ArticleJournal of neurochemistry2007
A novel PIP2 binding of epsilonPKC and its contribution to the neurite induction ability.
Article in Journal of neurochemistry, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Structural insights into C1-ligand interactions: Filling the gaps by in silico methods.Advances in biological regulation · 2021Review
- Ethanol-Induced Changes in PKCε: From Cell to Behavior.Frontiers in neuroscience · 2018Review
- PKC-ε pseudosubstrate and catalytic activity are necessary for membrane delivery during IgG-mediated phagocytosis.Journal of leukocyte biology · 2013Article
- Direct binding of RalA to PKCη and its crucial role in morphological change during keratinocyte differentiation.Molecular biology of the cell · 2011Article
- The role of protein kinase C epsilon in neural signal transduction and neurogenic diseases.Frontiers of medicine · 2011Review
- The substrates and binding partners of protein kinase Cepsilon.The Biochemical journal · 2010Review
- PKC epsilon facilitates recovery of exocytosis after an exhausting stimulation.Pflugers Archiv : European journal of physiology · 2009Article
Corrections and comments
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Authors and funding
5 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Protein kinase C-epsilon (epsilonPKC) induces neurite outgrowth in neuroblastoma cells but molecular mechanism of the epsilonPKC-induced neurite outgrowth is not fully understood. Therefore, we investigated the ability of phosphatidylinositol 4,5-bisphosphate (PIP(2)) binding of epsilonPKC and its correlation with the neurite extension. We found that full length epsilonPKC bound to PIP(2) in a 12-omicron-tetradecanoylphorbol-13-acetate dependent manner, while the regulatory domain of epsilonPKC (epsilonRD) bound to PIP(2) without any stimulation. To identify the PIP(2) binding region, we made mutants lacking several regions from epsilonRD, and examined their PIP(2) binding activity. The mutants lacking variable region 1 (V1) bound to PIP(2) stronger than intact epsilonRD, while the mutants lacking pseudo-substrate or common region 1 (C1) lost the binding. The PIP(2) binding ability of the V3-deleted mutant was weakened. Those PIP(2) bindings of epsilonPKC, epsilonRD and the mutants well correlated to their neurite induction ability. In addition, a chimera of pleckstrin homology domain of phospholipase Cdelta and the V3 region of epsilonPKC revealed that PIP(2) binding domain and the V3 region are sufficient for the neurite induction, and a first 16 amino acids in the V3 region was important for neurite extension. In conclusion, epsilonPKC directly binds to PIP(2) mainly through pseudo-substrate and common region 1, contributing to the neurite induction activity.
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