Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
4340497 | Neuroscience | 2008 | 5 Pages |
Abstract
The endopeptidase properties of β and γ splice forms of human MMEL were determined in HEK293T cells transduced with the human cDNAs for the two splice forms; this showed degradation of both Aβ42 and Aβ40 by hMMEL-β but not hMMEL-γ. hMMEL-β activity was found at the extracellular surface with no significant secreted activity. hMMEL-γ was not expressed at the extracellular surface. Finally, it was found that hMMEL cleaves Aβ near the α-secretase site (producing Aβ1-17â«Aβ1-16). These data establish hMMEL as a mediator of Aβ catabolism and raise the possibility of its involvement in the etiology of AD and as a target for intervention.
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Authors
J.Y. Huang, A.M. Bruno, C.A. Patel, A.M. Huynh, K.D. Philibert, M.J. Glucksman, R.A. Marr,