Cell Cycle, Apoptosis, and Cancer

Question 1

G1

Answer 1

RNA and protein synthesis occur in response to GFs.

Question 2

S

Answer 2

DNA is replicated. RNA and proteins continue to be syn

Question 3

G2

Answer 3

Integrity of DNA is checked. RNA and protein synthesis continue.

Question 4

M

Answer 4

Mitosis

Question 5

G0

Answer 5

Cells have exited the cell cycle; they are not growing or dividing.

Question 6

Restriction Point

Answer 6

When GFs are limited, cell cycle is stopped 2 hrs. After cells pass through, they are “GF independent”.

Question 7

G1 checkpoint

Answer 7

Verifies integrity of DNA.

Question 8

G2 checkpoint

Answer 8

Verifies completeness of genome.

Question 9

Metaphase checkpoint

Answer 9

Ensures attachment of chromosomes at mitotic spindle.

Question 10

Permanent cell

Answer 10

Remain in G0. Ex: cardiac cells, neurons, RBCs.

Question 11

Stable cells

Answer 11

Can reenter G0 w/ help of GFs. Ex: hepatocytes, epithelial cells of renal tubules.

Question 12

Labile cells

Answer 12

Never enter cell cycle. Constantly dividing. Ex: hair, skin, gut epithelium.

Question 13

Cyclin

Answer 13

Protein that partially activates CDKs and direct them to target to phosphorylate. Levels of cyclins can vary during the cell cycle.

Question 14

CAK

Answer 14

Fully activate CDKs with help of cyclins.

Question 15

Cyclin D (G1)

Answer 15

Helps cells pass through the restriction point in late G1 phase.
Complexes: cyclin D-CDK4, cyclin D-CDK6.

Question 16

Cyclin E (G1/S)

Answer 16

Helps cells at end of G1 to commit to DNA replication and enter S phase.
Complex: cyclin E-CDK2

Question 17

Cyclin A (S)

Answer 17

Necessary for initiation of DNA synthesis.

Complex: cyclin A-CDK2.

Question 18

Cyclins A and B (M)

Answer 18

Necessary for nuclear division.

Complexes: cyclin A-CDK1, cyclin B-CDK1

Question 19

Inhibition of CDK (2 main inhibitors)

Answer 19

WEE1 kinase adds another P to CDK, rendering it inactive.
p27: causes conformational change, rendering it inactive. Regulates in G1 to S transition.
Both affect CDK’s kinase activity.

Question 20

CAK and the T loop

Answer 20

T loop blocks active site, but is displaced when cyclin binds. CAK then phosphoryates T loop and fully activates enzyme.

Question 21

WEE1 kinase

Answer 21

Phosphorylates roof site inhibiting CDK.

Question 22

CDC25

Answer 22

Dephosphorylates roof site, activating CDK.

Question 23

APC/C (cytosome)

Answer 23

Regulates progression from metaphase to anaphase via degredation. Member of ubiquitin ligase family.

Question 24

p53

Answer 24

Transcription factor. Normally degraded by proteosome in quiescent cells.

Question 25

p53 affect on damaged DNA

Answer 25

p53 is phosphorylated and activates stimulates transcription of genes that inhibit progression of the cell cycle. (CKI inhibit cyclin-CDK complex from binding of p21).

Question 26

p53 affect on undamaged DNA

Answer 26

Rapidly degraded by MDM2, a ubiquitin ligase.

Question 27

p21

Answer 27

A CKI. The major target of p53 activity.

Question 28

Caspase activation

Answer 28

Exist as a zymogen. Must be activated to become active. Forms a small and large subunit.

Question 29

APAF1 and the Intrinsic pathway

Answer 29

Actuve BAX self-aggregates, release cyto-c. Cyto-c and APAF1 form apoptosome, which activates caspace-9 leading to apoptosis.

Question 30

Proto-oncogene

Answer 30

Encode proteins that encourage cell growth and division.

Question 31

Oncogene

Answer 31

Mutated version of proto-oncogene causing increase production of altered proteins (can contribute cancer growth).

Question 32

Hereditary form of Rb

Answer 32

Mutation or deletion of Rb1 (pt is heterozygous). cells are predispositioned for cancer. Somatic mutations eliminate last “good” copy (loss of heterozygosity).

Question 33

Sporatic form of Rb

Answer 33

Non heridary. Requires mutation of both RB1 (2 independent mutations).

Question 34

HER2

Answer 34

Proto-oncogene. Mutation results in overexpression. Changes Val to Glu. Receptors dimerize and TK activity is increased (doesn’t require ligand). Observed in many breast cancers.

Question 35

Tumor suppressors

Answer 35

Repress cell cycle, promote apoptosis.

Question 36

Metastasis suppressors

Answer 36

Prevents tumor cells from dispersing by blocking loss-of-contact inhibition.

Question 37

Herceptin

Answer 37

Monoclonal Ab (mAb) directed against HER2/NEU epidermal GF (EGF), which has been expressed in breast cancers.

Question 38

Gleevec

Answer 38

Binds to ABL tyrosine inase and inhibits its activity. Used for chronic myelogenous leukemia.

Question 39

Myc

Answer 39

Helps activate CDK

Question 40

BCL-2

Answer 40

Anti apoptotic