15 - Mitosis Flashcards
Review the cell cycle and mitosis.
Go back and review if needed.
Review the important stages of the cell cycle.
Review the steps and overview of regulation in mitosis.
What are CDKs (cyclin dependent kinases)?
What do CDKs (cyclin dependent kinases) do?
How are CDKs (cyclin dependent kinases) regulated?
Cdks Can Be Regulated in multiple ways
1. Cdk inhibitor proteins
2. Cdk expression (both mRNA expression and Ubiquitin-
mediated protein degradation)
3. Phosphorylation
Give a summary of cyclin-cdk activation and inhibition.
Where are the major cell cycle checkpoints?
Describe the G1 phase checkpoint.
G1 PHASE
* Cdks Are Stably Inactivated in G 1
* Mitogens Promote the Production of the
Cyclins That Stimulate Cell Division
* DNA Damage Can Temporarily Halt
Progression Through G 1
* Cells Can Delay Division for Prolonged Periods
by Entering Specialized Nondividing States
What is a mitogen and what does it do? When does it do its job? Give a clinically relevant example.
Rb was the first tumor suppressor identified. What is a tumor suppressor?
* Tumor suppressors work to stop cell proliferation when it is not needed.
* Mutated tumor suppressors like RB protein can lose their
ability to stop cell proliferation and lead to cancer formation.
What is an oncogene? Give a clinically relevant example.
What is an oncogene?
* Oncogenes are normal proteins that induce cell proliferation when activated (e.g., surface receptor that mediates mitogenic signaling or signal transduction proteins like Ras or MAP kinase acting downstream of the receptor).
* Activated oncogenes that do not turn “off’ (i.e., mutated
oncogenes) can lead to over proliferation and cancer formation.
What factor other than CDK dependent mechanisms is relevant in the G1 phase checkpoint?
- DNA Damage Can Temporarily Halt
Progression Through G1
What is Ataxia-Telangiectasia and why is it important in the cell cycle?
How does the checkpoint at the S/G2 phase transition function?
How does the checkpoint at the G2/M phase transition function?
G2/M transition is controlled by Cyclin B and Cdk1.
What is mitotic nondisjunction? When does it occur?
What other methods besides cyclin dependent mechanisms and DNA damage can regulate the cell cycle? Why is that clinically relevant?
