Cells surviving fractional killing by TRAIL exhibit transient but sustainable resistance and inflammatory phenotypes.
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Cell-to-cell variability in cell death: can systems biology help us make sense of it all?Rapid Assessment and Visualization of Normality in High-Content and Other Cell-Level Data and Its Impact on the Interpretation of Experimental Results.NF-κB signalling and cell fate decisions in response to a short pulse of tumour necrosis factor.Interaction of dietary fatty acids with tumour necrosis factor family cytokines during colon inflammation and cancer.Plasminogen activator urokinase expression reveals TRAIL responsiveness and supports fractional survival of cancer cells.Modeling dynamics of cell-to-cell variability in TRAIL-induced apoptosis explains fractional killing and predicts reversible resistanceSingle-cell variation leads to population invariance in NF-κB signaling dynamicsComputational analysis of signaling patterns in single cells.A multi-scale approach reveals that NF-κB cRel enforces a B-cell decision to divide.Fractional killing arises from cell-to-cell variability in overcoming a caspase activity thresholdNF-κB contributes to MMP1 expression in breast cancer spheroids causing paracrine PAR1 activation and disintegrations in the lymph endothelial barrier in vitro.Non-genetic diversity modulates population performance.Cell-to-Cell Variation in p53 Dynamics Leads to Fractional Killing.Adaptive resistance of melanoma cells to RAF inhibition via reversible induction of a slowly dividing de-differentiated state.Surviving apoptosis: life-death signaling in single cells.Control of cancer formation by intrinsic genetic noise and microenvironmental cues.Measuring Cancer Drug Sensitivity and Resistance in Cultured Cells.Systematic analysis of BRAF(V600E) melanomas reveals a role for JNK/c-Jun pathway in adaptive resistance to drug-induced apoptosis.Abstracting the dynamics of biological pathways using information theory: a case study of apoptosis pathway.Demystifying the cytokine network: Mathematical models point the way.The recurrent architecture of tumour initiation, progression and drug sensitivity.A dynamical framework for complex fractional killing.Dual role of DR5 in death and survival signaling leads to TRAIL resistance in cancer cells.Fundamental trade-offs between information flow in single cells and cellular populations.AHR/CYP1A1 interplay triggers lymphatic barrier breaching in breast cancer spheroids by inducing 12(S)-HETE synthesis.A mechanistic pan-cancer pathway model informed by multi-omics data interprets stochastic cell fate responses to drugs and mitogens.[Intraclonal heterogeneity in tumors and its impact on precision medicine].Microenvironmental Signals and Biochemical Information Processing: Cooperative Determinants of Intratumoral Plasticity and Heterogeneity.
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Cells surviving fractional killing by TRAIL exhibit transient but sustainable resistance and inflammatory phenotypes.
description
article científic
@ca
article scientifique
@fr
articolo scientifico
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artigo científico
@pt
bilimsel makale
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scientific article published on 22 May 2013
@en
vedecký článok
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vetenskaplig artikel
@sv
videnskabelig artikel
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vědecký článek
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name
Cells surviving fractional kil ...... e and inflammatory phenotypes.
@en
Cells surviving fractional kil ...... e and inflammatory phenotypes.
@nl
type
label
Cells surviving fractional kil ...... e and inflammatory phenotypes.
@en
Cells surviving fractional kil ...... e and inflammatory phenotypes.
@nl
prefLabel
Cells surviving fractional kil ...... e and inflammatory phenotypes.
@en
Cells surviving fractional kil ...... e and inflammatory phenotypes.
@nl
P2093
P2860
P356
P1476
Cells surviving fractional kil ...... e and inflammatory phenotypes.
@en
P2093
Deborah A Flusberg
Jérémie Roux
Peter K Sorger
Sabrina L Spencer
P2860
P304
P356
10.1091/MBC.E12-10-0737
P577
2013-05-22T00:00:00Z