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Journal ArticleDOI

Response to Comment on "Oscillations in NF-kappa B signaling control the dynamics of gene expression"

TLDR
In this paper, the experimental data showed no correlation between NF-kappa B (ReLA) expression level and oscillation dynamics, and a small change to the computational model used by Barken et al. to generate their theoretical data reduced the apparent discrepancies.
Abstract
Our experimental data shows no correlation between NF-kappa B (ReLA) expression level and oscillation dynamics. We show that a small change to the computational model used by Barken et al. to generate their theoretical data reduces the apparent discrepancies. Cell system differences and possible compensatory changes to normal signaling in their genetically engineered knockout cells may explain differences between the two studies.

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Citations
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Journal ArticleDOI

Pulsatile Stimulation Determines Timing and Specificity of NF-κB-Dependent Transcription

TL;DR: Altering the stimulation intervals gave different patterns of NF-κB–dependent gene expression, which supports the idea that oscillation frequency has a functional role in nuclear factor κB regulation.
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A Noisy Paracrine Signal Determines the Cellular NF-κB Response to Lipopolysaccharide

TL;DR: It is shown that mammalian cells can create “noisy” environments to produce diversified responses to stimuli and be linked to a secondary paracrine signal secreted at low concentrations, such that not all cells undergo a second round of NF-κB activation.
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Physiological levels of TNFα stimulation induce stochastic dynamics of NF-κB responses in single living cells

TL;DR: Deterministic and stochastic models simulated the experimentally observed activation threshold and gave rise to new predictions about the structure of the system and open the way for better mechanistic understanding of physiological TNFα activation of inflammatory responses in cells and tissues.
Journal ArticleDOI

Stochastic Regulation in Early Immune Response

TL;DR: This article reformulate the model of the NF-kappaB regulatory module to analyze a single cell regulation and hypothesize that this synchronization is crucial for proper activation of early genes controlling inflammation.
References
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Journal ArticleDOI

A synthetic oscillatory network of transcriptional regulators

TL;DR: This work used three transcriptional repressor systems that are not part of any natural biological clock to build an oscillating network, termed the repressilator, in Escherichia coli, which periodically induces the synthesis of green fluorescent protein as a readout of its state in individual cells.
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The IκB-NF-κB Signaling Module: Temporal Control and Selective Gene Activation

TL;DR: A computational model is presented that describes the temporal control of NF-κB activation by the coordinated degradation and synthesis of IκB proteins and demonstrates that IπκBα is responsible for strong negative feedback that allows for a fast turn-off of the NF-σB response.
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Requirement for glycogen synthase kinase-3β in cell survival and NF-κB activation

TL;DR: It is shown that disruption of the murine GSK-3β gene results in embryonic lethality caused by severe liver degeneration during mid-gestation, a phenotype consistent with excessive tumour necrosis factor (TNF) toxicity, as observed in mice lacking genes involved in the activation of the transcription factor activation NF-κB.
Journal ArticleDOI

Studying protein dynamics in living cells.

TL;DR: Live cell imaging, in combination with photobleaching, energy transfer or fluorescence correlation spectroscopy are providing unprecedented insights into the movement of proteins and their interactions with cellular components.
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