Cell Cycle Regulation

• Checkpoint


  Stages in eukaryotic cell cycle after G1, G2, and metaphase where it assesses whether or not it should continue with division
• G1 checkpoint


  Main decision point for the cell; here it can still go back to not dividing. If it chooses to continue, it will go through with mitosis barring major complications
• G1 checkpoint things that get checked:

  • Is the cell large enough
  • Does it have enough energy reserves
  • Is it receiving positive cues from neighbors like GF
  • Is any of the DNA damaged
• G2 checkpoint


  Happens right before mitosis, checks to ensure that DNA isn't damaged and replicated properly. If no, progress halts until repairs are made. If that's impossible, it undergoes apoptosis
• Spindle checkpoint


  Cell checks to make sure all sister chromatids are attached to their microtubules. Cycle will not proceed until everything is done properly
• Cyclins


  Related proteins that are important core cell cycle regulators. G1, G1/S, S, and M are the 4 main types, and they peak in the phase they're needed in to promote its events
• Cyclin dependant kinases 


  Cdks
• Cdks


  Enzymes that bind to cyclin and gets directed by it to phosphorylate its target, which is different dependant on the type of cyclin it binds to. Their levels remain constant but their targets change as the dominant cyclins change
• Maturation promoting factor


  MPF
• MPF


  Cdk that binds with M cyclin at the end of the G2 phase, creating a complex that adds phosphate tags to membrane proteins, causing the nuclear envelope to break down, marking the start of the mitotic phase
• Anaphase promoting complex / cyclosome 


  APC/C
• APC/C


  Protein complex activated by MPF complexes to destroy them (ending mitosis and starting G1 in the daughter cell), along with the proteins holding the sister chromatids together during anaphase
• Ubiquitin


  Small protein tag added to APC/C targets, which sends them to the proteasome to be disposed of
• Proteasome


  Recycling bin of the cell that ubiquitin-tagged proteins are sent to
• APC/C triggers the destruction of cohesin, the protein holding sister proteins together, by adding a ubiquitin tag to a protein called securin, which is sent for recycling. Without it in place, separase, the enzyme that securin inhibits, is free to do its job and lets the chromatids separate
• p53


  Famous tumor suppressor protein that ensures cells don't pass don damaged DNA by triggering Cdk inhibitor protein production during the G1 checkpoint to buy time for DNA repair and checking + repairing the DNA itself, then triggering cell death if it's beyond repair
• p53


  Single most mutated gene leading to cancer because of its tumore suppressant properties
• Contact inhibition


  When normal cells are overcrowded, they stop reproducing. Not present in cancer cells, which ignore all signs to stop dividing
• Telomerase


  Enzyme present in cancer cells which reverses the wearing down of the ends of chromosomes that normally happens at the end of a cell division
• Metastasis


  When a cancer cell gains the ability to migrate to other parts of the body
• Angiogenesis


  The production of new blood vessels, which gets triggered by cancer cells so they keep having a supply of oxygen and nutrients
• Cells become cancerous because after one mutation that causes them to sloppily and rapidly multiply, they mutate more and more until eventually something becomes malignant. This means that you can have multiple widescale mutations in different parts of the same patient
• Oncogenes


  Over active and cancer causing forms of genes that cause too much cell multiplication
• Proto-oncogenes


  Normal, not yet mutated form of a gene that could cause cancer
• Amplification


  When a cell gains extra copies of a gene and starts making too much protein, that can cause a proto-oncogene to become an oncogene
• Proto-oncogenes become oncogenes when they are too active, so mutations that force them to be constantly on are what make them cancerous