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Mitosis cells

Tubulins arose very early during the course of evolution of unicellular eukaryotes and provide the machinery for the equipartitioning of chromosomes in mitosis, cell locomotion, and the maintenance of cell shape. The primordial genes that coded for tubulins likely were few in number. As metazoan evolution progressed, natural selection processes conserved multiple and mutant tubulin genes in response to the requirements for differentiated cell types (Sullivan, 1988). [Pg.4]

Minshull, J., Blow, J. J., and Hunt, T. (1989a). Translation of cyclin mRNA is necessary for extracts of activated Xenopus eggs to enter mitosis. Cell 56 947-956. [Pg.46]

Moreno, S., Hayles, J., and Nurse, P. (1989). Regulation of p34cprotein kinase during mitosis. Cell 58 361-372. [Pg.46]

Morla, A. O., Draetta, G., Beach, D., and Wang, J. Y. J. (1989). Reversible tyrosine phosphorylation of cdc2 dephosphorylation accompanies activation during entry into mitosis. Cell 58 193-203. [Pg.46]

Russell, P and Nurse, P. (1987b). The mitotic inducer niml+ functions in a regulatory network of protein kinase homologs controlling the initiation of mitosis. Cell 49 569-579. [Pg.50]

The cell cycle is a key process that recurs in a periodic manner. Early cell cycles in amphibian embryos are driven by a mitotic oscillator. This oscillator produces the repetitive activation of the cyclin-dependent kinase cdkl, also known as cdc2 [131]. Cyclin synthesis is sufficient to drive repetitive cell division cycles in amphibian embryonic cells [132]. The period of these relatively simple cell cycles is of the order of 30 min. In somatic cells the cell cycle becomes longer, with durations of up to 24 h or more, owing to the presence of checkpoints that ensure that a cell cycle phase is properly completed before the cell progresses to the next phase. The cell cycle goes successively through the phases Gl, S (DNA replication), G2, and M (mitosis) before a new cycle starts in Gl. After mitosis cells can also enter a quiescent phase GO, from which they enter Gl under mitogenic stimulation. [Pg.273]

The simplest and most sensitive assays for detecting clastogenic (i.e. chromosomal breaking) effects involve the use of mammalian cells. Cultures of established cell lines (e.g. Chinese hamster ovary) as well as primary cell cultures (e.g. human l)nnphocyte) may be used. After exposure to a range of chemical concentrations in the presence and absence of an appropriate metabolic activation system, the cell cultures are treated with a spindle inhibitor (e.g. vinblastine) to accumulate cells in a metaphaselike stage of mitosis. Cells are harvested at appropriate times and chromosome preparations are made, stained with DNA-specific dye and the metaphase cells are analysed under the microscope for chromosome abnormalities. [Pg.132]

Morgan, T.H. (1911). Random segregation versus coupling in Mendelian inheritance. Science 34, 384. Murray, A. (1995). Cyclin ubiquitinization the destructive end of mitosis. Cell 81,149-152. [Pg.279]

Cells, removed from animal tissues or whole animals, will continue to grow if supplied with nutrients and growth factors, allowing single cells to act as independent units that are able to divide by mitosis. Cell lines can... [Pg.75]

Fig. 2. Morphology of aberrant mitosis induced by cisplatin. Following incubation with cis-platin, cells progress to G2 and eventually enter mitosis. The top left panel shows a cell undergoing mitosis, but the chromosomes appear to be pulled to three different loci in the cell. The top right is a mitotic cell stained with an anti-/Ltubulin antibody and shows the presence of multipolar mitotic spindles. The bottom panels show the consequence of aberrant mitosis cells form nuclear membranes around scattered chromosomes giving either many large nuclear particles (right), or a few micronuclei (left). The cells were stained with Giemsa so that the nuclei stain purple and the cytoplasm blue. Fig. 2. Morphology of aberrant mitosis induced by cisplatin. Following incubation with cis-platin, cells progress to G2 and eventually enter mitosis. The top left panel shows a cell undergoing mitosis, but the chromosomes appear to be pulled to three different loci in the cell. The top right is a mitotic cell stained with an anti-/Ltubulin antibody and shows the presence of multipolar mitotic spindles. The bottom panels show the consequence of aberrant mitosis cells form nuclear membranes around scattered chromosomes giving either many large nuclear particles (right), or a few micronuclei (left). The cells were stained with Giemsa so that the nuclei stain purple and the cytoplasm blue.
In a further difference with natural processes, no operation analogous to mitosis (cell division) exists in EAs, since the key aspect of the operation of the algorithm is the way in which the gene pool within the population changes from generation to generation, not the fate of a particular individual. [Pg.17]

