7 - Regulation of Cell Proliferation and Genome Stability

?
Describe Whole animal cloning and induced pluripotent stem cells (iPSCs)
Take an unfertilised egg and destroy the nucleus using UV light-> take the nucleus frm the skin cells od an adult from in a pipette-> inject the nucleus from the frog into the egg-> normal blastula formed -> tadpole
1 of 11
what happens differently to normal and cancerous cells traversing the cell cycle
normal: contact inhibition (signaling from cadherin-based adherens junctions stops cells from cycling. They arrest in G1/ Cncer cells: transformed cells continue to cell cycle
2 of 11
what needs to happen to form a fully metastatic tumour?
cell cyce de-regulated, self sufficiency in growth signals, insensitivity to antigrowth signals, evasion of apoptosis, limitless replictive potential, tissue invasion and metastasis, sustained angiongenesis (genetic factors&age&environ. factors)
3 of 11
How does a tumour evolve?
begins with a mutation that provides a cell with a competitive advantage e.g.by enabling the cell to proliferate more rapidly than its neighbors->descendants of mutant acquire additional mutations that allow them to overcome proliferation barriers
4 of 11
What is aneuploidy?
Aneuploidy (abnormal number of chromosomes) and genome instability is characteristic of aggressive human cancer cells
5 of 11
What are the 4 major transitions in the cell cycle? How are the controlled?
Restriction Point (in vertebrates) or START (in yeast)/ The G1/S transition/ The G2/M transition/ Metaphase-to-anaphase (sister chromatid separation) - controlled by Cyclin-Cdk activation and inactivation
6 of 11
What does Cdk activating kinase (CAK) do?
aids construction of Cdk / Cyclin complexes,repositions T loop away from active site so kinase can now transfer phosphate to target proteins(catalytic activity of complex is aided by phosphorylation of T loop by CAK
7 of 11
What do CDK inhibitors (CDKI) do?
bind&inhibit Cdk /Cyclin complexes(CDKIs(p16INK4)can block Cyclin D association to Cdk4, whereas others(p27)can block ATP binding by the Cdk2 /Cyclin A complex where others(p21)prevent substrate binding by Cdk1 / Cyclin and Cdk2 / Cyclin complexes
8 of 11
Describe Control of p27 (CDKI) proteolysis by SCF (Skp2, Cullin and F box) ubiquitin ligase
The Cdk inhibitor (p27) is only recognised by the F box recognition protein component of the SCF E3 ubiquitin ligase when it is phosphorylated. This triggers poly-ubiquitination of the Cdk inhibitor which targets it for destruction by the proteasome
9 of 11
Five ways Cyclin / Cdk complexes can be activated?
Transc&transl of cyclins/Phosphorylation of T loop of Cdk by CAK/Proteolytic destruction of Cdk inhibitor proteins by SCF ubiquitin ligase/Dephosof Tyrosine 15 in catalytic site of Cdk1 by Cdc25 phosphatase/Intracellular re-localisation of cyclin/CDK
10 of 11
Five ways Cyclin / Cdk complexes can be inactivated?
association w Cdk inhibitor-blocks:interaction of Cdk4 w cyclin D/ATP binding by Cdk2/substrate binding by both Cdk1&Cdk2. Tyrosine phos of Tyr15 in Cdk1 by Wee1 kinase. Proteolytic destruction of Cyclin following its ubiquitination by SCForAPC/C E3
11 of 11

Other cards in this set

Card 2

Front

what happens differently to normal and cancerous cells traversing the cell cycle

Back

normal: contact inhibition (signaling from cadherin-based adherens junctions stops cells from cycling. They arrest in G1/ Cncer cells: transformed cells continue to cell cycle

Card 3

Front

what needs to happen to form a fully metastatic tumour?

Back

Preview of the front of card 3

Card 4

Front

How does a tumour evolve?

Back

Preview of the front of card 4

Card 5

Front

What is aneuploidy?

Back

Preview of the front of card 5
View more cards

Comments

No comments have yet been made

Similar Biology resources:

See all Biology resources »See all MCB resources »