ArticlePloS one2012
Docking of LDCVs is modulated by lower intracellular [Ca2+] than priming.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 15 citations in OpenAlex.
- Highly adaptable deep-learning platform for automated detection and analysis of vesicle exocytosis.Nature communications · 2025Article
- Lytic granule exocytosis at immune synapses: lessons from neuronal synapses.Frontiers in immunology · 2023Review
- How does the stimulus define exocytosis in adrenal chromaffin cells?Pflugers Archiv : European journal of physiology · 2018Review
- The actin binding protein scinderin acts in PC12 cells to tether dense-core vesicles prior to secretion.Molecular and cellular neurosciences · 2017Article
- H/KDEL receptors mediate host cell intoxication by a viral A/B toxin in yeast.Scientific reports · 2016Article
- Behavior and Properties of Mature Lytic Granules at the Immunological Synapse of Human Cytotoxic T Lymphocytes.PloS one · 2015Article
- Super-resolution microscopy in studying neuroendocrine cell function.Frontiers in neuroscience · 2013Review
- Deciphering dead-end docking of large dense core vesicles in bovine chromaffin cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Membrane-proximal tryptophans of synaptobrevin II stabilize priming of secretory vesicles.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Many regulatory steps precede final membrane fusion in neuroendocrine cells. Some parts of this preparatory cascade, including fusion and priming, are dependent on the intracellular Ca(2+) concentration ([Ca(2+)](i)). However, the functional implications of [Ca(2+)](i) in the regulation of docking remain elusive and controversial due to an inability to determine the modulatory effect of [Ca(2+)](i). Using a combination of TIRF-microscopy and electrophysiology we followed the movement of large dense core vesicles (LDCVs) close to the plasma membrane, simultaneously measuring membrane capacitance and [Ca(2+)](i). We found that a free [Ca(2+)](i) of 700 nM maximized the immediately releasable pool and minimized the lateral mobility of vesicles, which is consistent with a maximal increase of the pool size of primed LDCVs. The parameters that reflect docking, i.e. axial mobility and the fraction of LDCVs residing at the plasma membrane for less than 5 seconds, were strongly decreased at a free [Ca(2+)](i) of 500 nM. These results provide the first evidence that docking and priming occur at different free intracellular Ca(2+) concentrations, with docking efficiency being the most robust at 500 nM.
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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.