Cell cycle activity

The very beginning of the first mitotic cell cycle of the mouse embryo seems to be controlled by the mechanisms characteristic for both meiotic and mitotic cell cycles. Active MAP kinase, its substrate p90rsk and the CSF activity itself could influence the cellular processes within the one-cell embryo. Indeed, we have observed that despite the entry into the interphase (as judged by the low activity of MPF) some proteins are actively phosphorylated as during the meiotic M phase (e.g. 35 kDa complex Howlett et al 1986, Szollosi et al 1993), the nuclei and the microtubule interphase network start to form only 1.5 hours after activation (Szollosi et al 1993). This delay in the phenomena characteristic for the interphase could be linked to the mixed meiotic/mitotic character of this early period. This delay probably allows the correct transformation of the sperm nucleus into the male pronucleus. In species like Xenopus or Drosophila the transitional period between the meiotic and the mitotic cell cycle control is probably much shorter since it is proportional to duration of the short first cell cycle of these rapidly cleaving embryos. Mammalian embryos are perhaps the most suitable to study this transition because of the exceptionally long first embryonic cell cycle. 

In summary, it will need to be demonstrated whether accelerated telomere shortening indeed represent the chronic phase clock reflecting both increased replicative aging of Ph-r HSC due to increased cell cycle activity as well as... 

Phosphorylation of H3 is not limited to mitosis and also occurs in G1 phase of the cell cycle. Activation of the Ras-Raf-MEK-ERK signal transduction pathway and/or of the p38 stress kinase pathway when cells are treated with epidermal growth factor (EGF), 12-G-tetradecanoylphorbol-13-acetate (TPA), anesomycin, okadiac acid, and stresses such as UV irradiation induces the rapid phosphorylation of H3 at Ser-10 and/or Ser-28 [68-72] (Figs. 5 and 6). Inhibition of the MEK1,2 activity with PD98059 prevents the activation of ERK and TPA-induced H3... 

Cell cycle activity of the active compounds was investigated. Propidium iodine (the marker for DNA content) was used as a marker of the cell cycle. This cytometric determination was calibrated separately and calculated for a related program to evaluate the percentage of cells in each phase of the cell cycle. The treated cells were compared with that of control HL-60 cancer cells for the percentage of cells in each cell cycle compartment over a period of 24 h. HL-60 cells treated with 10 pg... 

Kruman II, Wersto RP, Cardozo-Pelaez F, Smilenov L, Chan SL, Chrest FJ, Emokpae Jr R, Gorospe M, Mattson MP (2004) Cell cycle activation linked to neuronal cell death initiated by DNA damage. Neuron 41 549-561. 

In addition to serving as markers of renal dysfunction, it is now evident that the filtration of abnormal amounts and/or types of proteins influences the progression of renal disease by promoting secondary injury to tubular epithelial cells and interstitial structures. For example, the upregulation of various cytokines in tubular epithelial cells may contribute to the development of interstitial fibrosis and cell cycle activation leading to tubular cell proliferation and/or apoptosis [52-54],... 

Pasarica, M., Holland, T., and Dhurandhar, N. 2005. Enhanced cell cycle activation by adenovirus 36 contributes to increased lipid accumulation in 3T3-L1 cells. EASES J. 19, A91. 

Potapova TA, Daum JR, Byrd KS, Gorbsky GJ. 2009. Fine tuning the cell cycle activation of the Cdkl inhibitory phosphorylation pathway durine mitotic exit. Mol Biol Cell 20(6) 1737-1748. 

Note RepOTter systems STAT3 (cell surface receptor tyrosine kinase activation) SRE (Ras pathway activation) E2F1 (cell cycle activation) FLKHRLl (PI3K-mTOT activation). 

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