liquid
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儲存條件 |
Store at +4°C short term. For long-term storage, aliquot and store at -20°C or below. Stable for 12 months at -20°C. Avoid repeated freeze-thaw cycles.
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應(yīng)用 |
WB, IHC-P, E
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稀釋方法 |
IHC-P (2.5 μg/ml), WB (1:500-1:1000),
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別名 |
Amyloid beta A4 protein, ABPP, APPI, APP, Alzheimer disease amyloid protein, Cerebral vascular amyloid peptide, CVAP, PreA4, Protease nexin-II, PN-II, N-APP, Soluble APP-alpha, S-APP-alpha, Soluble APP-beta, S-APP-beta, C99, Beta-amyloid protein 42, Beta-APP42, Beta-amyloid protein 40, Beta-APP40, C83, P3(42), P3(40), C80, Gamma-secretase C-terminal fragment 59, Amyloid intracellular domain 59, AICD-59, AID(59), Gamma-CTF(59), Gamma-secretase C-terminal fragment 57, Amyloid intracellular domain 57, AICD-57, AID(57), Gamma-CTF(57), Gamma-secretase C-terminal fragment 50, Amyloid intracellular domain 50, AICD-50, AID(50), Gamma-CTF(50), C31, APP, A4, AD1
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圖像 |
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說明書 |
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數(shù)量 |
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