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SFM Biochemistry > Cell Cycle & Cell Death > Flashcards

Cell Cycle & Cell Death Flashcards

1
Q

What does autophagy look like?

A

cell membrane blebbing
2 vacuoles
partial chromatin condensation (no nuclear or FNA fragmentation)

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2
Q

What is the biochem result of autophagy?

A

caspase independent, increased lysosomal activity

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3
Q

What does necrosis look like?

A

swelling & rupture of cell membrane
bigger vacuole, mitochondrial swelling
degradation of nuclear chromatin/DNA

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4
Q

What main players target the mito in necrosis?

A

RIP1 & PARP1

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5
Q

What does apoptosis look like?

A

cell membrane blebbing into fragments
fragmentation & shrinkage of cytoplasm
nuclear chromatin condenses & degrades into fragments

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6
Q

What is an important biochem feature of apoptosis?

A

mitochondrial & caspase dependent!

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7
Q

What is the executioner caspase?

A

caspase 3 (some 6 & 7)

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8
Q

What are the initiating caspases?

A

caspases 8, 9, 10

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9
Q

What do Bax & Bak do in apoptosis?

A

stimulated by Bid to release cyt C from mito

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10
Q

What is the role of cyt C in apoptosis?

A

activates caspase 9 apoptosome complex which stimulates caspase 3 (for cell death)

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11
Q

What does mitotic catastrophe look like?

A 
no change in cell membrane
large cytoplasm (giant cell)
nucleus looks like mitosis, some fragmentation
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12
Q

What induces mitotic catastrophe?

A

defects at cycle checkpoints (G2, BUBR at spindle & APC)

hyperamplification of centrosomes
Caspase 2 activation in metaphase

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13
Q

What does senescence look like?

A

no change in cell membrane
flat & increase granules in cytoplasm
distinct heterochromatin structure in nucleus

LOOKS LIKE A FRIED EGG!

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14
Q

What pathways lead to senescence?

A

p53-p21 and p16-Rb

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15
Q

Radiation is effective on cells that…

A

high reproductive activity
long dividing future
morph/function are fixed

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16
Q

How does radiation work?

A

uses energy to break DNA bonds & hydrolyzes water to form damaging free radicals

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17
Q

Chemotherapy

A 
alkylating agents (crosslink DNA)
intercalating agents (structural change in DNA)
antimetabolites (structural analogues of bases, block synthesis of DNA)
mitostatic agents (inhibit tubulin synthesis so affects spindle)
platinum derivatives (role in DNA binding)
18
Q

Antitumor antibiotics

A

inhibit topoisomerase II, intercalation

19
Q

Antimetabolites

A

inhibit enzymes, introduce false substances into DNA, inhibit spindle division

20
Q

Enzymes in chemo

A

enzymatic cleave of asparagin

21
Q

Other chemotherapeutics

A

work via crosslinking DNA changes or destroying enzymes

22
Q

Tumor suppressor genes (3)

A

p53 (at cell cycle checkpoints, G1 to S and G2 to M)

p16INK4A (gene mutation & deletion, CpG methylation)

Rb

23
Q

Inheritance of tumor suppressor genes?

A

recessive, normal activity is to repress growth

need to lose function in both genes to lose function

24
Q

Oncogenes-how are they activated?

A

by mutations or overexpression

25
Q

How do oncogenes act?

A

dominant in action….gain of function mutation leads to overexpression or unregulated activity (only need mutation of 1 allele to get effect!)

26
Q

Viral Oncogenes

A

oncogenic element carried by retroviruses, integrate into host DNA & use machinery to replicate

27
Q

Name 7 Viral Oncogenes

A 
Henry (Herpesvirus)
And (Adenovirus)
Hershey (Hepadnavirus)
Prefer (Polyomavirus)
Protein (Papillomavirus)
Flavored (Falvivirus)
Reese's (Retroviruses)
28
Q

Hallmarks of Cancer

A 
I (inflammation)
A (angiogenesis)
M (metastasis)
G (genomic instability)
R (gROwth inhibitory signals insensitive)
E (evade cell death)
A (avoid immune destruction)
S (self-sufficient growth)
E (energy metabolism change)
R (replication potential unlimited)
29
Q

What helps move G1 to S?

A

cycD w/ CDK4,6

phosphorylation of Rb-E2F

30
Q

What helps move S to G2?

A

CycE, CDK2

CycA, CDK2

31
Q

What helps move G2 to M?

A

CycB, CDK1

32
Q

Role of Cdc25 phosphatases

A

act on CDK1 to promote G1 to S and G2 to M transitions

33
Q

Types of CKIs

A

INK & Kip/Cip

34
Q

What does p16INK inhibit?

A

cycD/CDK4, 6

35
Q

What do p27, p21, p57 inhibit?

A

cyc A & E w/ CDK2
CDC2

cell cycle arrest

36
Q

What does p21 inhibit & how is it activated?

A

inhibits most CDK-cyc complexes

activated by p53, cell cycle arrest post DNA damage

37
Q

What does p16INK inhibit & how activated?

A

blocks CDK4, 6

activated by Rb, leads to cell cycle arrest in senescence

38
Q

Where is the cell cycle restriction point?

A

from G1 to S, where cells commit to divide

39
Q

Where are the cell cycle checkpoints?

A

from G1 to S, from G2 to M

40
Q

What are the major players in G1 checkpoint?

A

DNA damage activates ATM that stimulates p53, p21

41
Q

What are the major players in G2 checkpoint?

A

DNA damage activates ATM (works thru p53, p21) and activates ATR (targets Chk1,2 to move Cdc25 out of nucleus)

SFM Biochemistry (2 decks)

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