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MeSH Review


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Disease relevance of Mitosis


Psychiatry related information on Mitosis


High impact information on Mitosis

  • The Wee1 kinase phosphorylates and inhibits cyclin-dependent kinase 1 (Cdk1), thereby delaying entry into mitosis until appropriate conditions have been met [7].
  • Our studies demonstrate that Set1 has important, unexpected functions in mitosis [8].
  • During mitosis, LGN recruits NuMA to the cell cortex, while cortical association of LGN itself requires the C-terminal Galpha binding domain [9].
  • Elimination of CDK activity at the end of mitosis allows Whi5 to reenter the nucleus to again repress G1/S transcription [10].
  • Since treatment with rapamycin induces a tight association between FKBP and FRAP, one would expect rapamycin to trap the FKBP-fused Golgi protein in the ER if it ever visits the ER during mitosis [11].

Chemical compound and disease context of Mitosis


Biological context of Mitosis

  • One simple model consistent with the roles of CDC28 and CDC37 in mitosis as well as in caryogamy is that these gene products are structural components of the nucleus that must be built into it during one cell cycle in order to permit successful caryogamy at the next G1 [17].
  • The concerted transition into mitosis involves both a reduction in the rate of p34cdc2 phosphorylation on tyrosine and an increase in its rate of dephosphorylation [18].
  • Phosphorylation of histone H3 at serine 10 occurs during mitosis in diverse eukaryotes and correlates closely with mitotic and meiotic chromosome condensation [19].
  • NuMA is a nuclear protein during interphase but redistributes to the spindle poles early in mitosis [20].
  • The presence of extended keratin fibril meshworks in these injected cells is compatible with cell growth and mitosis [21].

Anatomical context of Mitosis


Associations of Mitosis with chemical compounds

  • Pulse treatment of such cultures with thymidine at times corresponding to the S, G2, and M periods had no effect on further growth [27].
  • Moreover, okadaic acid and caffeine, which uncouple the dependence of mitosis on the completion of S phase, increase unphosphorylated p34cdc2 by attenuating tyrosine kinase function [28].
  • As cells enter mitosis, the protein-tyrosine kinase, p60c-src, is known to be extensively phosphorylated on threonine in its amino-terminal region [29].
  • The abnormal mitoses were associated with biochemical defects in the activation of separin, the sister-separating protease, rendering it unable to cleave the cohesin subunit Scc1 efficiently [30].
  • These data indicate that inositol-1,4-bisphosphate may function as an effector molecule in the activation of a low activity form of human DNA polymerase alpha and suggest that it may function as a second messenger during the initiation of mitosis in stimulated cells [31].

Gene context of Mitosis

  • In mammalian cells, LATS1 is phosphorylated in a cell-cycle-dependent manner and complexes with CDC2 in early mitosis [32].
  • Genetic and biochemical studies have indicated that the cdc25 protein controls the entry into mitosis by triggering tyrosine dephosphorylation of the cdc2 protein kinase [33].
  • Our results are consistent with CDC28 function being required in both G1 and mitosis [34].
  • Exit from mitosis is triggered by Tem1-dependent release of the protein phosphatase Cdc14 from nucleolar RENT complex [35].
  • We show here that CLB2 proteolysis, which is important for transition from mitosis to G1, is not confined to a narrow window at the end of mitosis as previously thought but continues until reactivation of CDC28 by CLN cyclins toward the end of the subsequent G1 period [36].

Analytical, diagnostic and therapeutic context of Mitosis

  • The WD repeat protein Cdc20 is essential for progression through mitosis because it is required to activate ubiquitin ligation by the anaphase-promoting complex (APC/C) [37].
  • Subsequently, cultures continuously exposed to urea showed a decline in the mitotic index, indicating that the entry rate of cells into mitosis is lower than the rate at which cells escape from the mitotic block [38].
  • CENP-E represents a link between attachment of spindle microtubules and the mitotic checkpoint signalling cascade, as depletion of this motor leads to profound checkpoint activation, whereas immunoprecipitation reveals a nearly stoichiometric association of CENP-E with the checkpoint kinase BubR1 during mitosis [39].
  • Almost half of them show keratin disruption as described previously: by immunofluorescence, filaments are replaced during mitosis by a 'speckled' pattern of discrete cytoplasmic dots [40].
  • Microinjection of antibody to Mad2 protein into mammalian cells in mitosis induces premature anaphase [41].


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  19. Phosphorylation of histone H3 is required for proper chromosome condensation and segregation. Wei, Y., Yu, L., Bowen, J., Gorovsky, M.A., Allis, C.D. Cell (1999) [Pubmed]
  20. A complex of NuMA and cytoplasmic dynein is essential for mitotic spindle assembly. Merdes, A., Ramyar, K., Vechio, J.D., Cleveland, D.W. Cell (1996) [Pubmed]
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  22. The AAA-ATPase Cdc48/p97 regulates spindle disassembly at the end of mitosis. Cao, K., Nakajima, R., Meyer, H.H., Zheng, Y. Cell (2003) [Pubmed]
  23. CDC27Hs colocalizes with CDC16Hs to the centrosome and mitotic spindle and is essential for the metaphase to anaphase transition. Tugendreich, S., Tomkiel, J., Earnshaw, W., Hieter, P. Cell (1995) [Pubmed]
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