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Cyclin-dependent kinase-5/p35 phosphorylates Presenilin 1 to regulate carboxy-terminal fragment stability

Lookup NU author(s): Professor Colin Dingwall

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Abstract

Mutations in the Presenilin 1 gene are the cause of the majority of autosomal dominant familial forms of Alzheimer's disease. Presenilin 1 (PS1) is produced as a holoprotein but is then rapidly processed to amino- (N-PS1) and carboxy-terminal (C-PS1) fragments that are incorporated into stable high molecular mass complexes. The mechanisms that control PS1 cleavage and stability are not property understood but sequences within C-PS1 have been shown to regulate both of these properties. Here we demonstrate that cyclin dependent kinase-5/p35 (cdk5/p35) phosphorylates PS1 on threonine(354) within CPS1 both in vitro and in vivo. Threonine(354) phosphorylation functions to selectively stabilize G-PS1. Our results demonstrate that cdk5/p35 is a regulator of PS1 metabolism.

Publication metadata

Author(s): Dingwall C; Lau KF; Howlett DR; Kesavapany S; Standen CL; McLoughlin DM; Miller CCJ

Publication type: Article

Publication status: Published

Journal: Molecular and Cellular Neuroscience

Year: 2002

Volume: 20

Issue: 1

Pages: 13-20

ISSN (print): 1044-7431

ISSN (electronic): 1095-9327

Publisher: Academic Press

URL: http://dx.doi.org/10.1006/mcne.2002.1108

DOI: 10.1006/mcne.2002.1108

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