Dynamic Regulation of N-Methyl-d-aspartate (NMDA) and α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid (AMPA) Receptors by Posttranslational Modifications
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Many molecular mechanisms underlie the changes in synaptic glutamate receptor content that are required by neuronal networks to generate cellular correlates of learning and memory. During the last decade, posttranslational modifications have emerged as critical regulators of synaptic transmission and plasticity. Notably, phosphorylation, ubiquitination, and palmitoylation control the stability, trafficking, and synaptic expression of glutamate receptors in the central nervous system. In the current review, we will summarize some of the progress made by the neuroscience community regarding our understanding of phosphorylation, ubiquitination, and palmitoylation of the NMDA and AMPA subtypes of glutamate receptors.
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All four AMPAR subunits are ubiquitinated, with major sites on GluA1 and GluA2 mapped to GluA1 K868 and GluA2 K870/K882.
“All four AMPAR subunit are also ubiquitinated. The major sites of ubiquitination on GluA1 and GluA2 have been mapped to GluA1 K868 and GluA2 K870/K882 (Widagdo et al., 2015, Widagdo et al., 2017, Lussier et al., 2015).”
From The AMPA Receptor Code of Synaptic Plasticity (2018) · cites this paper as Lussier et al., 2015
The Ubiquitination section (page not provided) reports that proteomic studies identified all four AMPAR subunits, GluA1–4, as ubiquitinated. Our copy does not identify GluA1 K868 or GluA2 K870/K882 as major ubiquitination sites; searches for those residues found no supporting passage. (LLM, conf=0.87)
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References 100 · Cited by 163
Research works printed but not linked: 8
- Ehlers, M. D. (2013) Dendritic trafficking for neuronal growth and plas- ticity. Biochem. Soc. Trans. 41, 1365-1382
- Derkach, V., Barria, A., and Soderling, T. R. (1999) Ca 2ϩ /calmodulin- kinase II enhances channel conductance of ␣-amino-3-hydroxy-5-meth- yl-4-isoxazolepropionate type glutamate receptors. Proc. Natl. Acad. Sci.
- Lu, W., Isozaki, K., Roche, K. W., and Nicoll, R. A. (2010) Synaptic tar- geting of AMPA receptors is regulated by a CaMKII site in the first intracellular loop of GluA1. Proc. Natl. Acad. Sci. U.S.A. 107, 22266 -22271
- Komander, D. (2009) The emerging complexity of protein ubiquitina- tion. Biochem. Soc. Trans. 37, 937-953
- Lussier, M. P., Herring, B. E., Nasu-Nishimura, Y., Neutzner, A., Kar- bowski, M., Youle, R. J., Nicoll, R. A., and Roche, K. W. (2012) Ubiquitin ligase RNF167 regulates AMPA receptor-mediated synaptic transmis- sion. Proc. Natl. Acad. Sci. U.S.A. 109, 19426 -19431
- Widagdo, J., Chai, Y. J., Ridder, M. C., Chau, Y. Q., Johnson, R. C., Sah, P., Huganir, R. L., and Anggono, V. (2015) Activity-dependent ubiquitina- tion of GluA1 and GluA2 regulates AMPA receptor intracellular sorting and degradation. Cell Rep. 10.1016/j.celrep.2015.01.015 · DOI · Paper page
- Planey, S. L., and Zacharias, D. A. (2009) Palmitoyl acyltransferases, their substrates, and novel assays to connect them (Review). Mol. Membr. Biol. 26, 14 -31
- Thomas, G. M., and Huganir, R. L. (2013) Palmitoylation-dependent regulation of glutamate receptors and their PDZ domain-containing partners. Biochem. Soc. Trans. 41, 72-78
- Authors
- Lussier, M. P., Sanz-Clemente, A., & Roche, K. W.
- Affiliations
- Université du Québec à Montréal (CA)
- Northwestern University (US)
- National Institutes of Health (US)
- Corresponding author
- Roche, Katherine W.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2015-11
- Volume
- 290
- Issue
- 48
- Pages
- 28596-28603
- ISSN
- 0021-9258 (ISSN-L)
- PMC
- PMC4661374
- OpenAlex
- W2176816948
- Cited by
- 163
- References
- 100
- Citations by year
- 2026: 7 · 2025: 9 · 2024: 12 · 2023: 16 · 2022: 11 · 2021: 19 · 2020: 22 · 2019: 20 · 2018: 23 · 2017: 15 · 2016: 7 · 2015: 2
- FWCI
- 1.86
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (1K99AG041225, K99AG041225, R00AG041225)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Receptor Mechanisms and Signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Amino Acid Enzymes and Metabolism
- Keywords
- NMDA receptor, AMPA receptors, glutamate receptors, post-translational modification, receptor phosphorylation, ubiquitination, palmitoylation, synaptic plasticity, receptor trafficking, receptor stability, synaptic transmission, learning and memory
- MeSH terms
- Animals, Humans, Phosphorylation, Receptors, N-Methyl-D-Aspartate, Receptors, AMPA, Protein Transport, Ubiquitination, Lipoylation
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