PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 12852997

[Deterministic differential equations in cytokinetics].

F Fourré·H Barbason
View original source ↗Export metadata ↓

Abstract

Carcinogenesis is generally viewed as the result of a disrupted equilibrium between the processes of proliferation, differentiation, migration and loss. In cell kinetics, perturbation of fundamental kinetic parameters such as the mitotic index or the growth fraction may reflect a carcinogenic process. In this paper, we present a system of deterministic differential equations describing the dynamical evolution of a cell population. We show that this model can account for asynchronicity of cells and simulate the fraction of labelled mitoses experiment as well.

Explore related subjects

Cell CycleCell DifferentiationCell DivisionMathematicsMitotic IndexModels, BiologicalEnglish AbstractJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

F Fourré, H Barbason. 2003. [Deterministic differential equations in cytokinetics].. https://doi.org/10.1016/s0369-8114(03)00028-2

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2017

Rapid DNA replication origin licensing protects stem cell pluripotency.

Complete and robust human genome duplication requires loading minichromosome maintenance (MCM) helicase complexes at many DNA replication origins, an essential process termed origin licensing. Licensing is restricted to G1 phase of the cell cycle, but G1 length varies widely among cell types. Using quantitative single-cell analyses, we found that pluripotent stem cells with naturally short G1 phases load MCM much faster than their isogenic differentiated counterparts with long G1 phases. During the earliest stages of differentiation toward all lineages, MCM loading slows concurrently with G1 lengthening, revealing developmental control of MCM loading. In contrast, ectopic Cyclin E overproduction uncouples short G1 from fast MCM loading. Rapid licensing in stem cells is caused by accumulation of the MCM loading protein, Cdt1. Prematurely slowing MCM loading in pluripotent cells not only lengthens G1 but also accelerates differentiation. Thus, rapid origin licensing is an intrinsic characteristic of stem cells that contributes to pluripotency maintenance.

Cell Cycle↗
PubMed2003

Hiding at the ends of yeast chromosomes: telomeres, nucleases and checkpoint pathways.

Telomeres stabilise DNA at the ends of chromosomes, preventing chromosome fusion and genetic instability. Telomeres differ from double strand breaks in that they activate neither DNA repair nor DNA damage checkpoint pathways. Paradoxically DNA repair and checkpoint genes play critical roles in telomere stability. Recent work has provided insights into the roles of DNA repair and DNA damage checkpoint pathways in the physiological maintenance of telomeres and in cellular responses when telomeres become uncapped. In budding yeast the Mre11p nuclease, along with other unidentified nucleases, plays critical roles in physiological telomere maintenance. However, when telomeres are uncapped, the 5'-to-3' exonuclease, Exo1p, plays a critical role in generating single-stranded DNA and activating checkpoint pathways. Intriguingly Exo1p does not play an important role in normal telomere maintenance. Although checkpoint pathways are not normally activated by telomeres, at least four different types of telomere defect activate checkpoint pathways. Interestingly, each of these telomere defects depends on a different subset of checkpoint proteins to induce cell cycle arrest. A model for how a spectrum of telomeric states might interact with telomerase and checkpoint pathways is proposed.

Cell Cycle↗
PubMed2003

Gaseous nitrogen oxides stimulate cell cycle progression by retinoblastoma phosphorylation via activation of cyclins/Cdks [correction].

Nitrogen oxides (NOx) are important indoor and outdoor air pollutants. Many studies have indicated that NOx gas causes lung tissue damage by its oxidation properties and its free radicals. In a previous study we demonstrated that NOx gas induced proliferation of human lung fibroblast MRC-5 cells. In this study we show that NOx gas stimulates MRC-5 cell proliferation by retinoblastoma (Rb) phosphorylation via activation of cyclin-cell division protein kinase (cdk) complexes [correction]. Western blot and immunoprecipitation data showed that NOx gas increased the expressions of cyclinA/cdk2, cyclinD1/cdk4, and cyclinE/cdk2 complexes in the cells at 9 h after treatment. The levels of phospho-Rb were also increased and cdk inhibitors (CKIs) p27 and p16 were apparently decreased. These data suggested that NOx gas stimulates cell-cycle progression by Rb phosphorylation via activation of cyclin-cdk complexes and inhibition of CKIs. In conclusion, the NOx-gas that induced lung fibroblast cell proliferation by stimulation of cell-cycle progression may contribute to lung fibrosis by NOx pollutants.

Cell Cycle↗