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Mol. Cells 2010; 29(1): 51-56

Published online January 31, 2010

https://doi.org/10.1007/s10059-010-0016-0

© The Korean Society for Molecular and Cellular Biology

Expression of p25, an Aberrant Cyclin-Dependent Kinase 5 Activator, Stimulates Basal Secretion in PC12 Cells

Mi-Young Son1,2, and Sul-Hee Chung1,*

1Graduate Program in Neuroscience, Institute for Brain Science and Technology, Inje University, Busan 614-735, Korea, 2Present address: Development and Differentiation Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 305-806, Korea; Department of Biological Sciences, Korean Advanced Institute of Science and Technology, Daejeon 305-701, Korea

Correspondence to : *Correspondence: sulchung@inje.ac.kr

Received: July 9, 2009; Revised: October 13, 2009; Accepted: November 2, 2009

Abstract

Although alterations in the functions of neurotransmitter systems have been implicated in the pathology of Alzhei-mer’s disease (AD), the mechanisms that give rise to these alterations are not well understood. The amount of p25, an aberrant cleavage product of p35 that activates cyclin-dependent kinase 5 (Cdk5), is elevated in AD brains. The role of Cdk5 in neurotransmitter release has been well established. In this study, we examined whether p25 was linked to altered neurotransmitter release in AD. Transient or stable expression of p25 significantly increased basal secretion of human growth hormone (hGH) or neurotransmitter in PC12 cells. Expression of a p25 phosphorylation-deficient mutant, T138A, inhibited basal hGH secretion relative to the p25 wild type, suggesting the involvement of Thr138 phosphorylation in secretion. The expression and activity of

Keywords Alzheimer’s disease, Cdk5, p25, PC12 cells, secretion

Article

Research Article

Mol. Cells 2010; 29(1): 51-56

Published online January 31, 2010 https://doi.org/10.1007/s10059-010-0016-0

Copyright © The Korean Society for Molecular and Cellular Biology.

Expression of p25, an Aberrant Cyclin-Dependent Kinase 5 Activator, Stimulates Basal Secretion in PC12 Cells

Mi-Young Son1,2, and Sul-Hee Chung1,*

1Graduate Program in Neuroscience, Institute for Brain Science and Technology, Inje University, Busan 614-735, Korea, 2Present address: Development and Differentiation Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 305-806, Korea; Department of Biological Sciences, Korean Advanced Institute of Science and Technology, Daejeon 305-701, Korea

Correspondence to:*Correspondence: sulchung@inje.ac.kr

Received: July 9, 2009; Revised: October 13, 2009; Accepted: November 2, 2009

Abstract

Although alterations in the functions of neurotransmitter systems have been implicated in the pathology of Alzhei-mer’s disease (AD), the mechanisms that give rise to these alterations are not well understood. The amount of p25, an aberrant cleavage product of p35 that activates cyclin-dependent kinase 5 (Cdk5), is elevated in AD brains. The role of Cdk5 in neurotransmitter release has been well established. In this study, we examined whether p25 was linked to altered neurotransmitter release in AD. Transient or stable expression of p25 significantly increased basal secretion of human growth hormone (hGH) or neurotransmitter in PC12 cells. Expression of a p25 phosphorylation-deficient mutant, T138A, inhibited basal hGH secretion relative to the p25 wild type, suggesting the involvement of Thr138 phosphorylation in secretion. The expression and activity of

Keywords: Alzheimer’s disease, Cdk5, p25, PC12 cells, secretion

Mol. Cells
May 31, 2022 Vol.45 No.5, pp. 273~352
COVER PICTURE
Fe2+ ion depletion-induced expression of BΔGFP at the early stage of leaf development (Choi et al., pp. 294-305).

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