S phase of cell cycle

Myc Transcription factor A transcription factor that increases concentrations of the enzymes reqnired for S-phase of cell cycle, so that DNA synthesis can proceed withont any limitation in precnrsor concentrations (chapter 20). 

S-phase of cell cycle 579 Saccharomyces cerevisiae figure 20... 

HI Holds ends of nucleosomal 12 6 S-phase of cell cycle... 

Traycoff CM, Halstead B, Rice S et al. Chronic myelogenous leukaemia CD34-r cells exit GO/Gl phases of cell cycle more rapidly than normal marrow CD34+ cells. Br.J.Haematol. 1998 102 759-767. 

Some drugs that exert their maximum cytotoxicity during the S-phase of the cycle also prevent cells from progressing through the cell cycle to the S-phase this is accomplished by sublethal inhibition of RNA and protein synthesis. The antimetabolites methotrexate, fluo-rouracU, and mercaptopurine all can inhibit RNA synthesis in Gi- and Gz-phases and inhibit DNA synthesis during S-phase. This inhibition of cell cycle progression actually may result in reduced cytotoxicity, and such agents have been termed S-phase-specific but self-limited. 

To optimize drug therapy, it is necessary to know in what phase of the cell cycle antineoplastic agents are effective. Which one of the following agents is cytotoxic only to cells in the S-phase of the cycle ... 

Cytarabine (cytosine arabinoside, ara-C, Cytosar-U) is an analogue of the pyrimidine nucleosides cytidine and deoxycytidine. It is one of the most active agents available for the treatment of acute myelogenous leukemia. Cytarabine kills cells in the S-phase of the cycle by competitively inhibiting DNA polymerase. The drug must... 

Table 8. Effects of resveratrol on apoptosis Go/Gl, S aad G2/M phase of cell cycle in LLC cells1...

M-phase of cell cycle 579 Macrodipole of helix 70 Macroglobulin(s) (IgM) 58, 629... 

To assess the percentage of MCF-7 cells that progressed through the S-phase of the cycle during incubation with EM-652, EM-800, or tamoxifen in the presence or absence of E2, the continous BrdUrd exposure technique was used. As measured after a 48-hour exposure to BrdUrd, 72-hour pretreatment with 1 nM EM-652, EM-800, or hydroxytamoxifen alone decreased the percentage of BrdUrd-positive cells from 43.6% to 20.2%, 21.5%, and 30.9%, respectively (p<. 01) (Fig. 22A). On the other... 

Site of action Like the other purine and pyrimidine antagonists, ara-C must be sequentially phosphorylated to the corresponding nucleotide, cytosine arabinoside triphosphate (ara-CTP), in order to be cytotoxic. It is S-phase (hence cell-cycle) specific. Ara-C is also incorporated into DNA and can terminate chain elongation. It can also inhibit the reduction of CDP to dCDP. 

Nevertheless, phosphonocarboxylate derivatives have been considered for treatment of diseases characterized by excessive osteoclast-mediated bone resorption. For example, it has been demonstrated that 3-PEHPC treatment in the 5T2MM model of multiple myeloma prevents the development of myeloma bone disease in vivo and reduces the myeloma burden by inhibiting osteoclastic bone resorption [29]. Similarly, it has been shown that 3-PEHPC dose-dependently increases apoptosis in human myeloma cells similar to risedronate. However, while risedronate causes apoptosis and induces cell cycle arrest in the S-phase, no cell cycle arrest was detected after treatment with 3-PEHPC due to its different mechanism of action [30]. 

A deficiency of zinc in . gracilis has been shown to affect adversely all the phases of cell cycle (Gi, S, G2, and mitosis), thus indicating that zinc is required for biochemical processes essential for cells to pass from G2 to mitosis, from S to G2, and from Gi to S (13). The effect of zinc on cell cycle is undoubtedly attributable to its vital role in DNA synthesis (90,9i). Many studies have shown that zinc deficiency in animals im-... 

Proliferation and migration of vascular smooth muscle cells (VSMC) is one of the hallmarks of atherosclerosis. Red wine polyphenols hinder the proliferation and migration of cultured SMCs stimulated by growth factors through inhibition of PI3K activity and p38 (MAPK) phosphorylation.In support, resveratrol reversibly arrests VSMC proliferation in early S phase of the cycle. Recent studies on SMCs demonstrate the anti-atherogenic actions of resveratrol via its ability to inhibit the autocrine secretion and the mitogenic effects of endothelin-... 

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