ArticleProceedings of the National Academy of Sciences of the United States of America1993
Regulatory subunits of cAMP-dependent protein kinases are degraded after conjugation to ubiquitin: a molecular mechanism underlying long-term synaptic plasticity.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
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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.
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Who cites it
81 citing papers in PubMed, 217 citations in OpenAlex.
- Regulation of Translation by PKA Signaling Pathway.International journal of molecular sciences · 2026Review
- The Ubiquitin-Proteasome System in Brain Disorders: Pathogenic Pathways, Post-Translational Tweaks, and Therapeutic Frontiers.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Review
- Article
- The PDE4DIP-AKAP9 axis promotes lung cancer growth through modulation of PKA signalling.Communications biology · 2025Article
- β-Amyloid impairs Proteasome structure and function. Proteasome activation mitigates amyloid induced toxicity and cognitive deficits.bioRxiv : the preprint server for biology · 2025Article
- Early disruption of the CREB pathway drives dendritic morphological alterations in FTD/ALS cortical neurons.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- The ubiquitin-proteasome system and learning-dependent synaptic plasticity - A 10 year update.Neuroscience and biobehavioral reviews · 2023Review
- Synaptic retrograde regulation of the PKA-induced SNAP-25 and Synapsin-1 phosphorylation.Cellular & molecular biology letters · 2023Article
- The proteasome: A key modulator of nervous system function, brain aging, and neurodegenerative disease.Frontiers in cell and developmental biology · 2023Review
- Review
- Neuronal activity regulates the nuclear proteome to promote activity-dependent transcription.The Journal of cell biology · 2021Article
- Historical perspective and progress on protein ubiquitination at glutamatergic synapses.Neuropharmacology · 2021Review
- PKA Cα subunit mutation triggers caspase-dependent RIIβ subunit degradation via SerScience advances · 2021Article
- Genome-Wide Association Analysis of Neonatal White Matter Microstructure.Cerebral cortex (New York, N.Y. : 1991) · 2021Article
- A Putative Role for Ubiquitin-Proteasome Signaling in Estrogenic Memory Regulation.Frontiers in behavioral neuroscience · 2021Article
- Balanced actions of protein synthesis and degradation in memory formation.Learning & memory (Cold Spring Harbor, N.Y.) · 2019Review
- PA28αβ overexpression enhances learning and memory of female mice without inducing 20S proteasome activity.BMC neuroscience · 2018Article
- Autophagy Enhances Memory Erasure through Synaptic Destabilization.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- The ubiquitin-proteasome system functionally links neuronal Tomosyn-1 to dendritic morphology.The Journal of biological chemistry · 2018Article
- Memory Takes Time.Neuron · 2017Review
21 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
In Aplysia, behavioral sensitization of defensive reflexes and the underlying presynaptic facilitation of sensory-to-motor neuron synapses lasts for several minutes (short term) or days to weeks (long term). Short-term sensitization has been explained by modulation of ion-channel function through cAMP-dependent protein phosphorylation. Long-term facilitation requires additional molecular changes including protein synthesis. A key event is the persistent activation of the cAMP-dependent protein kinase at baseline concentrations of cAMP. This activation is due to selective loss of regulatory (R) subunits of PKA without any change in catalytic (C) subunits. To understand the molecular mechanisms that produce the loss of R subunits in long-term facilitation, we investigated how R subunits are degraded in extracts of Aplysia nervous tissue and in rabbit reticulocyte lysates. Degradation of Aplysia R subunits requires ATP, ubiquitin, and a particulate component that appears to be the proteasome complex. Degradation is blocked by hemin, which causes the accumulation of high molecular weight derivatives of R subunits that are likely to be ubiquitin conjugates of R subunits and intermediates in the degradative pathway. We also show that vertebrate RI and RII subunits can be degraded through the ubiquitin pathway. We suggest that degradation is initiated by cAMP, which causes the holoenzyme to dissociate and, further, that the altered R-to-C ratio in Aplysia sensory neurons is maintained in long-term facilitation by newly synthesized proteins that help target R subunits for accelerated degradation.
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Registered trials
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.