ArticlePLoS biology2007
Depolarization and CaM kinase IV modulate NMDA receptor splicing through two essential RNA elements.
Article in PLoS biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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65 citing papers in PubMed, 106 citations in OpenAlex.
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- The calcium channel TRPC6 promotes chemotherapy-induced persistence by regulating integrin α6 mRNA splicing.Cell reports · 2023Article
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- Alternative splicing modulation by G-quadruplexes.Nature communications · 2022Article
- A paralog-specific role of COPI vesicles in the neuronal differentiation of mouse pluripotent cells.Life science alliance · 2020Article
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- Targeting RyR Activity Boosts Antisense Exon 44 and 45 Skipping in Human DMD Skeletal or Cardiac Muscle Culture Models.Molecular therapy. Nucleic acids · 2019Article
- The Ubiquitination of Spinal MrgC Alleviates Bone Cancer Pain and Reduces Intracellular Calcium Concentration in Spinal Neurons in Mice.Neurochemical research · 2019Article
- A unique de novo gain-of-function variant inCold Spring Harbor molecular case studies · 2018Article
- Regulation of Neuronal Differentiation, Function, and Plasticity by Alternative Splicing.Annual review of cell and developmental biology · 2018Review
- Identification and characterization of two novel alternatively spliced E2F1 transcripts in the rat CNS.Molecular and cellular neurosciences · 2018Article
- Protective effects ofToxicology research · 2018Article
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- Phenylbutazone induces expression of MBNL1 and suppresses formation of MBNL1-CUG RNA foci in a mouse model of myotonic dystrophy.Scientific reports · 2016Article
- RNA ligation in neurons by RtcB inhibits axon regeneration.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Evolutionary emergence of a novel splice variant with an opposite effect on the cell cycle.Molecular and cellular biology · 2015Article
- Histone hyperacetylation and exon skipping: a calcium-mediated dynamic regulation in cardiomyocytes.Nucleus (Austin, Tex.) · 2015Article
5 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Alternative splicing controls the activity of many proteins important for neuronal excitation, but the signal-transduction pathways that affect spliced isoform expression are not well understood. One particularly interesting system of alternative splicing is exon 21 (E21) of the NMDA receptor 1 (NMDAR1 E21), which controls the trafficking of NMDA receptors to the plasma membrane and is repressed by Ca(++)/calmodulin-dependent protein kinase (CaMK) IV signaling. Here, we characterize the splicing of NMDAR1 E21. We find that E21 splicing is reversibly repressed by neuronal depolarization, and we identify two RNA elements within the exon that function together to mediate the inducible repression. One of these exonic elements is similar to an intronic CaMK IV-responsive RNA element (CaRRE) originally identified in the 3' splice site of the BK channel STREX exon, but not previously observed within an exon. The other element is a new RNA motif. Introduction of either of these two motifs, called CaRRE type 1 and CaRRE type 2, into a heterologous constitutive exon can confer CaMK IV-dependent repression on the new exon. Thus, either exonic CaRRE can be sufficient for CaMK IV-induced repression. Single nucleotide scanning mutagenesis defined consensus sequences for these two CaRRE motifs. A genome-wide motif search and subsequent RT-PCR validation identified a group of depolarization-regulated alternative exons carrying CaRRE consensus sequences. Many of these exons are likely to alter neuronal function. Thus, these two RNA elements define a group of co-regulated splicing events that respond to a common stimulus in neurons to alter their activity.
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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.