Mathematical modeling and sensitivity analysis of G1/S phase in the cell cycle including the DNA-damage signal transduction pathway

Biosystems ◽  
2008 ◽  
Vol 94 (1-2) ◽  
pp. 109-117 ◽  
Author(s):  
Kazunari Iwamoto ◽  
Yoshihiko Tashima ◽  
Hiroyuki Hamada ◽  
Yukihiro Eguchi ◽  
Masahiro Okamoto
Life ◽  
2020 ◽  
Vol 10 (2) ◽  
pp. 15
Author(s):  
Novikova ◽  
Stepanchenko ◽  
Zorina ◽  
Nosov ◽  
Rakitin ◽  
...  

Recent studies indicate direct links between molecular cell cycle and cell differentiation machineries. Ethylene and abscisic acid (ABA) are known to affect cell division and differentiation, but the mechanisms of such effects are poorly understood. As ethylene and ABA signaling routes may interact, we examined their involvement in cell division and differentiation in cell tissue cultures derived from several Arabidopsis thaliana plants: wild type (Col-0), and ethylene-insensitive mutants etr1-1, ctr1-1, and ein2-1. We designed an experimental setup to analyze the growth-related parameters and molecular mechanisms in proliferating cells upon short exposure to ABA. Here, we provide evidence for the ethylene–ABA signaling pathways’ interaction in the regulation of cell division and differentiation as follows: (1) when the ethylene signal transduction pathway is functionally active (Col-0), the cells actively proliferate, and exogenous ABA performs its function as an inhibitor of DNA synthesis and division; (2) if the ethylene signal is not perceived (etr1-1), then, in addition to cell differentiation (tracheary elements formation), cell death can occur. The addition of exogenous ABA can rescue the cells via increasing proliferation; (3) if the ethylene signal is perceived, but not transduced (ein2-1), then cell differentiation takes place—the latter is enhanced by exogenous ABA while cell proliferation is reduced; (4) when the signal transduction pathway is constitutively active, the cells begin to exit the cell cycle and proceed to endo-reduplication (ctr1-1). In this case, the addition of exogenous ABA promotes reactivation of cell division.


1993 ◽  
Vol 3 (8) ◽  
pp. 256
Author(s):  
M. Peter ◽  
A. Gartner ◽  
J. Horecka ◽  
G. Ammerer ◽  
I. Herskowitz

2008 ◽  
Vol 40 (11) ◽  
pp. 730-741 ◽  
Author(s):  
Hong Yue ◽  
Martin Brown ◽  
Fei He ◽  
Jianfang Jia ◽  
Douglas B. Kell

2017 ◽  
Vol 4 (4) ◽  
pp. 1380 ◽  
Author(s):  
Jiahai Chen ◽  
Xiaoli Yang

Background: Hepatocellular carcinoma (HCC) is one of the most frequent malignant tumors. The objective was to investigate the role of serine/threonine kinase Pim-2 in apoptosis signal transduction pathway, because there is little study about its contribution to apoptosis in hepatocellular carcinoma.Methods: The Pim-2 gene and protein expression were examined by qRT-PCR, Western blot and immunohistochemical stain in HCC tissues and normal liver tissues. The plasmid pCI-neo-Pim2 was transfected into human hepatoma cell line SMMC7721 by lipofectamine. Total RNAs were extracted from SMMC7721 cell in logarithm growth phase. The mRNA expression of Pim-2, Akt-1 (protein kinase B), 4E-BP1 (translation repressor of mammalian target of rapamycln), SOCS-1 (repressor of cytokine), Bad(Bcl-xL/Bcl-2 associated death promoter, Bim(Bc1-2 interacting mediator of cell death)and Puma (p53 upregulated modulator of apoptosis) were identified by qRT-PCR. The cell cycle of post-transfected SMMC7721 cells was assessed by flow cytometry.Results: Pim-2 expression was enhanced in HCC. In post-transfected SMMC7721 cells, Pim-2 mRNA expression was up-regulated, level of Bad mRNA was attenuated, furthermore, the transcription level of Akt-1, SOCS-1, 4E-BP1, Bim and Puma gene wasn’t variety. Up-graulated Pim-2 can’t cause distinct change of cell cycle or apoptosis in hepatoma cell.Conclusions: The serine/threonine kinase Pim-2 plays an import role in the development of HCC, Pim-2 dependent maintenance of cell size and survival correlated with its ability to maintain down-regulated expression of the BH3 protein Bad. Pim-2 is not a trigger in cell-autonomous survival or inhibiting apoptosis in hepatocellular carcinoma. Pim-2 is a redundancy pathway of survival signaling.


Cell ◽  
1993 ◽  
Vol 73 (4) ◽  
pp. 747-760 ◽  
Author(s):  
Matthias Peter ◽  
Anton Gartner ◽  
Joe Horecka ◽  
Gustav Ammerer ◽  
Ira Herskowitz

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