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Your search keyword '"NF-κB cRel"' showing total 2 results
Start Over Descriptor "NF-κB cRel" Topic proto-oncogene proteins c-rel
2 results on '"NF-κB cRel"'

1. A multi-scale approach reveals that NF-κB cRel enforces a B-cell decision to divide.

Author

Shokhirev MN, Almaden J, Davis-Turak J, Birnbaum HA, Russell TM, Vargas JA, and Hoffmann A

Subjects
Animals, Apoptosis, B-Lymphocytes metabolism, Cell Proliferation, Mice, Models, Molecular, Sequence Analysis, RNA, Signal Transduction, Spleen cytology, B-Lymphocytes cytology, Cell Division, NF-kappa B metabolism, Proto-Oncogene Proteins c-rel metabolism
Abstract

Understanding the functions of multi-cellular organs in terms of the molecular networks within each cell is an important step in the quest to predict phenotype from genotype. B-lymphocyte population dynamics, which are predictive of immune response and vaccine effectiveness, are determined by individual cells undergoing division or death seemingly stochastically. Based on tracking single-cell time-lapse trajectories of hundreds of B cells, single-cell transcriptome, and immunofluorescence analyses, we constructed an agent-based multi-modular computational model to simulate lymphocyte population dynamics in terms of the molecular networks that control NF-κB signaling, the cell cycle, and apoptosis. Combining modeling and experimentation, we found that NF-κB cRel enforces the execution of a cellular decision between mutually exclusive fates by promoting survival in growing cells. But as cRel deficiency causes growing B cells to die at similar rates to non-growing cells, our analysis reveals that the phenomenological decision model of wild-type cells is rooted in a biased race of cell fates. We show that a multi-scale modeling approach allows for the prediction of dynamic organ-level physiology in terms of intra-cellular molecular networks., (© 2015 The Authors. Published under the terms of the CC BY 4.0 license.)

Published
2015
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2. A multi-scale approach reveals that NF-κB cRel enforces a B-cell decision to divide

Author

Jeremy Davis-Turak, Alexander Hoffmann, Jesse D. Vargas, Maxim N. Shokhirev, Jonathan Almaden, Harry Birnbaum, and Theresa M Russell

Subjects
Models, Molecular, Lymphocyte, Cell, Apoptosis, Transcriptome, B-lymphocyte, Mice, Models, Genetics, education.field_of_study, B-Lymphocytes, Applied Mathematics, apoptosis, NF-kappa B, Articles, Cell cycle, Phenotype, medicine.anatomical_structure, Computational Theory and Mathematics, NF‐κB cRel, cell cycle, General Agricultural and Biological Sciences, Sequence Analysis, Cell Division, Information Systems, Signal Transduction, Bioinformatics, 1.1 Normal biological development and functioning, Population, B‐lymphocyte, NF-kappa B cRel, Computational biology, Biology, General Biochemistry, Genetics and Molecular Biology, Underpinning research, medicine, Animals, education, B cell, Cell Proliferation, General Immunology and Microbiology, Sequence Analysis, RNA, Molecular, Proto-Oncogene Proteins c-rel, NF-κB cRel, RNA, cell fate decision, Generic health relevance, Biochemistry and Cell Biology, Other Biological Sciences, Decision model, Spleen
Abstract

Understanding the functions of multi-cellular organs in terms of the molecular networks within each cell is an important step in the quest to predict phenotype from genotype. B-lymphocyte population dynamics, which are predictive of immune response and vaccine effectiveness, are determined by individual cells undergoing division or death seemingly stochastically. Based on tracking single-cell time-lapse trajectories of hundreds of B cells, single-cell transcriptome, and immunofluorescence analyses, we constructed an agent-based multi-modular computational model to simulate lymphocyte population dynamics in terms of the molecular networks that control NF-κB signaling, the cell cycle, and apoptosis. Combining modeling and experimentation, we found that NF-κBcRel enforces the execution of a cellular decision between mutually exclusive fates by promoting survival in growing cells. But as cRel deficiency causes growing B cells to die at similar rates to non-growing cells, our analysis reveals that the phenomenological decision model of wild-type cells is rooted in a biased race of cell fates. We show that a multi-scale modeling approach allows for the prediction of dynamic organ-level physiology in terms of intra-cellular molecular networks.

Published
2015

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