ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Raf kinase inhibitory protein is required for cerebellar long-term synaptic depression by mediating PKC-dependent MAPK activation.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 30 citations in OpenAlex.
- Purkinje cell models: past, present and future.Frontiers in computational neuroscience · 2024Review
- Solid lipid nanoparticles loading with curcumin and dexanabinol to treat major depressive disorder.Neural regeneration research · 2021Article
- Feedback regulation of RTK signaling in development.Developmental biology · 2019Review
- Regulation and Interaction of Multiple Types of Synaptic Plasticity in a Purkinje Neuron and Their Contribution to Motor Learning.Cerebellum (London, England) · 2018Review
- Timely regulated sorting from early to late endosomes is required to maintain cerebellar long-term depression.Nature communications · 2017Article
- Hippocampal Cholinergic Neurostimulating Peptide as a Possible Modulating Factor against Glutamatergic Neuronal Disability by Amyloid Oligomers.Cell transplantation · 2017Article
- A Model of Induction of Cerebellar Long-Term Depression Including RKIP Inactivation of Raf and MEK.Frontiers in molecular neuroscience · 2017Article
- Multiple amygdaloid divisions of arcopallium send convergent projections to the nucleus accumbens and neighboring subpallial amygdala regions in the domestic chicken: a selective pathway tracing and reconstruction study.Brain structure & function · 2017Article
- Cerebellar Shank2 Regulates Excitatory Synapse Density, Motor Coordination, and Specific Repetitive and Anxiety-Like Behaviors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Stochastic Induction of Long-Term Potentiation and Long-Term Depression.Scientific reports · 2016Article
- Modulation, Plasticity and Pathophysiology of the Parallel Fiber-Purkinje Cell Synapse.Frontiers in synaptic neuroscience · 2016Review
- Functional and Physical Interaction of Diacylglycerol Kinase ζ with Protein Kinase Cα Is Required for Cerebellar Long-Term Depression.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Protein tyrosine phosphatase receptor type R is required for Purkinje cell responsiveness in cerebellar long-term depression.Molecular brain · 2015Article
- Raf kinase inhibitory protein (RKIP): functional pleiotropy in the mammalian brain.Critical reviews in oncogenesis · 2014Review
- Long-term depression and other synaptic plasticity in the cerebellum.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2013Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It was demonstrated previously that a positive feedback loop, including protein kinase C (PKC) and mitogen-activated protein kinase (MAPK), is required for the gradual expression of cerebellar long-term depression (LTD). PKC and MAPK are mutually activated in this loop. MAPK-dependent PKC activation is likely to be mediated by phospholipase A2. On the other hand, it is not clear how PKC activates MAPK. Therefore, the entire picture of this loop was not fully understood. We here test the hypothesis that this loop is completed by the PKC substrate, Raf kinase inhibitory protein (RKIP). To test this hypothesis, we used a mutant form of RKIP that is not phosphorylated by PKC and thus constitutively inhibits Raf-1 and MEK, upstream kinases of MAPK. When this RKIP mutant was introduced into Purkinje cells of mouse cerebellar slices through patch-clamp electrodes, LTD was blocked, while wild-type (WT) RKIP had no effect on LTD. Physiological epistasis experiments demonstrated that RKIP works downstream of PKC and upstream of MAPK during LTD induction. Furthermore, biochemical analyses demonstrated that endogenous RKIP dissociates from Raf-1 and MEK during LTD induction in a PKC-dependent manner, suggesting that RKIP binding-dependent inhibition of Raf-1 and MEK is removed upon LTD induction. We therefore conclude that PKC-dependent regulation of RKIP leads to MAPK activation, with RKIP completing the positive feedback loop that is required for LTD.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.