ArticleProceedings of the National Academy of Sciences of the United States of America2001
Calmodulin priming: nuclear translocation of a calmodulin complex and the memory of prior neuronal activity.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 33 papers.
What it found
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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
33 citing papers in PubMed, 104 citations in OpenAlex.
- Excitation-transcription coupling, neuronal gene expression and synaptic plasticity.Nature reviews. Neuroscience · 2023Review
- Calmodulin Regulates Transient Receptor Potential TRPM3 and TRPM8-Induced Gene Transcription.International journal of molecular sciences · 2023Article
- Neuronal activity regulates Matrin 3 abundance and function in a calcium-dependent manner through calpain-mediated cleavage and calmodulin binding.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- RyR-mediated CaProceedings of the National Academy of Sciences of the United States of America · 2021Article
- CaThe Journal of biological chemistry · 2020Article
- Memory Takes Time.Neuron · 2017Review
- Distinct roles of multiple isoforms of CaMKII in signaling to the nucleus.Biochimica et biophysica acta · 2015Review
- Evolutionary and functional perspectives on signaling from neuronal surface to nucleus.Biochemical and biophysical research communications · 2015Review
- γCaMKII shuttles Ca²⁺/CaM to the nucleus to trigger CREB phosphorylation and gene expression.Cell · 2014Article
- Molecular mechanisms of activity-dependent changes in dendritic morphology: role of RGK proteins.Trends in neurosciences · 2014Review
- Visualizing CaMKII and CaM activity: a paradigm of compartmentalized signaling.Journal of molecular medicine (Berlin, Germany) · 2013Review
- Enhanced striatal β1-adrenergic receptor expression following hormone loss in adulthood is programmed by both early sexual differentiation and puberty: a study of humans and rats.Endocrinology · 2013Article
- Calcium signaling in synapse-to-nucleus communication.Cold Spring Harbor perspectives in biology · 2011Review
- Mechanisms of specificity in neuronal activity-regulated gene transcription.Progress in neurobiology · 2011Review
- Excitation-transcription coupling in sympathetic neurons and the molecular mechanism of its initiation.Neuroscience research · 2011Review
- β1-Adrenergic receptors activate two distinct signaling pathways in striatal neurons.Journal of neurochemistry · 2011Article
- Using automated imaging to interrogate gonadotrophin-releasing hormone receptor trafficking and function.Molecular and cellular endocrinology · 2011Review
- Pulsatile and sustained gonadotropin-releasing hormone (GnRH) receptor signaling: does the Ca2+/NFAT signaling pathway decode GnRH pulse frequency?The Journal of biological chemistry · 2009Article
- Isoflurane inhibits cyclic adenosine monophosphate response element-binding protein phosphorylation and calmodulin translocation to the nucleus of SH-SY5Y cells.Anesthesia and analgesia · 2009Article
- Inactivation of CREB mediated gene transcription by HDAC8 bound protein phosphatase.Biochemical and biophysical research communications · 2009Article
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The neuronal nucleus plays a vital role in information processing, but whether it supports computational functions such as paired-pulse facilitation, comparable to synapses, is unclear. Ca(2+)-dependent movement of calmodulin (CaM) to the nucleus is highly responsive to Ca(2+) entry through L-type channels and promotes activation of the transcription factor CREB (cAMP-responsive element binding protein) through phosphorylation by CaM-sensitive kinases. We characterized key features of this CaM translocation and its possible role in facilitation of nuclear signaling. Nuclear CaM was elevated within 15 s of stimulus onset, preceding the first signs of CREB phosphorylation in hippocampal pyramidal neurons. Depolarization-induced elevation of nuclear CaM also was observed in cerebellar granule cells, neocortical neurons, and dentate gyrus granule cells. Nuclear translocation of CaM was not blocked by disruption of actin filaments or microtubules, or by emptying endoplasmic reticulum Ca(2+) stores with thapsigargin. Translocation of fluorescently tagged CaM was prevented by fusing it with the Ca(2+)/CaM binding peptide M13, suggesting that nuclear CaM accumulation depends on association with endogenous Ca(2+)/CaM binding proteins. To determine whether increased nuclear [CaM] might influence subsequent nuclear signal processing, we compared responses to two consecutive depolarizing stimuli. After a weak "priming" stimulus that caused CaM translocation, CREB phosphorylation caused by a subsequent stimulus was significantly faster, more sensitive to Ca(2+) elevation, and less specifically dependent on Ca(2+) influx through L-type channels. CaM translocation not only supports rapid signaling to the nucleus, but also could provide a "memory" for facilitatory effects of repeated neural activity, seen in altered phosphorylated CREB dynamics and Ca(2+) channel dependence.
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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.