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First published online 10 October 2006
doi: 10.1242/jcs.03219

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14-3-3 affects dynamics and integrity of glial filaments by binding to phosphorylated GFAP

¹ The Key Laboratory of Cell Proliferation and Differentiation of Ministry of Education and The State Key Laboratory of Bio-membrane and Membrane Bio-engineering, Peking University, Beijing 100871, China
² The Department of Cell Biology and Genetics, College of Life Sciences, Peking University, Beijing 100871, China
³ The Center for Theoretical Biology, Peking University, Beijing 100871, China
⁴ Neuroscience Research Institute, Peking University, Beijing 100083, China
⁵ Hong Kong DNA Chips Limited, Hong Kong SAR, China

^* Author for correspondence (e-mail: chenjg{at}pku.edu.cn)

Accepted 16 August 2006

Recent findings indicated a protective role of GFAP in ischemic brain, injured spinal cord, and in neurodegenerative disease. We previously demonstrated that 14-3-3, once thought to be neuronal specific, was up-regulated by ischemia in astrocytes and may play a specific protective role in astrocytes. Here we report that 14-3-3 associates with both soluble and filamentous GFAP in a phosphorylation- and cell-cycle-dependent manner in primary cultured astrocytes. The amount of association increases during G2/M phase due to more phosphorylated GFAP. Moreover, this interaction is independent of vimentin, another type III intermediate filament protein in astrocytes which forms glial filaments with GFAP. A series of domain deletion mutants and substitution mutations at phosphorylation sites (from serine to alanine) on GFAP demonstrated that serine 8 in the head domain is essential for the direct association of GFAP to 14-3-3. Overexpression of 14-3-3 destroyed the integrity and affected the movement of GFAP intermediate filaments. This data demonstrates that 14-3-3 contributes to the regulation of dynamics of GFAP filaments, which may contribute to the stability of the cytoskeleton and the mechanisms of central nervous system neurodegenerative disease.

Key words: , GFAP, Vimentin, Astrocytes, Phosphorylation

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