Respuesta :
Answer: seen below.
Explanation:
The cyclin-dependent kinases (CDKs) are a family of serine or threonine kinases which controls progression through the cell cycle. It is regulated by the subunit cyclins which forms a complex. Any Abnormalities that occur in any of the phases (from the resting state (G0), growth phase (G1), through DNA replication (S) to cell division (M) ) initiate a signal that triggers a cell cycle arrest until the issue is resolved.
CDKs have been shown to regulate other processes, particularly various aspects of transcription, different CDK isoforms have key roles in cancer cell proliferation through loss of regulation of the cell cycle. kinases inhibits several family members, preventing cell-cycle progression, for instance, in response to DNA damage, elimination of the phosphates involves in inhibition by phosphatases of the Cdc25 family is then required for activation of CDKs and cell-cycle progression. Loss of control of the cell cycle leads to the formation of cancer as stated earlier. Therefore, the presence of cyclin-dependent kinases inhibitors might play a role in normal cells becoming cancer cells by preventing cell cycle progression in response to DNA damage which can lead to the formation of cancer cells. It has been stated that the presence of CDK inhibitors is also useful in the treatment of cancerous tumor.
The abnormal expression of activators or inhibitors of cyclin-dependent kinases (CDKs) leads to abnormal phosphorylation of protein targets associated with the disruption of the cell cycle.
- The cyclins and cyclin-dependent kinases (CDKs) are proteins whose interaction is fundamental for controlling the progression through the cell cycle.
- A cyclin binds to its corresponding CDK to activate its kinase domain, which then phosphorylates different protein targets during the cell cycle.
- Cancer is often associated with mutations in proteins that regulate the activity of CDKs, thereby also dysregulating check restriction points in normal cells.
- The abnormal expression of activators and/or inhibitors of CDKs drives the abnormal functioning of these proteins, thereby they then are no longer able to phosphorylate (and thus regulate) targets associated with the progression or disruption of the cell cycle.
In conclusion, the abnormal expression of activators or inhibitors of cyclin-dependent kinases (CDKs) leads to abnormal phosphorylation of protein targets associated with the disruption of the cell cycle.
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