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COM SFM > Cell Cycle, Cancer, Cell Death > Flashcards

Cell Cycle, Cancer, Cell Death Flashcards

1
Q

G1 cyclins include

A

C, D1

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2
Q

S cyclins include

A

Cyclin A

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3
Q

G2/M cyclins include

A

B 1-2

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4
Q

Cyclin H

A

Constitutive expression

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5
Q

Cdk4/Cdk6

A

Binds with cyclin D
Phosphorylation of retinoblastoma susceptibility protein (pRb) in G1
Triggers passage of the restriction point, and cyclin E synthesis in some cells

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6
Q

Cdk2

A

Binds with cyclin E and A

Triggers G1–>S transition

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7
Q

Cdk1

A

Binds with Cyclin B, triggers G2–>M transition

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8
Q

Cdk activation

A

Cdks have 3 phosphate binding sites. Phosphorylation of one of these sites activates it, while phosphorylation of the other 2 sites inactivates it.
The complex must be phosphorylated on the first site, and dephosphorylated (by protein phosphatase cdc25) on the other two sites to be active

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9
Q

Cdc25A phosphatase

A

Acts on Cdk1, Cdk2

Promotes G1–>S and G2–>M transitions

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10
Q

Cdc25B phosphatase

A

Acts on Cdk1

Promotes G2–>M transition

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11
Q

Cdc25C phosphatase

A

Acts on Cdk1
Promotes G2–>M transition
Dephosphorylates Cdk1 complexed to cyclins A/B

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12
Q

CKI: p21

A

Induced by p53 tumor suppressor. Cell cycle arrest after DNA damage. Binds most Cdk-cyclin complexes

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13
Q

CKI: p27

A

Cell cycle arrest in response to growth suppressors like TGF-b
Binds Most Cdk cyclin complexes

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14
Q

INK4: p16

A

Cooperates with retinoblastoma susceptibility protein pRb in growth regulation. Cell cycle arrest in senescence.

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15
Q

What are the common substrates for all INK4 cyclin inhibitors

A

Cdk4 and Cdk6

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16
Q

What is the predominant cyclin during G1 phase

A

Nuclear D1

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17
Q

Explain cyclin/Cdk activity during the G1/S transition

A

E-CDK2 complexes hyperphosphorylate pRb, which liberates E2F transcription factors from pRb control, enabling E2Fs to trigger increased transcription of the cyclin E and E2F1 genes. This leads to synthesis of more cyclin E and formation of more E-CDK2 complexes, which then amplify the process by hyperphosphorylating more pRb. E2F1 amplifies its own activity

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18
Q

G2/M transition cyclin/CDK activity

A

Activation of CDK1/Cyclin B at the G2/M boundary by Cdc25 phosphatase. CDK1/Cyclin B translocate to nucleus and initiate spindle assembly. Activated anaphase promoting complex APC destroy CDK1, freeing cyclin B for degradation

19
Q

What happens if DNA damage is detected during G1 checkpoint (fast and slow pathways)

A

Slow pathway involves stabilization of p53 and upregulation of p21 which inhibits cyclin/Cdk complexes
Fast pathway activates Chk2 and inactivates Cdc25 so that inhibitory phosphates of Cyclin E/Cdk2 complexes are not removed

20
Q

p16 function during G1 checkpoint damage

A

p16 prevents pRb phosphorylation via inhibition of Cdk4/Cdk6 kinases

21
Q

What protein is responsible for activating the inhibitory proteins such as p53 and Chk2

A

ATM

22
Q

Is the initiation step of carcinogenesis reversible

A

No

23
Q

Is the promotion step of carcinogenesis reversible

A

Only in its early stages

24
Q

Initiation vs promotion

A

Initiation is the original even that causes a change in cellular DNA sequence
Promotion involves gene activation or repression such that the latent phenotype of the initiated cell becomes expressed through cellular selection and clonal expansion

25
Q

Progression of carcinogenesis

A

Involves further complex irreversible genetic changes such as translocations, deletions, gene amplifications.
Results in the conversion of benign tumors into malignant neoplasms

26
Q

Retrovirus type 1- transducing viruses

A

Cellular oncogene is carried in retrovirus

27
Q

Retrovirus type 2- non transducing viruses

A

Cellular oncogene activated by proviral insertion/integration

28
Q

Retrovirus type 3 non transducing long latency viruses

A

Retroviral transactivating protein disrupting normal regulation of cellular transcription

29
Q

Retrovirus type 4- retroviruses that contain an envelope that signals

A

Inappropriate cellular signaling resulting from viral envelope/cell receptor interaction (acts like mitogen)

30
Q

Tumor suppressor genes are all what type of proteins

A

Cell cycle regulatory proteins such as p53, Rb, p16

31
Q

Radiation is most effective on cells which have

A

Reproductive activity

Longer dividing future ahead

32
Q

Alkylating agents

A

Denature DNA macromolecules

33
Q

Intercalating agents

A

Intercalate b/w two bases, inducing structural/functional changes- capable of breaking DNA molecuels

34
Q

Antimetabolites

A

Structural analogs of purines/pyrimidines- block the synthesis of corresponding bases

35
Q

Mitostatic agents

A

Inhibit tubulin synthesis- cell spindle poisons

36
Q

Platinum derivatives

A

Bind DNA

37
Q

Main proteins involved in necrosis

A

Receptor-interacting protein 1 RIP1

Poly (ADP-ribose) polymerase 1 PARP-1

38
Q

Necrosis mechanism

A 
Ca2+ overload
Mitochondrial uncoupling
Increased O2 consumption and excess ROS production
ATP depletion
No caspases involved
39
Q

Does apoptosis cause inflammation

A

No, necrosis does

40
Q

Apoptosis mechanisms

A

ATM/p53 activation by DNA damage
Death receptors- Fas, TNF- Caspase 8 mediated
Sphyngomyelinase activation–>ceramide formed
Mitochondrial damage mediated by ceramide

41
Q

Bax/Bak, BH3 only function

A

Bax/Bak induce permeabilization by forming pores
BH3-only family members activate Bax/Bak by binding/inhibiting anti-apoptotic Bcl-2 proteins and directly bind Bax/Bak and activate them (apoptosis)

42
Q

Major differences b/w autophagy and apoptosis

A

No nuclear or DNA fragmentation

43
Q

Autophagy quick overview

A

Release of beclin from Bcl-2, which can then form the PI3K that contributes to formation of nucleation complex.
Two independent conjugation cascades mediated by LC3-II and Atg5-12
Transmembrane Atg9 delivers additional membranes

44
Q

Mitotic catastrophe

A

Caused by aberrant mitosis
Mainly associated with deficiencies in cell cycle checkpoints
-Involves formation of giant cell with large cytoplasm, no change in membrane
Formation of nuclear envelopes around clusters of mis-segregated chromosomes
Abnormal Cdk1/Cyclin B activation

COM SFM (31 decks)

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