Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
29 Cards in this Set
- Front
- Back
|
FGFs, TGF-beta, IGFs, Wnts are growth factors that activate and inhibit the cell cycle. Which one's activate/deactive? Are these external or internal factors?
|
Activate: FGF, IGF, Wnts
Deactive: TGF-beta All are external factors |
|
|
There are two types of Internal Factors for cell-cycle control:
|
Early Response Genes and Delayed Response Genes
|
|
|
What are the Early Response Genes?
|
myc, fos
|
|
|
What are the Delayed Response Genes?
|
cdks, cyclins
|
|
|
Name the CDKs and Cyclins. Describe if they have catalytic or regulatory activity. Also, describe their relative levels during the cell cycle.
|
CDKs 1,2,4 are CATALYTIC. Their content is constant during the cell cycle.
Cyclins DEAB are REGULATORY. Their content increases during the cell-cycle |
|
|
What are the four cell-cycle checkpoints:
|
1. G1-Phase
2. S-Phase 3. M-Phase 4. Anaphase |
|
|
How is G1-Phase activated and what happens?
|
Cyclin D binds CDK4 to phosphorylate retinoblastoma (Rb) - releasing its hold in E2F1. E2F1 activates genes for cyclins E&A.
|
|
|
How is S-Phase activated and what happens?
|
Restriction checkpoint (R) is overcome by cyclin E + CDK2. Cyclin A + CDK2 then activates origins of DNA replication. All DNA is duplicated.
|
|
|
How is M-Phase activated and what happens?
|
Cdc25 de-phosphorylates cyclin B+CDK1 --> it enters the nucleus --> phosphorylates protein.
|
|
|
What is Anaphase activated?
|
Activated by Anaphase Promoter Complex (APC) that contains ubiquitin.
|
|
|
G1 Phase has four choices - what are they?
|
1. Senescence (G0)
2. Differentiation (G0) 3. Apoptosis --> cell death 4. Proliferation --> entry into cell-cycle |
|
|
Two major events happen in S-Phase:
|
1. Chromosomes 2N DNA --> 4N DNA
2. Histones are synthesized |
|
|
What two things go on during G2-Phase?
|
1. Preparation for mitosis; centrosome is duplicated (that perpendicular structure with 9 triplet MT arrangement)
2. Hyperphophorylation of histones and non-histone proteins |
|
|
What are the four events in M-Phase.
|
1. Cells round-up
2. Nuclear membrane disintegrates 3. Chromatin condenses (chromosomes) 4.Segregation of chromosomes into "daughter" cells |
|
|
Of the four phases of the cell cycle, which one's duration is variable?
|
G1
|
|
|
As we age, our cells evolve toward ? and cause cancer.
|
Malignancy
|
|
|
What are the five gene categories that are mutated in cancer?
|
1. Proto-oncogenes
2. Tumor suppressor genes 3. Apoptosis genes 4. Genes that induce Cellular Immortality 5. Genes that repair DNA |
|
|
What do proto-oncogenes do? Give examples.
|
They encode proteins that activate the cell-cycle. Cell surface receptors, second messengers, transcription factors, cyclins, and CDKs.
|
|
|
Oncogenes (mutated proto-oncogenes that are now tumor inducing) upregulate or downregulate genes? How
|
Upregulate. Either by overexpressing a gene or increasing a proteins activity
|
|
|
In general, how do Tumor Suppressor Genes work?
|
They inhibit the cell-cylce bc the proteins involved are cell cycle proteins that are deactivated by the tumor suppressors.
|
|
|
Give examples of Tumor Suppressor Genes:
|
p21 (inhibits CDKs 2&4)
p53 (is mutated in more than half of all cancers) Rb binds to E2F BRCA |
|
|
When mutated, how does p53 cause cancer?
|
Normally, p53 activates p21 that inhibit CDKs 2 and 4. Mutated p53 does not do that and the cell is free to continue dividing.
|
|
|
Describe the steps of Apoptosis:
|
1. Macrophages release TNF
2. TNF binds TNFR cell membrane receptor 3. Pro-apoptotic signals induce leakiness of outer cell membrane of Mito 4. CytC escapes cytoplasm 5. CytC activates Caspase, a protease that destroys cell organelles 6. Chromatin fragments (200bp) 7. Blebs are seen on the cell surface and the cell explodes. |
|
|
What does telomerase do?
|
It restores the original length of telomeres after each cell division.
|
|
|
Name an apoptosis gene that is often mutated, causing cancer. Does mutation activate or inhibit apotosis?
|
bcl-2. Activates
|
|
|
How do mutated DNA repair genes cause cancer?
|
Normally, DNA damage causes the cell cycle to stop until repair enzymes fix the damaged DNA. If repair genes are mutated, clones of abnormal cells arise. Eg in colorectal cancer.
|
|
|
What are the three strategies to targeting cancer?
|
1. Targeting metastasis
2. Targeting angiogenesis 3. Targeting specific, sick molecules |
|
|
What is the principle behind the therapy that targets metastasis?
|
Inhibiting proteases that inhibit the spread of cancers that eat through extracellular matrix. TIMPS for tissue inhibitors of metalloproteinases.
|
|
|
What are the two methods used to target specific, sick molecules that cause cancer?
|
Neutralizing monoclonal antibodies and small inhibitory RNAs (siRNA)
|
