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Eukaryotic Cell Cycle (eukaryotic + cell_cycle)
Selected AbstractsDNA polymerases ,, ,, and , localize and function together at replication forks in Saccharomyces cerevisiaeGENES TO CELLS, Issue 4 2005Shin-Ichiro Hiraga Early in eukaryotic cell cycle, a pre-RC is assembled at each replication origin with ORC, Cdc6, Cdt1 and Mcm2-7 proteins to license the origin for use in the subsequent S phase. Licensed origin must then be activated by S-Cdk and Ddk. At the onset of S phase, RPA is loaded on to the ARS in a reaction stimulated by S-Cdk and Ddk, followed by Cdc45-dependent loading of pol ,, -,, and -,. This study examines cell cycle-dependent localization of pol ,, -, and -, in Saccharomyces cerevisiae using immuno-histochemical and chromatin immuno-precipitation methods. The results show that pol ,, -,, or -, localizes on chromatin as punctate foci at all stages of the cell cycle. However, some foci overlap with or are adjacent to foci pulse-labeled with bromodeoxyuridine during S phase, indicating these are replicating foci. DNA microarray analysis localized pol ,, -,, and -, to early firing ARSs on yeast chromosome III and VI at the beginning of S phase. These data collectively suggest that bidirectional replication occurs at specific foci in yeast chromosomes and that pol ,, -,, and -, localize and function together at multiple replication forks during S phase. [source] Exploring the link between microorganisms and oral cancer: A systematic review of the literatureHEAD & NECK: JOURNAL FOR THE SCIENCES & SPECIALTIES OF THE HEAD AND NECK, Issue 9 2009Samuel J. Hooper PhD Abstract The majority of cases of oral cancer have been related to tobacco use and heavy alcohol consumption. However, the incidence of oral cavity carcinoma appears to be increasing in many parts of the world in a manner that it is difficult to explain with traditional risk factors alone. Meanwhile, interest in the possible relationships between microorganisms and the different stages of cancer development has been rising and numerous mechanisms by which bacteria and yeast may initiate or promote carcinogenesis are currently under investigation. In particular, a persuasive body of evidence suggests a possible etiological role involving the metabolism and production of carcinogenic products, such as acetaldehyde. Other suggested mechanisms include the induction of chronic inflammation and direct interference with eukaryotic cell cycle and signaling pathways. This review aims to summarize the known associations between microbial infection and cancer and draw attention to how they may relate to oral carcinoma. © 2009 Wiley Periodicals, Inc. Head Neck, 2009 [source] Expression of a cyclin E1 isoform in mice is correlated with the quiescent cell cycle status of hepatocytes in vivo,HEPATOLOGY, Issue 1 2006Nils-Holger Zschemisch Cyclin E1 controls G1/S phase transition of the eukaryotic cell cycle. We report the impact of alternative spliced cyclin E1 isoforms on cell cycle regulation in hepatocytes. We show that expression of new cyclin E1 mRNA variants IN3, ,4, and ,5 is associated with retarded proliferation in murine hepatocellular carcinoma. Additionally, we demonstrate that a new cyclin E1 isoform ,3/8 lacking the central part of wild-type mRNA is expressed predominantly in nonproliferating murine hepatocytes. Following partial hepatectomy, ,3/8 is downregulated when hepatocytes enter the cell cycle from quiescence. The ,3/8 protein does not exhibit any cyclin box motif but binds cyclin-dependent kinase 2 without stimulating kinase activity. We demonstrate that ,3/8 lacks any nuclear localization signal and is exclusively located in the cytoplasm. Overexpression of ,3/8 in cultured cells leads to a delayed G0-G1 transition, indicating that this splice variant helps to maintain a quiescent state of hepatocytes. In conclusion, we identified an isoform of cyclin E1 involved in G0 maintenance and suggest an additional mechanism for cell cycle control. (HEPATOLOGY 2006;44:164,173.) [source] Zinc regulates the ability of Cdc25C to activate MPF/cdk1JOURNAL OF CELLULAR PHYSIOLOGY, Issue 1 2007Lu Sun Zn2+ is an essential micronutrient for the growth and development of multicellular organisms, as Zn2+ deficiencies lead to growth retardation and congenital malformations (Vallee, BL, Falchuk, KH. 1993. Physiol Rev., 73:79,118). At the cellular level Zn2+ depravation results in proliferation defects in many cell types (Vallee, BL, Falchuk, KH. 1993. Physiol Rev., 73:79,118), however the molecular pathways involved remain poorly defined. Here we show that the transition metal chelator TPEN (N,N,N,,N,-tetrakis(2-pyridylmethyl) ethylene diamine) blocks the G2/M transition of the meiotic cell cycle by inhibiting Cdc25C-cdk1 activation. ICP-MS analyses reveal that Cdc25C is a Zn2+ -binding metalloprotein, and that TPEN effectively strips Zn2+ away from the enzyme. Interestingly, although apo-Cdc25C (Zn2+ -deficient) remains fully catalytically active, it is compromised in its ability to dephosphorylate and activate MPF/cdk1. Thus, Zn2+ is an important regulator of Cdc25C function in vivo. Because of the conserved essential role of the Cdc25C-cdk1 module in the eukaryotic cell cycle, these studies provide fundamental insights into cell cycle regulation. J. Cell. Physiol. 213: 98,104, 2007. © 2007 Wiley-Liss, Inc. [source] | |||||||||||||