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Cell Biology for Bioprocessing
Published in Wei-Shou Hu, Cell Culture Bioprocess Engineering, 2020
The progression through the cell cycle (G1, S, G2, and M) is positively regulated by cyclins and cyclin-dependent kinases (CDKs) and negatively controlled by CDK inhibitors (CDIs). Stage-specific cyclins for the G1, G1/S, S, and M phases rise and fall during the cell cycle and interact with different CDKs to form cell cycle stage-specific Cyclin-Cdk complexes. The different Cyclin-Cdk complexes are further regulated at activity levels by activating and inactivating phosphorylation and by complexing with CDI. Additionally, Cyclin-Cdk complexes are subject to proteolytic regulation (Figure 2.20).
Cell Cycle
Published in Mihai V. Putz, New Frontiers in Nanochemistry, 2020
Grdisa Mira, Ana-Matea Mikecin
The CC is controlled by numerous mechanisms that ensure accurate cell division. These mechanisms include the regulation of cyclin-dependent kinases (CDK) by cyclins, CDK inhibitors (CKI), phosphorylating events, as well as the activation of checkpoints after DNA damage.
Illuminating the cycle of life
Published in Raquel Seruca, Jasjit S. Suri, João M. Sanches, Fluorescence Imaging and Biological Quantification, 2017
Anabela Ferro, Patrícia Carneiro, Maria Sofia Fernandes, Tânia Mestre, Ivan Sahumbaiev, João M. Sanches, Raquel Seruca
The cell cycle consists of three gap phases, G0, G1, and G2, which are interspersed between the DNA synthesis phase (S phase) and the mitosis phase (M phase). The G0/G1, S, and G2 phases are collectively known as interphase. The cell cycle is a coordinated network of genes and proteins, cyclically regulated by transcription, posttranslational modifications, as well as dynamic genetic and protein interactions [8,9]. Key regulatory molecules include the cyclin-dependent kinases (CDK), a family of serine/threonine kinases that are specifically activated at different phases of the cell cycle by cyclins. Cell-cycle progression is driven by the periodic oscillation of CDK/cyclin activities, which are in turn regulated by a number of mechanisms, including (1) cyclin synthesis; (2) activation of CDKs by CDK activating kinases (CAKs); (3) inhibition of CDKs by CDK inhibitors (CKIs); and (4) ubiquitin-mediated proteasomal degradation of cyclins [9]. Indeed, protein degradation plays a key role in driving cell-cycle transitions through two major E3 ubiquitin ligases, the Skp1–Cul1-F box protein (SCF) complex and the anaphase-promoting complex/cyclosome (APC/C), which ubiquitinate G1 cyclins from late G1 to early M phase and mitotic cyclins from anaphase till the end of G1 phase, respectively [9,10]. Further regulation is accomplished by a myriad of cell-cycle checkpoints that induce cell-cycle arrest on detection of defects and ensure the progression of the cycle in an orderly fashion while minimizing genomic instability [11,12]. Briefly, the G1/S checkpoint induces an arrest induced by DNA damage in a p53-dependent manner, whereas the S phase checkpoint delays initiation or elongation of DNA replication to minimize replications errors. The G2/M checkpoint restricts entry into mitosis minimizing chromosome missegregation, whereas the spindle assembly checkpoint (SAC) detects improper alignment of chromosomes on the mitotic spindle thus ensuring fidelity of chromosome segregation. Finally, postmitotic arrest prevents abnormal daughter cells from entering the next interphase [2,12]. A schematic representation of the cell cycle is displayed in Figure 12.1.
Theoretical, antimicrobial, antioxidant, in vitro cytotoxicity, and cyclin-dependent kinase 2 inhibitor studies of metal(II) complexes with bis(imidazol-1-yl)methane-based heteroscorpionate ligands
Published in Journal of Coordination Chemistry, 2019
S. Jayakumar, D. Mahendiran, A. Kalilur Rahiman
Cell cycle progression is controlled by cyclin-dependent kinases (CDKs) counter balanced by CDK inhibitors. The CDKs are a family of heterodimeric Ser/Thr protein kinases each consisting of a catalytic CDK subunit and an activating cyclin subunit. CDKs coordinate the eukaryotic cell division cycle and serve to integrate diverse growth-regulatory signals, and also strongly inhibit the tumor cell growth [50, 51]. For this reason, we have been interested to study the interaction of the synthesized heteroscorpionate-based homoleptic metal(II) complexes with CDK2 receptor (Figure 5). The observed docked values of complexes 1-9 are –4.31, –4.51, –4.18, –4.99, –5.07, –4.93, –5.14, –6.26, and –5.09, respectively. It can be seen that the complexes most likely bind to the hydrophobic pocket. All the complexes potentially interact with CDKs via π-π, π-σ, hydrogen bonding, electrostatic and van der Waals interactions. The interaction of nickel(II) and copper(II) complexes 3, 5, 7, and 8 are explained herewith.