Cancer Biology

Gap 1
Synthesis
Gap 2
Mitosis

It regulates the checkpoint between G1 and S phase that checks for damaged DNA. Mutations of this protein often seen in cancer. When expressed in high levels, it binds to DNA, initially arresting the cell cycle and eventually leading to apoptosis if left unchecked.

It binds to p53 and breaks it down. When there is DNA damage, MDM2 stops binding to p53, which raises the levels of p53 and allows it to halt the cell cycle or cause apoptosis.

They regulate a DNA damage checkpoint in G2 and possibly S phase.

They recieve signals from growth factors, which prompt them to bind to CDKs (Cyclin dependent kinases) to activate them.

They phosphorilate things, such as Rb, when activated by being bound to cyclin.

It prevents the cells from entering the S phase. It gets phosphorilated by CDKs and upon being phosphorilated stops preventing the cell from begining DNA replication, transitioning from G1 to S.

It binds to the cyclin CDK complex and inactivates it.

Nucleoside, a sugar and a base. The sugar can have 1 or 2 OH groups (DNA vs RNA)

Nucleotide, a sugar, base, and phosphate

Nucleotide triphosphate, a sugar, base, and triphosphate chain

Purine

Adenine
Guanine

Pyrimidine

Cytosine
Thymine
Uracil

It opens up the double stranded DNA and unwinds it to allow synthesis.

It copies the DNA in order to synthesis a new strand of DNA.

It relieves stress on DNA during replication by breaking the DNA strands ahead of where replication is occuring and religating them once the stress has been reduced. Type 1 breaks 1 strand, type 2 breaks 2 strands.

Regular proteins in cells that have the potential to lead to cancer if mutated or misregulated, things that control cell growth and proliferation.

proto-oncogenes that have mutated to increase the rate of growth and proliferation of the cell.

Genes that limit cell growth and serve as a check to cancer. Often mutated to not be functional in cancer.