Biology 1002B Lecture Notes - Lecture 20: Cyclin-Dependent Kinase, Tumor Suppressor Gene, Oncogene
19 Mar 2015
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Divide like crazy because they keep their genes turned on for replication and they ignore any signals that tell them to stop. Able to attract their own blood supply: cells that don"t respect their cell cycle check points = cancer. Cdk cyclin dependent kinase (phosphorylase) phosphorylates target proteins either turning them on or off in order to break the g1 checkpoint. Cdk not active and need cyclin to get passed check point. Cyclin produced only at certain times, cdk always expressed (constitutive) role of proto-oncogenes, tumor suppressor genes and oncomirs in caner: expression of proto-oncogenes promotes cell cycling (ex egfr, proto-oncogenes (gene waiting to become a cancer gene) When up-regulated lead to increased cell division: normal genes that just decided to become cancerous (not really cancer genes, egf epidermal growth factor (protein) Cells need to know that egf is available so need a receptor (egfr) When binds then sends signal to nucleus to stimulate cell to divide.
