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Increased microtubule assembly rates influence chromosomal instability in colorectal cancer cells
An increase in microtubule plus-end assembly rates is identified as a mechanism influencing CIN in colorectal cancer cells and its adverse consequence on tumour growth is revealed.
The CHK2–BRCA1 tumour suppressor pathway ensures chromosomal stability in human somatic cells
A function of Chk2, independent of p53 and DNA damage, is reported that is required for proper progression of mitosis, and for the maintenance of chromosomal stability in human somatic cells.
Crosstalk of the mitotic spindle assembly checkpoint with p53 to prevent polyploidy
It is shown that not only p53 but also a functional spindle assembly checkpoint is required for postmitotic G1 checkpoint function, and that polyploid cells are inhibited to re-enter mitosis by an additional checkpoint acting in G2.
Yeast Shuttling SR Proteins Npl3p, Gbp2p, and Hrb1p Are Part of the Translating mRNPs, and Npl3p Can Function as a Translational Repressor
The cytoplasmic rearrangement for shuttling mRNA binding proteins in Saccharomyces cerevisiae during translation is described and evidence that the import receptor Mtr10p, but not the SR protein kinase Sky1p is involved in the timely regulated release of Npl3p from polysome-associated mRNAs is provided.
Cell cycle-regulated proteolysis of mitotic target proteins.
It is reported that injection of dominant negative Ubc3/Cdc34, whose role in G1-S control is well established and has been implicated in kinetochore function during mitosis in yeast, dramatically interferes with congression of chromosomes to the metaphase plate.
Mitotic drug targets and the development of novel anti-mitotic anticancer drugs.
Mechanisms of mitotic cell death induced by chemotherapy-mediated G2 checkpoint abrogation.
A highly improved strategy for an anticancer treatment is shown by the combined use of UCN-01 with abrogators of the survivin/Aurora B-dependent antiapoptotic pathway that retains the selectivity for p53-defective cancer cells.
Partial downregulation of MAD1 causes spindle checkpoint inactivation and aneuploidy, but does not confer resistance towards taxol
It is reported that the stable partial downregulation of the spindle checkpoint gene MAD1 leads to a functional inactivation of theSpindle checkpoint resulting in gross aneuploidy, and it is shown that normal levels of Mad2, but not of Mad1, are required for preventing premature sister chromatid separation and for maintaining the timing of an undisturbed mitosis.
Tumor Suppressor CHK2: Regulator of DNA Damage Response and Mediator of Chromosomal Stability
Another, DNA-damage–independent function of Chk2 during mitosis that is required for proper mitotic spindle assembly and maintenance of chromosomal stability is revealed and may be able to exploit the loss of CHK2 in human tumors to develop novel therapies based on synthetic lethal interactions.
Centromere localization of INCENP-Aurora B is sufficient to support spindle checkpoint function
It is demonstrated that treatment of mitotic cells with the antibiotic actinomycin D causes a displacement of an intact and active CPC from centromeres onto chromosome arms, which results in chromosome misalignment, cytokinesis failure and SAC override, but still preserves histone H3 phosphorylation on chromosome arms.