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Exam 2 > Cell Cycle > Flashcards

Cell Cycle Flashcards

1
Q

prophase

A

DNA disentangled and condensed

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2
Q

metaphase

A

chromosomes line up at equator

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3
Q

anaphase

A

separation of chromosomes

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4
Q

telophase

A

chromosomes packed into new nuclei

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5
Q

cytokinesis

A

cytoplasm division

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6
Q

Interphase

A

G1 + S + G2

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7
Q

Metaphase

A

mitosis and cytokinesis

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8
Q

G1 phase

A

most cells are here! most cells have 2n chromosomes (4n after replication)

in dividing cells

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9
Q

G0 phase

A

quiescent cells - not dividing but can be stimulated to divide (enter cell cycle) if enough nutrients etc

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10
Q

post-mitotic cells

A

incapable of cell divisions

i.e. neurons - made synaptic connections - lost when cell divides

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11
Q

R checkpoint

A

right before G1/S - beginning cell replication

enter cell cycle and leave G0

is environment favorable?

don’t want to divide if the cells can’t grow

once pass R check pt - have to finish unless catastrophe

cells check GROWTH conditions before commiting - before: how much GF signalling is there? after: doesn’t matter

NOT G1/S

only unexpected disasters can stop

stays in G0 if not enough extracelular signals to proceed through R

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12
Q

G2/M checkpoint

A

before cells enter mitosis

is environment favorable?

is all DNA replicated?

crisis?

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13
Q

metaphase to anaphase checkpoint

A

trigger anaphase and proceed to cytokinsesis

are all chromosomes attached to the spindle?

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14
Q

CDKs

A

inactive unless bound to cyclin

cyclin dependent kinase

activated to start and inactivated to stop

regulated by transcription, phosphorylation, protein degredation

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15
Q

G1(R)-CDK

A

Cyclin D, CDK4 and CDK6

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16
Q

G1-S CDK

A

Cyclin E, CDK2

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17
Q

S-CDK

A

Cyclin A, CDK2 and CDK1

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18
Q

G2/M-CDK

A

Cyclin B, CDK1

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19
Q

Cyclin-CDK inhibitors

A

p27, p21 - binds to cyclin cdk and inactivates it

i.e. if UV DNA damage - p53 (tumor suppressor) is activated –> nucleus –> transcribes p21 –> binds to G1/S CDK and S-CDK - inactivates it

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20
Q

CDK phosphorylation

A

to signal completion of S phase!

if fails - premature M entry - cell has too much DNA

During S:

wee1 phosphorylates and inhibits CDK1 activity

at G2/M:

Cdc25 removes phosphatases and activates cdk1

21
Q

Cyclin levels oscillation

A
22
Q

how do cells progress through the R phase?

A

cyclin D!

Wnt/beta catenin stimulate cyclin D transcription

APC blocks Wnt - if no APC - a lot of Wnt - lots of growth and deregulation (colon cancer)

other growth signals affect transcription of Cyclin D

23
Q

Progression from Cyclin D to Cyclin E

A

from R phase to G1/S phase

E2F is transcription factor for Cyclin E

pRB - bound to E2F so it’s supporessed

Cyclin D is activated by GF –> phosphorylate Rb –> Rb drops E2F –> E2F goes into nucleus to stim Cyclin E synthesis

initiates DNA replication

if mutation in Rb –> cells always entering cell cycle even if not ready

24
Q

Cyclin E - how does it trigger?

A

prereplicative complexes put on DNA in G1

Cyclin E - phosphorylates complexes so they are degraded! - preinitiation can bind and synthesis can occur -

don’t want more than 1 round of DNA synthesis

triggers DNA replication activity

DNA syn can’t be triggered after S phase because prereplicative complexes are gone

25
Q

ubiquitin system

A

E1, E2, E3

E1 - uses ATP to make a high E bond, ubiquitin activating enzyme, E1 + ATP binds to upiquitin

E2- ubiquitin carrier, E1 transferes activated ubiquitin, conjugation protein

E3 - E2 complexes with E3, recognizes which proteins need ubiquitin - puts ubiquitin on it - repeats until there is a chain and rounds it up in proteosome - degrades

if no E1 - stops cell cycle

26
Q

SFC complex

A

multisubunit ubiquitin ligase

Skp, Cul, F-box

F-box = specificity - interchangeable, belongs to specific target proteins and brings them close to E2 for ubiquitin tag

Rbx = E2

F-box - mostly degrades phosphoproteins, cyclins and CDKs phosphorylate

allows substrates to be degraded at specific phases (i.e. Cyclin E is degraded!)

