ch17 Flashcards
CDKs (cyclin-dependent kinases)
-accelerators
-cdk level does not change
Cyclins
substrate for CDK’s
-non-enzymatic
-brakes
-cdk level changes
1. bind to CDK
2. phosphorylate CDK
3. Involvement of inhibitory proteins
positive feedback loop
-control when cells decide to grow to stop growing
-help cells switch between stages
-Cdc25 is stimulated by active M-Cdk
negative feedback loop
-causes a system to change in the opposite direction from which it is moving
-M-Cdk sets in motion a regulatory process that leads to its own inactivation
accelerator pedals
-G1-Cdk
-G1/S-Cdk
-S-Cdk
-M-Cdk
brake pedals
provide information about extracellular environment, DNA damage, and spindle assembly
G zero
-Terminally differentiated cells (neurons)
-Cells enter in low nutrient conditions or damaged (cell cycle arrest)
Cell cycle arrest
-when DNA damage blocks cell division
-protein kinases are recruited to damage site and initiate signaling pathway
-p21 binds and inactivates G1/S-Cdk and S-Cdk complexes, arrested the cell in G1.
Anaphase promoting complex
Initiates the metaphase-to-anaphase transition & assembles polyubiquitin chains on target protein
2 substrates: Mitotic cyclin & Securin
-Activated by Cdc20
Story of M-Cdk
Rb and E2F check everything before division
M-CDK directs chromosomes to line up, APC gives signal to move to final division stage
p53 will send alerts if it notices danger
Rb
controls when a cell grows, divides, and stops dividing
E2F
activating genes necessary for cell division
p53
preventing cells w/ damaged DNA from proliferating and becoming cancerous through repair or apoptosis
Tyrosine kinase receptor
Mitogens stimulate G1-Cdk and G1/S-Cdk activities
Receive signal, pass it on, start cell jobs, cell cycle connection, keep balance
Myc
increases the expression of many delayed-response genes
-team boss, gives instructions