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    BIOMARKER:

    APP overexpression

    i
    Other names: APP, Amyloid Beta Precursor Protein, Amyloid Beta (A4) Precursor Protein, Alzheimer Disease Amyloid Protein, Cerebral Vascular Amyloid Peptide, Amyloid-Beta Precursor Protein, Amyloid Precursor Protein, Peptidase Nexin-II, Protease Nexin-II, PreA4, ABPP,Beta-Amyloid Precursor Protein, Testicular Tissue Protein Li, Beta-Amyloid Peptide(1-40), Beta-Amyloid Peptide(1-42), Amyloid Beta A4 Protein, CTFgamma
    Entrez ID:
    351
    Related biomarkers:
    Fusion
    7ms
    AAV mediated carboxyl terminus of Hsp70 interacting protein overexpression mitigates the cognitive and pathological phenotypes of APP/PS1 mice. (PubMed, Neural Regen Res)
    Our research shows that CHIP effectively reduces the behavior and pathological manifestations of APP/PS1 mice. Indeed, overexpression of CHIP could be a beneficial approach for the treatment of Alzheimer's disease.
    Preclinical • Journal
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    DNAJB1 (DnaJ Heat Shock Protein Family (Hsp40) Member B1) • ADAM10 (ADAM Metallopeptidase Domain 10)
    |
    APP overexpression
    over1year
    APP and Bace1: Differential effect of cholesterol enrichment on processing and plasma membrane mobility. (PubMed, iScience)
    Analogue results were obtained for cells overexpressing an APP mutant that cannot be processed by α-secretase, highlighting the major influence of cholesterol enrichment on the cleavage of APP carried out by Bace1. By contrast, the cholesterol content was not correlated with changes in membrane dynamics of APP and Bace1 analyzed with single molecule tracking, indicating that the effect of cholesterol enrichment on APP processing by Bace1 is uncoupled from changes in their lateral diffusion.
    Journal
    |
    APP (Amyloid Beta Precursor Protein)
    |
    APP overexpression
    over2years
    Overexpression of CCN1 in esophageal squamous cell carcinoma attenuates cell proliferation through amyloid precursor protein without DR6 involvement. (PubMed, Hum Cell)
    Overexpression of CCN1 in ESCC cells induced cell cycle arrest rather than apoptosis through upregulation of APP and its association with p53 without DR6 involvement. Overexpression of APP stopped cell growth, but overexpression of DR6 did not cause any form of programmed cell death or cell cycle arrest whatsoever.
    Journal
    |
    APP (Amyloid Beta Precursor Protein) • CCN1 (Cellular Communication Network Factor 1)
    |
    APP overexpression
    over2years
    CCN1 suppresses cell proliferation of esophageal squamous cell carcinoma through amyloid precursor protein without DR6 participation. (PubMed, Cell Signal)
    Overexpression of CCN1 in ESCC cells inhibited cell proliferation through upregulation of APP and its association with p53 without DR6 involvement. Overexpression of APP stopped cell growth, but overexpression of DR6 did not affect cell growth or cell death whatsoever.
    Journal
    |
    APP (Amyloid Beta Precursor Protein) • CCN1 (Cellular Communication Network Factor 1)
    |
    APP overexpression
    over2years
    Effect of Sulindac in an in vitro AD Model Under hypoxic conditions. (PubMed, FASEB J)
    Further, reduced cell proliferation was seen under hypoxic conditions compared to normoxic conditions indicating that hypoxic conditions further exacerbateAD pathology. Our findings in an in vitro AD model, suggest that sulindac has a potential therapeutic value to ameliorate AD pathology.
    Preclinical • Journal
    |
    APP (Amyloid Beta Precursor Protein)
    |
    APP overexpression
    almost3years
    The microRNA-455 Null Mouse Has Memory Deficit and Increased Anxiety, Targeting Key Genes Involved in Alzheimer's Disease. (PubMed, Int J Mol Sci)
    In the hippocampus of miR-455 null mice at 14 months of age, the levels of protein for APP, BACE1 and TAU were all increased. Such findings reinforce the involvement of miR-455 in AD progression and demonstrate its action on cognitive performance.
    Preclinical • Journal
    |
    MIR455 (MicroRNA 455)
    |
    APP overexpression
    almost3years
    O-GlcNAcylation Inhibits Endocytosis of Amyloid Precursor Protein by Decreasing Its Localization in Lipid Raft Microdomains. (PubMed, Membranes (Basel))
    These results indicate that O-GlcNAcylation can regulate lipid raft-dependent APP endocytosis via translocation of APP into non-raft microdomains. Our findings showed a new functional role of O-GlcNAcylation for the regulation of APP trafficking, offering new mechanistic insight for Aβ production.
    Journal
    |
    APP (Amyloid Beta Precursor Protein)
    |
    APP overexpression