scholarly journals A Predictive Mathematical Model of Cell Cycle, Metabolism, and Apoptosis of Monoclonal Antibody‐Producing GS–NS0 Cells

2019 ◽  
Vol 14 (11) ◽  
pp. 1800573 ◽  
Author(s):  
António L. Grilo ◽  
Athanasios Mantalaris
Keyword(s):  
Mathematical Model ◽  
Cell Cycle ◽  
Monoclonal Antibody ◽  
Ns0 Cells

Cell cycle-dependent reactivity with the monoclonal antibody Ki-67 during myeloid cell differentiation

1988 ◽  
Vol 179 (1) ◽  
pp. 79-88 ◽  
Author(s):  
Robert P. Wersto ◽  
Fritz Herz ◽  
Robert E. Gallagher ◽  
Leopold G. Koss
Keyword(s):  
Cell Cycle ◽  
Monoclonal Antibody ◽  
Cell Differentiation ◽  
Myeloid Cell ◽  
Ki 67 ◽  
Cycle Dependent

Cell cycle controls and the role of nerves and the regenerate epithelium in urodele forelimb regeneration: possible modifications of basic concepts

1987 ◽  
Vol 65 (8) ◽  
pp. 739-749 ◽  
Author(s):  
Roy A. Tassava ◽  
David J. Goldhamer ◽  
Bruce L. Tomlinson
Keyword(s):  
Cell Cycle ◽  
Monoclonal Antibody ◽  
Limb Regeneration ◽  
Blastema Formation ◽  
Basic Concepts ◽  
Regenerate Epithelium ◽  
Early Wound ◽  
Skin Epidermis ◽  
Wound Epithelium

Data from pulse and continuous labeling with [3H]thymidine and from studies with monoclonal antibody WE3 have led to the modification of existing models and established concepts pertinent to understanding limb regeneration. Not all cells of the adult newt blastema are randomly distributed and actively progressing through the cell cycle. Instead, many cells are in a position that we have designated transient quiescence (TQ) and are not actively cycling. We postulate that cells regularly leave the TQ population and enter the actively cycling population and vice versa. The size of the TQ population may be at least partly determined by the quantity of limb innervation. Larval Ambystoma may have only a small or nonexisting TQ, thus accounting for their rapid rate of regeneration. Examination of reactivity of monoclonal antibody WE3 suggests that the early wound epithelium, which is derived from skin epidermis, is later replaced by cells from skin glands concomitant with blastema formation. WE3 provides a useful tool to further investigate the regenerate epithelium.

scholarly journals Mathematical Model of Tumour Spheroid Experiments with Real-Time Cell Cycle Imaging

2021 ◽  
Vol 83 (5) ◽  
Author(s):  
Wang Jin ◽  
Loredana Spoerri ◽  
Nikolas K. Haass ◽  
Matthew J. Simpson
Keyword(s):  
Mathematical Model ◽  
Cell Cycle ◽  
Real Time ◽  
Tumour Spheroid

scholarly journals The Contribution of p53 in the Dynamics of Cell Cycle Response to DNA Damage Interpreted by a Mathematical Model

Cell Cycle ◽  
2007 ◽  
Vol 6 (8) ◽  
pp. 943-950 ◽  
Author(s):  
Monica Lupi ◽  
Giada Matera ◽  
Claudia Natoli ◽  
Valentina Colombo ◽  
Paolo Ubezio
Keyword(s):  
Mathematical Model ◽  
Cell Cycle ◽  
Dna Damage

scholarly journals A Branching Process to Characterize the Dynamics of Stem Cell Differentiation

2015 ◽  
Author(s):  
david miguez
Keyword(s):  
Mathematical Model ◽  
Cell Cycle ◽  
Stem Cell ◽  
Cycle Length ◽  
Branching Process ◽  
Stem Cell Differentiation ◽  
Stem Cell Population ◽  
Mathematical Framework ◽  
Average Cell ◽  
Cell Cycle Length

The understanding of the regulatory processes that orchestrate stem cell maintenance is a cornerstone in developmental biology. Here, we present a mathematical model based on a branching process formalism that predicts average rates of proliferative and differentiative divisions in a given stem cell population. In the context of vertebrate spinal neurogenesis, the model predicts complex non-monotonic variations in the rates of pp, pd and dd modes of division as well as in cell cycle length, in agreement with experimental results. Moreover, the model shows that the differentiation probability follows a binomial distribution, allowing us to develop equations to predict the rates of each mode of division. A phenomenological simulation of the developing spinal cord informed with the average cell cycle length and division rates predicted by the mathematical model reproduces the correct dynamics of proliferation and differentiation in terms of average numbers of progenitors and differentiated cells. Overall, the present mathematical framework represents a powerful tool to unveil the changes in the rate and mode of division of a given stem cell pool by simply quantifying numbers of cells at different times.

Bifurcation Analysis of a Model Accounting for the 14-3-3s Signalling Compartmentalisation

2012 ◽  
pp. 61-70
Author(s):  
S. Nikolov ◽  
J. Vera ◽  
O. Wolkenhauer
Keyword(s):  
Mathematical Model ◽  
Cell Cycle ◽  
Phase Portrait ◽  
Bifurcation Analysis ◽  
Subcellular Localisation ◽  
Loss Of Stability ◽  
Cycle Arrest ◽  
Reversible Loss ◽  
Analytical Tools

Bifurcation theory studies the qualitative changes in the phase portrait when we vary the parameters of the system. In this book chapter we adapt and extend a mathematical model accounting for the subcellular localisation of 14-3-3s, a protein involved in cell cycle arrest and the regulation of apoptosis. The model is analysed with analytical tools coming from Lyapunov-Andronov theory, and our analytical calculations predict that soft (reversible) loss of stability takes place.

scholarly journals Inhibition of human lymphocyte proliferation by monoclonal antibody to transferrin receptor

Blood ◽  
1983 ◽  
Vol 62 (4) ◽  
pp. 821-826 ◽  
Author(s):  
J Mendelsohn ◽  
I Trowbridge ◽  
J Castagnola
Keyword(s):  
Cell Cycle ◽  
Monoclonal Antibody ◽  
Lymphocyte Proliferation ◽  
Human Lymphocytes ◽  
Nitrilotriacetic Acid ◽  
S Phase ◽  
Inhibitory Effects ◽  
Mitogenic Response ◽  
Cell Cycle Inhibition ◽  
Partial Reversal

Abstract A monoclonal antibody, 42/6, which blocks the binding of transferrin to its receptor on the cell membrane, inhibits proliferation of human lymphocytes stimulated by phytohemagglutinin. Anti-receptor antibody B3/25, which does not block transferrin binding, does not alter the mitogenic response. Addition of soluble iron, in the form of ferric nitrilotriacetic acid, results in partial reversal of inhibition. Lymphocytes in the quiescent phase of the cell cycle at the time of 42/6 antibody addition are unable to traverse S phase, whereas cells actively proliferating when antibody is added are sensitive to its inhibitory effects throughout all phases of the cell cycle. Inhibition is static rather than cidal, since it can be reversed by removal of antibody after up to 48 hr of exposure.

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