Cig2, a cyclin that plays a pivotal role in cell cycle transitions, is intricately linked to cyclin-dependent kinases (CDKs). The chemicals listed as activators largely belong to a class that either directly or indirectly affects CDK activity. This modulation, especially in yeast organisms, can drive a compensatory surge in certain cyclin levels, including Cig2. This compensatory response ensures the preservation of cell cycle fidelity, particularly during G1/S and G2/M transitions. The precision of this response underscores the intricacy and the balance the cell maintains to ensure timely cell division.
These chemicals, primarily characterized as CDK, reveal the fine-tuned balance within the cell. Their selective action on specific CDKs means that while certain parts of the cell cycle might be inhibited, other segments, reliant on different cyclins and CDKs, can proceed. It is in this nuanced environment that Cig2 can become more active, ensuring that the cell cycle progresses despite challenges. Understanding these dynamics provides a deeper insight into the regulatory networks governing cell cycle progression and the indirect pathways that might be harnessed to influence specific cyclin activities.
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