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Cell Cycle Inhibitor

The process of cell cycle regulation is the activation or inactivation of various regulatory factors under the surveillance of checkpoints, thereby initiating the process of cell DNA replication and division into two daughter cells.<br>

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Cell Cycle Inhibitor

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  1. Cell Cycle Inhibitor The process of cell cycle regulation is the activation or inactivation of various regulatory factors under the surveillance of checkpoints, thereby initiating the process of cell DNA replication and division into two daughter cells. Among many cell cycle regulators, cyclin-dependent kinase (CDK) is at the core, and it is a network system that regulates the cell cycle with cyclin and cyclin-dependent kinase inhibitors (CKIs). CDKs are a class of serine/threonine kinases, and currently, 13 species are found, including CDK1~13, which play a role in cell cycle regulation of CDKs and transcriptional regulation of CDKs. The regulation of the cell cycle is, in fact, the regulation of checkpoints, with G1/S regulatory points being the most important. When the cell cycle is stimulated by external signals such as growth factors, the catalytic subunit CDK4/CDK6 binds to the regulatory subunit CyclinD, and the CDKs residues are activated by phosphorylation/dephosphorylation. After activation of CDKs, the Rb protein is phosphorylated. The rb gene, also known as the retinoblastoma gene, is the first cloned tumor suppressor gene, and its ability to form a complex with transcription factors (such as E2F) after phosphorylation of the protein is lost. E2F plays an important role in cell cycle regulation and induces the expression of CyclinE and CDK2 and forms a CyclinE/CDK2 complex, which further phosphorylates Rb protein and fully releases E2F. Subsequently, E2F enters the nucleus to activate a series of cell cycles into S phase. In the late phase of DNA replication during S phase, CDK2 is activated by cyclinE, which inactivates transcription factor E2F in time, preventing apoptosis caused by persistently activated E2F. Research statistics show that more than 90% of human cancers have mutations in related genes in the CDK, Cyclin, CKI, and Rb pathways, with CDK and its corresponding regulatory subunit Cyclin being the most frequently dysfunctional. In addition, fluctuations in the cell cycle promote chemotherapy resistance and reduce the effects of chemotherapy. Therefore, the regulation of CDK/Cyclin activity, which restores normal cell cycle, is one of the strategies for treating tumors.

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