ArticleBiochemical and biophysical research communications2009
The actin cytoskeleton differentially regulates NG115-401L cell ryanodine receptor and inositol 1,4,5-trisphosphate receptor induced calcium signaling pathways.
Article in Biochemical and biophysical research communications, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
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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
5 citing papers in PubMed, 12 citations in OpenAlex.
- Cyclic versus hemi-bastadins. pleiotropic anti-cancer effects: from apoptosis to anti-angiogenic and anti-migratory effects.Molecules (Basel, Switzerland) · 2013Article
- Two distinct phases of calcium signalling under flow.Cardiovascular research · 2011Article
- Actin microfilament involved in regulation of pacemaking activity in cultured interstitial cells of Cajal from murine intestine.The Journal of membrane biology · 2010Article
- Control of intracellular calcium signaling as a neuroprotective strategy.Molecules (Basel, Switzerland) · 2010Review
- Role of Fyn kinase in oocyte developmental potential.Reproduction, fertility, and development · 2010Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Regulation of bi-directional communication between intracellular Ca(2+) pools and surface Ca(2+) channels remains incompletely characterized. We report Ca(2+) release mediated by inositol 1,4,5-trisphosphate receptor (IP(3)R) and ryanodine receptor (RyR) pathways is diminished under actin cytoskeleton disruption in NG115-401L (401L) neuronal cells, yet despite truncated Ca(2+) release, Ca(2+) influx was not significantly altered in these experiments. However, disruption of cortical actin networks completely abolished IP(3)R induced Ca(2+) release, whereas RyR-mediated Ca(2+) release was preserved, albeit attenuated. Moreover, cortical actin disruption completely abolished IP(3)R and RyR linked Ca(2+) influx even though Ca(2+) pool sensitivities were different. These findings suggest discrete Ca(2+) store/Ca(2+) channel coupling mechanisms in the IP(3)R and RyR pathways as revealed by the differential sensitivity to actin perturbation.
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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.