ArticleEuropean journal of pharmacology2008
Negative regulation of cyclin-dependent kinase 5 targets by protein kinase C.
Article in European journal of pharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Protein Kinase C-Delta Mediates Cell Cycle Reentry and Apoptosis Induced by Amyloid-Beta Peptide in Post-Mitotic Cortical Neurons.International journal of molecular sciences · 2024Article
- Dopamine: Functions, Signaling, and Association with Neurological Diseases.Cellular and molecular neurobiology · 2019Review
- Dopamine receptors - IUPHAR Review 13.British journal of pharmacology · 2015Review
- Ischemic stroke injury is mediated by aberrant Cdk5.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Analysis of Cdk5-related phosphoproteomics in growth cones.Journal of molecular neuroscience : MN · 2014Article
- D1 dopamine receptor coupling to PLCβ regulates forward locomotion in mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Cdk5: An Emerging Kinase in Pain Signaling.Brain disorders & therapy · 2013Article
- Attention-deficit/hyperactivity phenotype in mice lacking the cyclin-dependent kinase 5 cofactor p35.Biological psychiatry · 2010Article
- PKCdelta regulates cortical radial migration by stabilizing the Cdk5 activator p35.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Cyclin-dependent kinase 5 (Cdk5) is a proline-directed protein serine/threonine kinase essential for brain development and implicated in synaptic plasticity, dopaminergic neurotransmission, drug addiction, and neurodegenerative disorders. Relatively little is known about the molecular mechanisms that regulate the activity of Cdk5 in vivo. In order to determine whether protein kinase C (PKC) regulates Cdk5 activity in the central nervous system, the phosphorylation levels of two Cdk5 substrates were evaluated under conditions of altered PKC activity in vivo. Treatment of acute striatal slices with a PKC-activating phorbol ester caused a time- and dose-dependent decrease in the levels of phospho-Ser6 inhibitor-1, phospho-Ser67 inhibitor-1, and phospho-Thr75 dopamine- and cAMP-regulated phosphoprotein, Mr 32,000 (DARPP-32). This effect was reversed by the PKC inhibitor, Ro-32-0432. Moreover, phospho-Ser6 inhibitor-1, phospho-Ser67 inhibitor-1, and phospho-Thr75 DARPP-32 levels were elevated in brain tissue from mice lacking the gene for PKC-alpha. PKC did not phosphorylate Cdk5 or its cofactor, p25, in vitro. Striatal levels of the Cdk5 cofactor, p35, did not change in response to phorbol ester treatment. Furthermore, Cdk5 immunoprecipitated from striatal slices treated with phorbol ester had unaltered activity toward a control substrate in vitro. These results suggest that PKC exerts its effects on the phosphorylation state of Cdk5 substrates through an indirect mechanism that may involve the regulatory binding partners of Cdk5 other than its neuronal cofactors.
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Registered trials
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