BIOM 500 QUIZ 3 / WEEK 3 LECTURE 1 NOTES
Chapter 11 – Cell Cycle Regulation
Phases
- Phases of cell cycle is divided into 2 sections:
o Interphase G1 S (synthesis) G2 (G – Gap)
o Mitotic M
- G initial (Cell is not replicated) quiescence
o Cells exit the cell cycle due to absence of growth signal or presence of prodifferentiation signal
o Cell cycle arrest
- Dysregulation failed development neoplasia
Cyclin – dependent kinase (CDK)
- Regulate cell cycle progression
- Binary enzymes with catalytic subunits allosterically regulated by cyclin binding
o Cyclin binding to CDK T- loop relieving the substrate binding site of CDK.
o Then T-loop is further displaced by CAK (CDK7) 0 dependent phosphorylation of a threonine within the T- loop
o CDK7 (TF1 1H) which is phosphorylates RNA polymerase II (transcriptional regulations)
o CDK7 (CDK – activating kinase) is constitutively active
o Phosphorylation of the N-terminal Thre/Tyr in the ATP-binding pocket of CDK is inhibitory
o Wee 1 and Myt 1 mediate this inhibitory phosphorylation
o CDC25A, 25B or 25C are phosphatases to ensure CDK activity
▪ Increase activity will removes the N-terminal domains
- In Summary:
o CDK are cell cycle regulators, they have a catalytic subunit that is regulated by the cyclin. The cyclinbinding to
the catalytic subunit of the CDK is part of how the CDK’s get activated
o CDK’s can also be covalently modified in order to get them active
o Cycling binding initiates the activity of the cyclin kinases
o N-terminals can be phosphorylated and in turn can inhibit CDK
- CDK 7 is also called a CAK (cyclin dependent activating kinase)
o Cyclin partner H is
▪ Job is to activate all the CDK’s (CDK 1 CDK 4 & CDK 6) so they can work on their targets
Chapter 11 – Cell Cycle Regulation
Phases
- Phases of cell cycle is divided into 2 sections:
o Interphase G1 S (synthesis) G2 (G – Gap)
o Mitotic M
- G initial (Cell is not replicated) quiescence
o Cells exit the cell cycle due to absence of growth signal or presence of prodifferentiation signal
o Cell cycle arrest
- Dysregulation failed development neoplasia
Cyclin – dependent kinase (CDK)
- Regulate cell cycle progression
- Binary enzymes with catalytic subunits allosterically regulated by cyclin binding
o Cyclin binding to CDK T- loop relieving the substrate binding site of CDK.
o Then T-loop is further displaced by CAK (CDK7) 0 dependent phosphorylation of a threonine within the T- loop
o CDK7 (TF1 1H) which is phosphorylates RNA polymerase II (transcriptional regulations)
o CDK7 (CDK – activating kinase) is constitutively active
o Phosphorylation of the N-terminal Thre/Tyr in the ATP-binding pocket of CDK is inhibitory
o Wee 1 and Myt 1 mediate this inhibitory phosphorylation
o CDC25A, 25B or 25C are phosphatases to ensure CDK activity
▪ Increase activity will removes the N-terminal domains
- In Summary:
o CDK are cell cycle regulators, they have a catalytic subunit that is regulated by the cyclin. The cyclinbinding to
the catalytic subunit of the CDK is part of how the CDK’s get activated
o CDK’s can also be covalently modified in order to get them active
o Cycling binding initiates the activity of the cyclin kinases
o N-terminals can be phosphorylated and in turn can inhibit CDK
- CDK 7 is also called a CAK (cyclin dependent activating kinase)
o Cyclin partner H is
▪ Job is to activate all the CDK’s (CDK 1 CDK 4 & CDK 6) so they can work on their targets