Cell cycle-selective agents comprise antimetabolites (of DNA synthesis) and inhibitors of mitosis (cell division see below). A widely used example of an antimetabolite is 5-fiuorouracil (5-FU Figure 13.11). Before this drug actually does something interesting, it needs to be converted to the nucleotide analog 5-fluoro-deoxyuridinemonophos-phate (5-FdUMP), which occurs in the same way as with normal uracil. [Pg.126]

Fig. 12.1 The phases between the end and the start of mitosis are the interphases. Gi and G2- In clockwise direction, between the end of Gi and the start of G2 comes the S-phase, when DNA is synthesized and replicated. After mitosis cells may enter a quiescent phase, Gq, or proceed to Gi and eventually to the S-phase. Checkpoint controls sense DNA damage and arrest the cell cycle in either Gi or G2. These controls prevent DNA synthesis and replication and mitosis, either when DNA is damaged or when DNA has not been properly replicated. Fig. 12.1 The phases between the end and the start of mitosis are the interphases. Gi and G2- In clockwise direction, between the end of Gi and the start of G2 comes the S-phase, when DNA is synthesized and replicated. After mitosis cells may enter a quiescent phase, Gq, or proceed to Gi and eventually to the S-phase. Checkpoint controls sense DNA damage and arrest the cell cycle in either Gi or G2. These controls prevent DNA synthesis and replication and mitosis, either when DNA is damaged or when DNA has not been properly replicated.
Lowe M, Rabouille C, Nakamura N, Watson R, Jackman M, Jamsa E, Rahman D, Pappin DJ, Warren G. Cdc2 kinase directly phosphorylates the cis-Golgi matrix protein GM130 and is required for Golgi fragmentation in mitosis. Cell 1998 94 783-793. [Pg.164]

Ault JG, Rieder CL, Chromosome mal-orientation and reorientation during mitosis. Cell Motil. Cytoskeleton 1992 22 155-159. 57. [Pg.196]

Inhibit polymerization of tubulin, which is necessary for the formation of mitotic spindles for mitosis. Cell cycle specific for M phase of cell cycle. [Pg.148]

Dibenzofuran scaffold-based P-tum mimetic Inhibition of WW domain of PIN1, a mitosis cell cycle regulator Improved solubility and resistance to aggregation without compromising thermodynamic stability [89]... [Pg.157]

Golgi membranes are absorbed into and reemerge from the ER timing mitosis. Cell 99, 589-601. [Pg.368]

Stem cells are undifferentiated cells fonnd in all mnl-ticellular organisms stem cells are capable of renewing themselves indefinitely via mitosis (cell division), sometimes after extended periods of inactivity. As long as the animal in which the stem cells are present is living, stem cells can divide essentially withont limit to repair or replenish other types of cells and rehabih-tate the necessary functionality of the organ or tissne in which the stem cells are present. [Pg.504]

Gerace, L., and Blobel, G. (1980). The nuclear envelope lamina is reversibly depolymerized during mitosis. Cell (Cambridge, Mass.) 19, 277-288. [Pg.21]

Debec ZA, Sullivan W, Bettencourt-Dias M. Centrioles active players or passengers during mitosis Cell Mol Life Sci. 2010 67 2173-94. [Pg.735]

Manchado, E., Guillamot, M., and Malumbres, M. (2012) Killing cells by targeting mitosis. Cell Death Differernti-ation, 19, 369-377. [Pg.247]

Yao LJ, Fan HY, Tong C, Chen DY, Schatten H, Srm QY. 2003. Polo-like kinase-1 in porcine oocyte meiotic maturation, fertilization and early embryonic mitosis. Cell Mol Biol (Noisy-le-grand) 49(3) 399-405. [Pg.497]


See other pages where Mitosis cells is mentioned: [Pg.40]    [Pg.38]    [Pg.71]    [Pg.44]    [Pg.319]    [Pg.456]    [Pg.334]    [Pg.193]    [Pg.160]    [Pg.124]    [Pg.209]    [Pg.157]    [Pg.5079]    [Pg.215]    [Pg.157]    [Pg.1259]    [Pg.430]    [Pg.592]    [Pg.262]    [Pg.21]    [Pg.21]   
See also in sourсe #XX -- [ Pg.284 ]




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