BACKGROUND: [Ca(2+)](i) oscillations are irregular and heterogeneous. RESULTS: The correlations between NFκB/STAT3-GFP transcription and [Ca(2+)](i) spike amplitude/cumulative spike duration are revealed by simultaneous monitoring in single cells and validated in cell population. CONCLUSION: [Ca(2+)](i) oscillations regulate transcription through [Ca(2+)](i) spike amplitude and cumulative spike duration. SIGNIFICANCE: How irregular [Ca(2+)](i) oscillations control transcription is crucial for understanding biological [Ca(2+)](i) signal-regulated events. Agonist-stimulated [Ca(2+)](i) oscillations are universally irregular in their kinetics. How irregular [Ca(2+)](i) oscillations dynamically regulate agonist-stimulated downstream events has not been studied. To overcome the obstacles of irregularity and heterogeneity of [Ca(2+)](i) oscillations, agonist-stimulated [Ca(2+)](i) signaling and NFκB/STAT3-GFP nuclear translocation were simultaneously monitored in each single cell examined. The cause-effect relationship between [Ca(2+)](i) oscillation parameters and transcriptional activities was validated in cell populations through irregular [Ca(2+)](i) oscillations with varied parameters. The time duration of cumulative [Ca(2+)](i) elevations reaching the threshold [Ca(2+)](i) level for a transcriptional factor activation and [Ca(2+)](i) spike amplitude was found to control agonist-stimulated transcription and gene expression.
BACKGROUND: [Ca(2+)](i) oscillations are irregular and heterogeneous. RESULTS: The correlations between NFκB/STAT3-GFP transcription and [Ca(2+)](i) spike amplitude/cumulative spike duration are revealed by simultaneous monitoring in single cells and validated in cell population. CONCLUSION: [Ca(2+)](i) oscillations regulate transcription through [Ca(2+)](i) spike amplitude and cumulative spike duration. SIGNIFICANCE: How irregular [Ca(2+)](i) oscillations control transcription is crucial for understanding biological [Ca(2+)](i) signal-regulated events. Agonist-stimulated [Ca(2+)](i) oscillations are universally irregular in their kinetics. How irregular [Ca(2+)](i) oscillations dynamically regulate agonist-stimulated downstream events has not been studied. To overcome the obstacles of irregularity and heterogeneity of [Ca(2+)](i) oscillations, agonist-stimulated [Ca(2+)](i) signaling and NFκB/STAT3-GFP nuclear translocation were simultaneously monitored in each single cell examined. The cause-effect relationship between [Ca(2+)](i) oscillation parameters and transcriptional activities was validated in cell populations through irregular [Ca(2+)](i) oscillations with varied parameters. The time duration of cumulative [Ca(2+)](i) elevations reaching the threshold [Ca(2+)](i) level for a transcriptional factor activation and [Ca(2+)](i) spike amplitude was found to control agonist-stimulated transcription and gene expression.
Authors: Jiwei Zhang; Juan Zhou; Lei Cai; Yankai Lu; Tao Wang; Liping Zhu; Qinghua Hu Journal: Antioxid Redox Signal Date: 2012-01-25 Impact factor: 8.401
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Authors: Kevin Thurley; Stephen C Tovey; Gregor Moenke; Victoria L Prince; Abha Meena; Andrew P Thomas; Alexander Skupin; Colin W Taylor; Martin Falcke Journal: Sci Signal Date: 2014-06-24 Impact factor: 8.192