ArticleMolecular biology of the cell2009
Cortical F-actin, the exocytic mode, and neuropeptide release in mouse chromaffin cells is regulated by myristoylated alanine-rich C-kinase substrate and myosin II.
Article in Molecular biology of the cell, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 18 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
18 citing papers in PubMed, 29 citations in OpenAlex.
- The neuronal calcium sensor Synaptotagmin-1 and SNARE proteins cooperate to dilate fusion pores.eLife · 2021Article
- Striatal dopamine neurotransmission: regulation of release and uptake.Basal ganglia · 2016Article
- Huntingtin-associated protein 1 regulates exocytosis, vesicle docking, readily releasable pool size and fusion pore stability in mouse chromaffin cells.The Journal of physiology · 2014Article
- Secretagogue stimulation of neurosecretory cells elicits filopodial extensions uncovering new functional release sites.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Glucose principally regulates insulin secretion in mouse islets by controlling the numbers of granule fusion events per cell.Diabetologia · 2013Article
- Multiple roles for the actin cytoskeleton during regulated exocytosis.Cellular and molecular life sciences : CMLS · 2013Review
- Article
- MARCKS protein is phosphorylated and regulates calcium mobilization during human acrosomal exocytosis.PloS one · 2013Article
- Protein kinase C-delta deficiency perturbs bone homeostasis by selective uncoupling of cathepsin K secretion and ruffled border formation in osteoclasts.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2012Article
- Activity-dependent fusion pore expansion regulated by a calcineurin-dependent dynamin-syndapin pathway in mouse adrenal chromaffin cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Myosin motor proteins are involved in the final stages of the secretory pathways.Biochemical Society transactions · 2011Review
- Chemical analysis of single cells.Analytical chemistry · 2011Review
- Regulation of fusion pore closure and compound exocytosis in neuroendocrine PC12 cells by SCAMP1.Traffic (Copenhagen, Denmark) · 2011Article
- Frequency-dependent modes of synaptic vesicle endocytosis and exocytosis at adult mouse neuromuscular junctions.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Spatial regulation of exocytic site and vesicle mobilization by the actin cytoskeleton.PloS one · 2011Article
- Article
- Dynamin and myosin regulate differential exocytosis from mouse adrenal chromaffin cells.Cellular and molecular neurobiology · 2010Review
- Suppression of Ca2+ syntillas increases spontaneous exocytosis in mouse adrenal chromaffin cells.The Journal of general physiology · 2009Article
Corrections and comments
- Retraction · 2013-04-01Falsification/Fabrication of Data · Investigation by Company/Institution · Investigation by ORI · Misconduct - Official Investigation(s) and/or Finding(s) · Misconduct by Author · · Bryan Dorejean named in NIH finding of misconduct:https://grants.nih.gov/grants/guide/notice-files/NOT-OD-13-039.html;
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Adrenal medullary chromaffin cells are innervated by the sympathetic splanchnic nerve and translate graded sympathetic firing into a differential hormonal exocytosis. Basal sympathetic firing elicits a transient kiss-and-run mode of exocytosis and modest catecholamine release, whereas elevated firing under the sympathetic stress response results in full granule collapse to release catecholamine and peptide transmitters into the circulation. Previous studies have shown that rearrangement of the cell actin cortex regulates the mode of exocytosis. An intact cortex favors kiss-and-run exocytosis, whereas disrupting the cortex favors the full granule collapse mode. Here, we investigate the specific roles of two actin-associated proteins, myosin II and myristoylated alanine-rich C-kinase substrate (MARCKS) in this process. Our data demonstrate that MARCKS phosphorylation under elevated cell firing is required for cortical actin disruption but is not sufficient to elicit peptide transmitter exocytosis. Our data also demonstrate that myosin II is phospho-activated under high stimulation conditions. Inhibiting myosin II activity prevented disruption of the actin cortex, full granule collapse, and peptide transmitter release. These results suggest that phosphorylation of both MARCKS and myosin II lead to disruption of the actin cortex. However, myosin II, but not MARCKS, is required for the activity-dependent exocytosis of the peptide transmitters.
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What 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.