ArticleASN neuro2009
Regulation of store-operated and voltage-operated Ca2+ channels in the proliferation and death of oligodendrocyte precursor cells by golli proteins.
Article in ASN neuro, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
29 citing papers in PubMed, 47 citations in OpenAlex.
- Prenatal Exposure to Tobacco Smoke and Vaping Aerosols: Mechanisms Disrupting White-Matter Formation.Toxics · 2025Review
- STIM Proteins: The Gas and Brake of Calcium Entry in Neurons.Neuroscience bulletin · 2025Review
- Article
- Characterizing spontaneous CaBiophysical journal · 2022Article
- Oscillatory calcium release and sustained store-operated oscillatory calcium signaling prevents differentiation of human oligodendrocyte progenitor cells.Scientific reports · 2022Article
- Proteins Interacting with STIM1 and Store-Operated CaProgress in molecular and subcellular biology · 2021Review
- Transcriptional regulators of the Golli/myelin basic protein locus integrate additive and stealth activities.PLoS genetics · 2020Article
- Article
- Target Molecules of STIM Proteins in the Central Nervous System.Frontiers in molecular neuroscience · 2020Review
- Enhanced oligodendrocyte maturation and myelination in a mouse model of Timothy syndrome.Glia · 2018Article
- Teriflunomide promotes oligodendroglial differentiation and myelination.Journal of neuroinflammation · 2018Article
- Conditional Deletion of the L-Type Calcium Channel Cav1.2 in NG2-Positive Cells Impairs Remyelination in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Store-operated calcium entry is essential for glial calcium signalling in CNS white matter.Brain structure & function · 2017Article
- Conditional Deletion of the L-Type Calcium Channel Cav1.2 in Oligodendrocyte Progenitor Cells Affects Postnatal Myelination in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Golli Myelin Basic Proteins Modulate Voltage-Operated Ca(++) Influx and Development in Cortical and Hippocampal Neurons.Molecular neurobiology · 2016Article
- Article
- Voltage-gated Ca2+ entry promotes oligodendrocyte progenitor cell maturation and myelination in vitro.Experimental neurology · 2015Article
- Prenatal stress-induced programming of genome-wide promoter DNA methylation in 5-HTT-deficient mice.Translational psychiatry · 2014Article
- Store-operated calcium entry in neuroglia.Neuroscience bulletin · 2014Review
- TRP channels coordinate ion signalling in astroglia.Reviews of physiology, biochemistry and pharmacology · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
OPCs (oligodendrocyte precursor cells) express golli proteins which, through regulation of Ca2+ influx, appear to be important in OPC process extension/retraction and migration. The aim of the present study was to examine further the role of golli in regulating OPC development. The effects of golli ablation and overexpression were examined in primary cultures of OPCs prepared from golli-KO (knockout) and JOE (golli J37-overexpressing) mice. In OPCs lacking golli, or overexpressing golli, differentiation induced by growth factor withdrawal was impaired. Proliferation analysis in the presence of PDGF (platelet-derived growth factor), revealed that golli enhanced the mitogen-stimulated proliferation of OPCs through activation of SOCCs (store-operated Ca2+ channels). PDGF treatment induced a biphasic increase in OPC intracellular Ca2+, and golli specifically increased Ca2+ influx during the second SOCC-dependent phase that followed the initial release of Ca2+ from intracellular stores. This store-operated Ca2+ uptake appeared to be essential for cell division, since specific SOCC antagonists completely blocked the effects of PDGF and golli on OPC proliferation. Additionally, in OPCs overexpressing golli, increased cell death was observed after mitogen withdrawal. This phenomenon could be prevented by exposure to VOCC (voltage-operated Ca2+ channel) blockers, indicating that the effect of golli on cell death involved increased Ca2+ influx through VOCCs. The results showed a clear effect of golli on OPC development and support a role for golli in modulating multiple Ca2+-regulatory events through VOCCs and SOCCs. Our results also suggest that PDGF engagement of its receptor resulting in OPC proliferation proceeds through activation of SOCCs.
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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.