ArticleThe Journal of biological chemistry2010
Ribosomal protein S6 kinase is a critical downstream effector of the target of rapamycin complex 1 for long-term facilitation in Aplysia.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 31 citations in OpenAlex.
- Leptin and Associated Neural Pathways Underlying Obesity-Induced Hypertension.Comprehensive Physiology · 2025Review
- Unraveling the Role of Ras Homolog Enriched in Brain (Rheb1 and Rheb2): Bridging Neuronal Dynamics and Cancer Pathogenesis through Mechanistic Target of Rapamycin Signaling.International journal of molecular sciences · 2024Review
- Nociceptive Biology of Molluscs and Arthropods: Evolutionary Clues About Functions and Mechanisms Potentially Related to Pain.Frontiers in physiology · 2018Review
- Selective Erasure of Distinct Forms of Long-Term Synaptic Plasticity Underlying Different Forms of Memory in the Same Postsynaptic Neuron.Current biology : CB · 2017Article
- Dietary and donepezil modulation of mTOR signaling and neuroinflammation in the brain.Biochimica et biophysica acta · 2016Article
- Bidirectional regulation of eEF2 phosphorylation controls synaptic plasticity by decoding neuronal activity patterns.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Doxorubicin attenuates serotonin-induced long-term synaptic facilitation by phosphorylation of p38 mitogen-activated protein kinase.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Translational control in synaptic plasticity and cognitive dysfunction.Annual review of neuroscience · 2014Review
- Cellular, molecular, and epigenetic mechanisms in non-associative conditioning: implications for pain and memory.Neurobiology of learning and memory · 2013Review
- S6 kinase localizes to the presynaptic active zone and functions with PDK1 to control synapse development.The Journal of cell biology · 2011Article
- A histone deacetylase-dependent screen in yeast.Bioorganic & medicinal chemistry · 2010Article
- Translational control mechanisms in long-lasting synaptic plasticity and memory.The Journal of biological chemistry · 2010Review
- Mechanisms of translational regulation in synaptic plasticity.Current opinion in neurobiology · 2010Review
- Association of the small GTPase Rheb with the NMDA receptor subunit NR3A.Neuro-Signals · 2010Article
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3 authors at 2 institutions in 1 country.
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Abstract
Long-term facilitation (LTF) in Aplysia is a leading cellular model for elucidating the biochemical mechanisms of synaptic plasticity underlying learning. In Aplysia, LTF requires translational control downstream of the target of rapamycin (TOR) complex 1 (TORC1). The major known downstream targets of TORC1 are 4E binding protein (4E-BP) and S6 kinase (S6K). By removing the site within these regulators required for their interaction with TORC1, we have generated dominant negative proteins that disrupt specific pathways downstream of TORC1. Expression of dominant negative S6K, but not dominant negative 4E-BP, in Aplysia sensory neurons (SNs) blocked 24-h LTF. TORC1 is directly activated by the small GTP-binding protein, Ras homologue enriched in brain (Rheb). To determine the effects of TORC1 activation on translation in Aplysia neurons, we have examined the effects of expressing a constitutively active form of the Aplysia orthologue of Rheb, ApRheb (ApRheb(Q63L)). Expression of ApRheb(Q63L) increased 4E-BP phosphorylation and the level of general, cap-dependent translation within the SN cell soma in a rapamycin-sensitive manner. This increase in cap-dependent translation was blocked neither by dominant negative 4E-BP nor dominant negative S6K. Thus, we demonstrate that S6K is an important downstream target of TORC1 in Aplysia and that it is necessary for 24-h LTF, but not for TORC1-mediated increases in somatic cap-dependent translation.
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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.