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Phosphorylation of rabphilin-3A by Ca2+/calmodulin- and cAMP-dependent protein kinases in vitro

EM Fykse, C Li and TC Sudhof
Journal of Neuroscience 1 March 1995, 15 (3) 2385-2395; https://doi.org/10.1523/JNEUROSCI.15-03-02385.1995
EM Fykse
Department of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas 75235.
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C Li
Department of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas 75235.
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TC Sudhof
Department of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas 75235.
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Abstract

Regulation of neurotransmitter release is thought to involve modulation of the release probability by protein phosphorylation. In order to identify novel targets for such regulatory processes, we have studied the phosphorylation of rabphilin-3A in vitro. Rabphilin-3A is a synaptic vesicle protein that interacts with rab3A in a GTP-dependent manner and binds Ca2+ in a phospholipid-dependent manner. Here we show that rabphilin-3A is an efficient substrate for Ca2+/calmodulin- dependent protein kinase II, which phosphorylates rat rabphilin-3A at residue 234 and 274, and for cAMP-dependent protein kinase, which phosphorylates rat rabphilin-3A at residue 234. This identifies the middle region of rabphilin-3A situated between the N-terminal rab3A- binding sequences and the C-terminal C2-domains involved in Ca2+/phospholipid binding as a regulatory domain. Thus, rabphilin-3A is a second phosphoprotein on synaptic vesicles that, similar to synapsin I, may integrate phosphorylation signals from multiple protein kinase signaling pathways in the cell.

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The Journal of Neuroscience: 15 (3)
Journal of Neuroscience
Vol. 15, Issue 3
1 Mar 1995
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Phosphorylation of rabphilin-3A by Ca2+/calmodulin- and cAMP-dependent protein kinases in vitro
EM Fykse, C Li, TC Sudhof
Journal of Neuroscience 1 March 1995, 15 (3) 2385-2395; DOI: 10.1523/JNEUROSCI.15-03-02385.1995

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Phosphorylation of rabphilin-3A by Ca2+/calmodulin- and cAMP-dependent protein kinases in vitro
EM Fykse, C Li, TC Sudhof
Journal of Neuroscience 1 March 1995, 15 (3) 2385-2395; DOI: 10.1523/JNEUROSCI.15-03-02385.1995
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