YRP01654P-01
[Polyclonal Antibody]
Phospho-Amyloid Precursor Protein(Y757) Rabbit Polyclonal Antibody
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Species: |
Rabbit |
Applications: |
IHC IF |
Immunogen Range: |
KLH conjugated synthetic phosphopeptide derived from human APP around the phosphorylation site of Tyr757 |
Clonality: |
Polyclonal Antibody |
Isotype: |
IgG |
GENE ID: |
351 |
Swiss Prot: |
P05067 |
Synonyms: |
AAA, AD1, PN2, ABPP, APPI, CVAP, ABETA, PN-II, CTFgamma, Amyloid beta A4 protein, APP, Alzheimer disease amyloid protein, Cerebral vascular amyloid peptide, PreA4, Protease nexin-II, A4 |
Purification: |
Purified by Protein A. |
Storage: |
Aqueous buffered solution containing 100ug/ml BSA, 50% glycerol and 0.09% sodium azide. Store at -20℃ for 12 months |
Background: |
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. 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. |
Caculated MW: |
/ |
Observed MW: |
Refer to Figures |
Applications: |
IHC 1:100-1:500 IF 1:50-1:200
|
Reacitivity: |
Human, Mouse, Rat |
For research use only. Not intended for diagnostic or therapeutic use!