Volume 6 Issue 2, February 2004

In the post-genome era, there is increasing interest in developing quantitative models of cell function at the molecular level. Although data describing the role of individual proteins in cell behaviour remain rate-limiting for such efforts, large-scale screening approaches are providing results that can be used to map the protein–protein interactions of a living biological system.

Genotoxic stress induces a survival response by releasing the transcription factor NF-κB from its inhibitor IκBα. In response to DNA damage, this initially requires the nuclear modification of the IκB kinase regulator NEMO/IKKγ by SUMO and ubiquitin.

Specific gene expression patterns must be tightly regulated for eukaryotic cells to acquire unique structural and functional features. A key step is transcriptional initiation, during which epigenetic activators are thought to facilitate the process by establishing and maintaining transcription-competent chromatin structures. Accumulating evidence shows that an epigenetic regulator can also control the next step — transcriptional elongation.

The kinetochore attaches the centromeric region of chromosomes to spindle microtubules, allowing equatorial chromosome segregation during mitosis. Proteomic analyses suggest that the kinetochore is a supramolecular complex containing more than 65 proteins that surpasses the size of a ribosome. From within this complex web, stable protein sub-complexes have been extracted, revealing the building blocks for kinetochore assembly.