- The Molecular Biology of HIV/AIDS
- The epigenetics of cancer, a recent view
- Rolling Circle Amplification Technology–Technical Details
- Structure of an enzyme and its in hibitor
- Development and morphogenesis: potentialities from common patterns
- Cancer as a Disease of the Cell Cycle
- Employment Opportunities
- Employment Opportunities at MSI
- Human skin analysis
- HYBRIDIZATION METHODS IN LIQUID PHASE
- PROPERTIES OF DNA
- The mitofusin 2 in mitochondrial energization
- Apoptotic mechanisms of granzymes in CTL lysis
- Induction therapy of autophagy and apoptosis in melanoma cells
- Parallel evolution of the venom of snakes and integrin
Who controls centrosome duplication?
The transition between each of the phases of the cell cycle is controlled by phosphorylation processes carried out by enzymes known as cyclin dependent kinase (CDK). In mammalian cells, the enzyme bound to CDK2 cyclin A acts as the main promoter of the transition from G1 to S phase cell cycle progression and S phase, when DNA replication. Thus, the cyclin A-CDK2 complex binds to a large number of regulatory proteins at different times during cell cycle progression.
Within this general scheme, CDK2 has been proposed as a key regulator of centrosome duplication. Research published in Oncogene, with Spanish participation Mariano Barbacid group, the National Cancer Centre (CNIO), has used mouse embryonic fibroblasts with the Cdk2 gene deletions, to show the effect of this protein in the process of doubling DNA during the S phase The authors have observed that CDK2 is not required for normal duplication of centrosomes or for mitotic spindle formation.
By contrast, Cdk2 deficiency appears to suspend the aberrant centrosome duplication induced by the activity of a viral oncogene, used as a tool for determining mechanisms of progression and tumor development. The results indicate a differential requirement for CDK2 activity in normal and impaired duplication of centrosomes, suggesting a role of CDK2 in licensing requirements for aberrant duplication of centrosomes. The conclusions of the work affect the chances of CDK2 as a potential therapeutic target for inhibition of chromosomal instability associated with the development of tumor cells.