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N. H. Greig [5]N. Greig [1]
  1.  22
    Lessons from a BACE1 inhibitor trial: off-site but not off base.D. K. Lahiri, B. Maloney, J. M. Long & N. H. Greig - 2014 - Alzheimers Dement 10:S411-9.
    Alzheimer's disease is characterized by formation of neuritic plaque primarily composed of a small filamentous protein called amyloid-beta peptide . The rate-limiting step in the production of Abeta is the processing of Abeta precursor protein by beta-site APP-cleaving enzyme . Hence, BACE1 activity plausibly plays a rate-limiting role in the generation of potentially toxic Abeta within brain and the development of AD, thereby making it an interesting drug target. A phase II trial of the promising LY2886721 inhibitor of BACE1 was (...)
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  2.  20
    Taking down the unindicted co-conspirators of amyloid beta-peptide-mediated neuronal death: shared gene regulation of BACE1 and APP genes interacting with CREB, Fe65 and YY1 transcription factors. [REVIEW]D. K. Lahiri, Y. W. Ge, J. T. Rogers, K. Sambamurti, N. H. Greig & B. Maloney - 2006 - Curr Alzheimer Res 3:475-83.
    Major hallmarks of Alzheimer's disease include brain deposition of the amyloid-beta peptide , which is proteolytically cleaved from a large Abeta precursor protein by beta and gamma- secretases. A transmembrane aspartyl protease, beta-APP cleaving enzyme , has been recognized as the beta-secretase. We review the structure and function of the BACE1 protein, and of 4129 bp of the 5'-flanking region sequence of the BACE1 gene and its interaction with various transcription factors involved in cell signaling. The promoter region and 5'-untranslated (...)
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