ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2003
Interactions with PDZ proteins are required for L-type calcium channels to activate cAMP response element-binding protein-dependent gene expression.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 132 citations in OpenAlex.
- Voltage-Gated and Chemogenetic Modulation of Calcium Signaling in Oligodendrocyte Development and Synaptic Integration.Journal of neurochemistry · 2025Review
- CaMKII clusters neuronal LTCCs in biomolecular condensates to gate excitation-transcription coupling.bioRxiv : the preprint server for biology · 2025Article
- Excitation-transcription coupling, neuronal gene expression and synaptic plasticity.Nature reviews. Neuroscience · 2023Review
- Clustering of CaJournal of neurochemistry · 2023Article
- Integrative Roles of Dopamine Pathway and Calcium Channels Reveal a Link between Schizophrenia and Opioid Use Disorder.International journal of molecular sciences · 2023Article
- BK channel activation by L-type CaJournal of neurophysiology · 2021Article
- Neuronal L-Type Calcium Channel Signaling to the Nucleus Requires a Novel CaMKIIα-Shank3 Interaction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Article
- Molecular mimicking of C-terminal phosphorylation tunes the surface dynamics of CaThe Journal of biological chemistry · 2018Article
- L-Type Calcium Channels Modulation by Estradiol.Molecular neurobiology · 2017Review
- Shank is a dose-dependent regulator of CaeLife · 2017Article
- Densin-180 Controls the Trafficking and Signaling of L-Type Voltage-Gated CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- GDF-15 enhances intracellular Ca2+ by increasing Cav1.3 expression in rat cerebellar granule neurons.The Biochemical journal · 2016Article
- The PDZ motif of the α1C subunit is not required for surface trafficking and adrenergic modulation of CaV1.2 channel in the heart.The Journal of biological chemistry · 2015Article
- L-type CaWiley interdisciplinary reviews. Membrane transport and signaling · 2014Article
- Palmitoylation of estrogen receptors is essential for neuronal membrane signaling.Endocrinology · 2013Article
- Alternative splicing: functional diversity among voltage-gated calcium channels and behavioral consequences.Biochimica et biophysica acta · 2013Review
- An L-type calcium channel agonist, bay K8644, extends the window of intervention against ischemic neuronal injury.Molecular neurobiology · 2013Article
- cAMP promotes the differentiation of neural progenitor cells in vitro via modulation of voltage-gated calcium channels.Frontiers in cellular neuroscience · 2013Article
- Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
After brief periods of heightened stimulation, calcium entry through L-type calcium channels leads to activation of the transcription factor cAMP response element-binding protein (CREB) and CRE-dependent transcription. Many of the details surrounding the mechanism by which L-type calcium channels are privileged in signaling to CREB, to the exclusion of other calcium entry pathways, has remained unclear. We hypothesized that the PDZ interaction sequence contained within the last four amino acids of the calcium channel alpha1C (Ca(V)1.2) subunit [Val-Ser-Asn-Leu (VSNL)] is critical for L-type calcium channels (LTCs) to interact with the signaling machinery that triggers activity-dependent gene expression. To disrupt this interaction, hippocampal CA3-CA1 pyramidal neurons were transfected with DNA encoding for enhanced green fluorescent protein tethered to VSNL (EGFP-VSNL). EGFP-VSNL significantly attenuated L-type calcium channel-induced CREB phosphorylation and CRE-dependent transcription, although somatic calcium concentrations after stimulation remained unchanged. The effect of EGFP-VSNL was specific to the actions of L-type calcium channels, because CREB signaling after NMDA receptor stimulation remained intact. The importance of the PDZ interaction sequence was verified using dihydropyridine (DHP)-insensitive alpha1C subunits. Neurons transfected with alpha1C lacking the terminal five amino acids (DHP-LTCnoPDZ) exhibited attenuated CREB responses in comparison with cells expressing the full-length subunit (DHP-LTC). Collectively, these data suggest that localized calcium responses, regulated by interactions with PDZ domain proteins, are necessary for L-type calcium channels to effectively activate CREB and CRE-mediated gene expression.
Indexed as
Identifiers
12716953PMC6742301W1878905851What OpenQuestion holds
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.