Cell Cycle, Cell Death, Cancer Flashcards
Which 5 steps are included in the M phase (mitosis)
- Prophase
- Prometaphase
- Metaphase
- Anaphase
- Telophase
What will keep a cell recently made by mitosis in the G0 phase?
If sufficient stimulus, or conditions, are absent, the cell remains in G0 and does not fo on to the growth and division cycle
What is the correct order of cell cycle phases
- Synthesis
- G2
- M
- G0 or G1
SGMO!!!!
Events in S-phase
“Replicatin”
DNA replication
Events in G2 phase
“Waiting”
DNA has finished replication. Waiting to initiate cell division aka waiting to enter the M phase
Events in M phase
“Dividing”
Mitosis (IPMAT)
Events in G0 phase
“Chillin”
Quiescent, non-cycling. Proliferation capacity is intact
Events in G1 phase
“Building”
The cell has finished dividing and it is now building cell mass to begin initiation of DNA replication
When using a flow cytometer to detect the cell cycle phase, within which phase is the most fluorescence seen?
There are more fluorescent cells in G1 because this is when the cells are building mass to initiate DNA replication in the synthesis phase
What kinds of molecules regulate the cell cycle
Cyclins
Cyclin-dependent kinases (CDKs)
Cyclin-dependent kinase inhibitors (CKIs)
Kinase vs. Phosphatase
Kinase: Attaches a phosphate group to a protein
Phosphatase: Removes a phosphate group from a protein
What are positive cell cycle regulators
Cyclins
CDKs
What are negative cell cycle regulators
CKIs
What is happening on a cyclin cycle graph? (Slide 16)
When a cell is transitioning between phases, it is regulated by various cyclins, CKDs, CDIs, etc. These regulators are seen in higher quantities where it is needed for transition.
What is present on a CDK to ensure cyclin binding
PSTAIRE alpha-helix
What must be phosphorylated on a threonine residue by a CDK-activating kinase (CAK) for the catalytic fx of a CDK to become activated?
The activation loop, or T-loop, must get phosphorylated
How do protein kinases and protein phosphatases work in tandem to activate a cyclin-CDK complex?
Protein kinases add the phosphates to inhibitory and activating sites on the CDK. Activating protein phosphatases, such as Cdc25, remove the inhibitory phosphate thereby activating the cyclin-CDK complex
Which cyclins bind to CDK1 (p34 cdc2)
A
B1
B2
Cdk1-cyclin B binds Cdk1 (Cdc kinase subunit)
Which cyclins bind to Cdk2
A, E
Which cyclins bind to Cdk4, Cdk 6
D1-D3
What is the action of CKIs
Block CDK action and ensure control over the cell cycle. CKIs are activated upon cell cycle activation checkpoint.
How do CKIs negatively regulate the cell cycle
Based on the particular regulator, the CKI may:
- Twist the upper lobe of the CDK to block cyclin binding
- Interfere with ATP hydrolysis
- A loop is insinuated in the upper lobe of the CDK to block ATP binding
How does INK4 function
Functions to negatively regulate the cell cycle in 2 ways. If it binds BEFORE the cyclin, it inhibits cyclin binding. If it binds AFTER the cyclin has bound, it interferes with ATP use.
How does p27 function?
Works after the cyclin has bound. A loop is insinuated into the upper lobe of the CDK to block ATP binding.
What gene induces CKI:p21
Induced by p53 tumor suppressor. Makes sense because when we want to SUPPRESS tumors, we want to arrest the cell cycle and this is possible with CKI:p21 (blocks ATP binding)
How is CKI:p27 and INK4:p16 regulated?
They both arrest cells in response to growth suppressors and transforming growth factors like TGF-beta. INK4:p16 action is altered in many cancers…will lead to uncontrollable growth because the CKI is not functioning well.
How so Ras proteins receive their signaling and what is the overall function of Ras signaling?
Ras proteins (aka small G proteins or small GTPases) receive their signals from catalytic receptors that have been activated by a ligand. Overall fx of Ras signaling involves proliferation.
Where is MAPK located?
In the cytoplasm
Where is Myc gene located
In the nucleus
Myc gene alters cyclin D gene, SCF subunit gene, and E2F gene. What is the effect of these?
They all lead to increased E2F activity. Cyclin D gene and SCF subunit gene lead to increase E2F activity INDIRECTLY by activating G1-Cdk and G1-S-Cdk cyclins which go on to carry out Rb phosphorylation.