| Term | Definition |
|---|
| Cell proliferation | cell division resulting in cell number increase. |
| The cell cycle | 4 phases: G1--> S --> G2 --> M. G0 - Resting "Cell cycle exit" |
| G1 phase | G1 "Gap between M/S" - Cell growth. * Cellular material production * Active transcription/translation * Production of enzymes necessary for DNA replication * Active metabolic pathways (nucleotide synthesis, energy production) * Require nutrients and growth signals. |
| S phase | DNA replication. |
| G2 phase | G2 "Gap between S/M" - Preparation of M phase. * Active transcription/translation. * Production of proteins and lipids necessary for DNA segregation and cell division. |
| M Phase | Mitosis: 3 steps. 1. Assembly of mitotic spindle: Sister Chromatids attached to microtubules at the site called kinetochores. The other end of each microtubule is attached to the centrosome (also known as spindle pole body or microtubule organizing center). 2. Anaphase: Two sister chromotids move to the opposite poles. 3. Cytokinesis: Cells physically separate into two daughter cells. |
| Cell cycle exit | Cells can undergo Irreversible exit: Terminal differentiation, Senescence (End of its replicative potential (aging) or cell damage) or Reversible exit: Quiescence: cell resting state brought upon by external cues such as lack of nutrients, cell-cell contact, growth inhibitory signals. |
| What drives the cell cycle? | Cyclin dependent kinases (Cdks): * Composed of Cdk kinase subunit and Cyclin regulatory subunit. * Activity regulated by production followed by rapid destruction of the cyclin subunit. * Different Cyclins are produced at specific times at the cell cycle. * Cdk complexes phosphorylate their substrates and activate them. |
| which cyclins/cdks are associated with each phase | G1 - Cyclin D/Cdk4, Cyclin D/Cdk6. G1/S - Cyclin E/Cdk2. S - Cyclin A/Cdk2. M - Cyclin B/Cdk1. |
| how does G1-Cdk activate G1/S Cdk? | phosphorylation of RB turns on Cyclin E gene. Allows Cdk2 to act on cyclin E. |
| What are the Cdk inhibitors and where do they act? | p21 - G1, G1/GS. p27 - G1, G1/S, S. p16 - G1/S. |
| G1 DNA damage checkpoint p53 transcription factor, what is the mechanism? | DNA damage --> dissociation of Mdm2/p53 complex --> p53 (transcription factor) turns on p21 gene. p21 Cdk inhibitor acts on Cyclin E/Cdk2, Cyclin A/Cdk2 --> Cell cycle arrest, which leads to DNA repair or prolonged arrest without DNA repair. If DNA repaired, then Mdm2/p53 complex forms, p53 degradation, and cell cycle progression. If there is prolonged arrest without DNA repair, p53 turns on PUMA gene, which activates PUMA channel leading to cytochrome C release and Apoptosis. |
| How are the molecules in the cell cycle tied to the external signals? | Growth signal = mitogenic signal (example: Epidermal Growth Factor (EGF) --> pro Cdks + anti Cdk-inhibitors. Growth Inhibitory signal = Anti-mitogenic signal (Example: Transforming Growth Factor beta (TGF-beta) --> anti Cdks + pro Cdk-inhibitors. |
| The Epidermal Growth Factor pathway | EGF binds to Receptor Tyrosine Kinase --> autophosphorylates tyrosine, bind Grb2, Sos binds Grb2. Sos turns Ras-GDP --> Ras-GTP. Ras-GTP binds RAF which starts the MAP kinase cascade. MAPK acts on target to turn on MYC --> Cyclin D --> G1-Cdk activation --> Cell cycle progression. |
| The Transforming Growth Factor Beta pathway | TGF-beta binds Ser/Thr Receptor kinase. SMAD transcription factor is turned on. p27 gene is "on" p27 is a Cdk inhibitor of CyclinD/Cdk4, CyclinE/Cdk2, CyclinA/Cdk2. This leads to Cell cycle inhibition and the cell cycle exit to G0. |
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