Tag: Cancer biology
Cdh1
Cdh1 is a major activator of the APC/C complex, responsible for mitotic exit, G1 maintenance and replication licensing. By degrading Cyclin B, Aurora A, Plk1 and Geminin, Cdh1 prevents premature S‑phase entry and maintains genomic stability. Its dysregulation contributes to replication stress, chromosomal instability and cancer development.
Cdc20
Cdc20 is a key activator of the APC/C complex, initiating the metaphase‑to‑anaphase transition by promoting securin and Cyclin B degradation. Regulated by checkpoint proteins such as Mad2 and BubR1, Cdc20 safeguards chromosome segregation, while its dysregulation contributes to aneuploidy and cancer progression.
Cancer
Cancer is a multifaceted disease caused by the uncontrolled growth of abnormal cells. It develops through genetic and epigenetic alterations, environmental exposures, and interactions within the tumour microenvironment. Understanding these processes is essential for improving prevention, diagnosis, and treatment.
Cdh1
Cdh1 is a major activator of the APC/C complex, responsible for mitotic exit, G1 maintenance and replication licensing. By degrading Cyclin B, Aurora A, Plk1 and Geminin, Cdh1 prevents premature S‑phase entry and maintains genomic stability. Its dysregulation contributes to replication stress, chromosomal instability and cancer development.
Cdc20
Cdc20 is a key activator of the APC/C complex, initiating the metaphase‑to‑anaphase transition by promoting securin and Cyclin B degradation. Regulated by checkpoint proteins such as Mad2 and BubR1, Cdc20 safeguards chromosome segregation, while its dysregulation contributes to aneuploidy and cancer progression.
Cancer
Cancer is a multifaceted disease caused by the uncontrolled growth of abnormal cells. It develops through genetic and epigenetic alterations, environmental exposures, and interactions within the tumour microenvironment. Understanding these processes is essential for improving prevention, diagnosis, and treatment.