Advanced molecular biology: a concise reference by Richard Twyman

By Richard Twyman

This e-book emphasises the unifying ideas and mechanisms of molecular biology, with common use of tables and containers to summarise experimental info and gene and protein features.

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Sample text

Weel and Cdc25 process intrinsic signals and integrate signals from the environment, and are probably the main checkpoint regulators. Weel activation is regulated by a kinase Niml, which is responsive to the nutritional status of the cell. The downstream targets for thesesignals may be Cdc25 or Weel or both. Rad3has recently been shown to phosphorylate Chkl, which in turn phosphorylates Cdc25 and causes it to be sequestered in a complex with 14-3-3 protein. In animals, there may also be a mechanism which regulates CDC2 kinase activity independently of phosphorylation on Tyr-15.

Incomplete DNA replication, nutritional status), as discussed in the text. Causes (This is likely to be an indirect transient spike of M-phase kinase activity at onset of the M phase substrate) Histone H1, HMG proteins Condensation chromatin of TFIID,TFIIIB,poly(A)polymeraseInhibitionofbasal transcription Regulation of transcription (phosphorylation of SW15 inhibits nuclear SBF, SW15 (S. cerevisiae) import) Lamins Phosphorylation nuclear lamins causes of dissociation into subunits which breaks down nuclear lamina and may drive dissolution the of nuclear membrane Mitotic spindle assembly RMSA (regulator ofmitotic spindle assembly) Vimentin Reorganization of cytoskeleton Caldesmon is an actin filament regulator and MLC interacts with actin Caldesmon, Myosin light chain to form contractilering at the site of cytokinesis.

Other APC targets include proteins required for maintaining the association of sister chromatids, possibly kinetochore components or perhaps a more generally distributed factor -a candidate is S. cerevisiue PDS1, as discussed above. Degradation of cyclin B is dependent upon chromatin alignment the on mitotic spindle, so it is possiblethat formation of the APC is dependent upon kinetochore attachment and inhibited by unattached kinetochores. The inactivation of M-phase kinase (triggered by degradationof cyclin B) allows M-phase kinase substrates such as myosin to be dephosphorylated, thus facilitating the cytoskeletal organization which precludes cytokinesis, the reconstruction of the nuclear lamina and decondensation of chromatin.

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