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  • HAT Assay Buffer, 5X - 3850735

    Document Type:
    Certificate of Analysis
    Lot Number:
    3850735
    Product Catalog Number:
    20-148
    Product Catalog Name:
    HAT Assay Buffer, 5X

  • HAT Assay Buffer, 5X -2660620

    Document Type:
    Certificate of Analysis
    Lot Number:
    2660620
    Product Catalog Number:
    20-148
    Product Catalog Name:
    HAT Assay Buffer, 5X

  • HAT Assay Buffer, 5X - 3725367

    Document Type:
    Certificate of Analysis
    Lot Number:
    3725367
    Product Catalog Number:
    20-148
    Product Catalog Name:
    HAT Assay Buffer, 5X

  • HAT Assay Buffer, 5X -2838810

    Document Type:
    Certificate of Analysis
    Lot Number:
    2838810
    Product Catalog Number:
    20-148
    Product Catalog Name:
    HAT Assay Buffer, 5X

  • HAT Assay Buffer, 5X - 3493369

    Document Type:
    Certificate of Analysis
    Lot Number:
    3493369
    Product Catalog Number:
    20-148
    Product Catalog Name:
    HAT Assay Buffer, 5X

  • Tip60 HAT Action Mediates Environmental Enrichment Induced Cognitive Restoration. 27454757

    Environmental enrichment (EE) conditions have beneficial effects for reinstating cognitive ability in neuropathological disorders like Alzheimer's disease (AD). While EE benefits involve epigenetic gene control mechanisms that comprise histone acetylation, the histone acetyltransferases (HATs) involved remain largely unknown. Here, we examine a role for Tip60 HAT action in mediating activity- dependent beneficial neuroadaptations to EE using the Drosophila CNS mushroom body (MB) as a well-characterized cognition model. We show that flies raised under EE conditions display enhanced MB axonal outgrowth, synaptic marker protein production, histone acetylation induction and transcriptional activation of cognition linked genes when compared to their genotypically identical siblings raised under isolated conditions. Further, these beneficial changes are impaired in both Tip60 HAT mutant flies and APP neurodegenerative flies. While EE conditions provide some beneficial neuroadaptive changes in the APP neurodegenerative fly MB, such positive changes are significantly enhanced by increasing MB Tip60 HAT levels. Our results implicate Tip60 as a critical mediator of EE-induced benefits, and provide broad insights into synergistic behavioral and epigenetic based therapeutic approaches for treatment of cognitive disorder.
    Document Type:
    Reference
    Product Catalog Number:
    17-408
    Product Catalog Name:
    EZ-Magna ChIP™ A - Chromatin Immunoprecipitation Kit

  • HAT Assay Buffer, 5X -2631536

    Document Type:
    Certificate of Analysis
    Lot Number:
    2631536
    Product Catalog Number:
    20-148
    Product Catalog Name:
    HAT Assay Buffer, 5X

  • Restoring Tip60 HAT/HDAC2 Balance in the Neurodegenerative Brain Relieves Epigenetic Transcriptional Repression and Reinstates Cognition. 29654189

    Cognitive decline is a debilitating hallmark during preclinical stages of Alzheimer's disease (AD), yet the causes remain unclear. Because histone acetylation homeostasis is critical for mediating epigenetic gene control throughout neuronal development, we postulated that its misregulation contributes to cognitive impairment preceding AD pathology. Here, we show that disruption of Tip60 histone acetlytransferase (HAT)/histone deacetylase 2 (HDAC2) homeostasis occurs early in the brain of an AD-associated amyloid precursor protein (APP) Drosophila model and triggers epigenetic repression of neuroplasticity genes well before Aβ plaques form in male and female larvae. Repressed genes display enhanced HDAC2 binding and reduced Tip60 and histone acetylation enrichment. Increasing Tip60 in the AD-associated APP brain restores Tip60 HAT/HDAC2 balance by decreasing HDAC2 levels, reverses neuroepigenetic alterations to activate synaptic plasticity genes, and reinstates brain morphology and cognition. Such Drosophila neuroplasticity gene epigenetic signatures are conserved in male and female mouse hippocampus and their expression and Tip60 function is compromised in hippocampus from AD patients. We suggest that Tip60 HAT/HDAC2-mediated epigenetic gene disruption is a critical initial step in AD that is reversed by restoring Tip60 in the brain.SIGNIFICANCE STATEMENT Mild cognitive impairment is a debilitating hallmark during preclinical stages of Alzheimer's disease (AD), yet its causes remain unclear. Although recent findings support elevated histone deacetylase 2 (HDAC2) as a cause for epigenetic repression of synaptic genes that contribute to cognitive deficits, whether alterations in histone acetlytransferase (HAT) levels that counterbalance HDAC2 repressor action occur and the identity of these HATs remain unknown. We demonstrate that disruption of Tip60 HAT/HDAC2 homeostasis occurs early in the AD Drosophila brain and triggers epigenetic repression of neuroplasticity genes before Aβ plaques form. Increasing Tip60 in the AD brain restores Tip60 HAT/HDAC2 balance, reverses neuroepigenetic alterations to activate synaptic genes, and reinstates brain morphology and cognition. Our data suggest that disruption of the Tip60 HAT/HDAC2 balance is a critical initial step in AD.
    Document Type:
    Reference
    Product Catalog Number:
    17-408
    Product Catalog Name:
    EZ-Magna ChIP™ A - Chromatin Immunoprecipitation Kit