27
Q

APC - Anaphase Promoting Complex

A

E3 ubiquitin ligase

targets cell cycle proteins for degredation via ubiquitin by proteosome

triggers transition from metaphase to anaphase by triggering proteins for degredation

CDC20 - activates APC + ubiquitin + E2 and E3, polyubiquitination chain on G2/M cyclin (cyclin B) -degrade in proteasome!

ALSO:

cohesin holds chromosomes together - activated APC cleaves securin from separase - separace can cleave cohesin and allow the chromosomes to separate

28
Q

Growth Factor signalling affects?

A

Cyclin D

29
Q

Degredation by proteasome affects?

A

Cyclin E (ubiquitin), Cyclin B (apc/ubiquitin)

also sep chromosomes in Mphase

30
Q

characteristics of apoptosis

A

active - proteins are made

cells shrink - use E

intact membrane

nuclear condensation

phagocytosis of cell corpse

31
Q

characteristics of necrosis

A

passive! damaged

cells swell

membranes rupture

inflammatory response

32
Q

TUNEL

A

mark to see where DNA is fragmenting

33
Q

casparases

A

executioners of apoptosis

cystein in the active site but cut at D (aspartic acid)

active only when cells need to die

cascade - 1 molecule of active initiator caspacse cuts a ton of proteins including executioner caspases

34
Q

CAD

A

DNAase

ICAD - inhibits CAD and is normally bound - ICAD is cleaved by effector caspase and CAD can cleave DNA

35
Q

extrinisic pway

A

apoptosis triggered from the outside

Fas ligand - binds to Fas death receptor - Fas R trimerize –> Fadd adaptor proteins bind –> procaspases bind –> initator caspases cut each other and gain activity –> cut self to increase activity and cut executioners for cascade

36
Q

caspase 8

A

used in intrinsic pway

form DISC complex w FADD adaptor proteins and Fas death receptor

37
Q

intrinic pathway

A

mitochondria –> release cytochrome c from intermembrane space –> activates Apaf1 and hydrolysis of ATP to ADP –> conf change –> all bind together to form apoptosome –> recruit procaspase 9 –> acleave and activate and cleave executioner procaspases

38
Q

caspase 9

A

caspase activated by intrinsic pway

39
Q

Bcl2

A

4 BH domains - 1, 2, 3, 4

anti-apoptosis

regulates cytochrome c release

oncogene - prevents cells from dying!

40
Q

BH123

A

pro-apoptotic - 3 BH domains

41
Q

BH3-only protein

A

pro-apoptotic - when activated - inhibits Blc-2 (antiapoptotic) an tips balance toward apoptosis

BH123 protein aggregate and make a pore so mitochondria proteins leave

42
Q

ABT737

A

Bcl-2 inhibitor

potential anti-cancer drug

acts like BH3-only!

Bcl-2 is increased in cancer cells - keeps them alive, ABT looks like BH-3 and neutralizes Bcl2 which allows cells to die

43
Q

IAP

A

inhibitor of apoptosis proteins - bind to caspaces to inactivate

tumor - increased IAP! blocks cell death - bind and block unnecesary caspase activation

anti-IAP - blocks IAP so cells can die

44
Q

Smac

A

IAP antagonist

IAPs binding to caspases to inhibit apoptosis

Smac inactivates IAPs so there is apoptosis!

cancer treatments

45
Q

p53 and apoptosis

A

p53 can induce BH3 only protein transcriptions –> apoptosis

46
Q

summary of extrinsic apoptotic pway

A
47
Q

summary of intrinsic apoptotic pway

A
48
Q

TNF alpha

A

hits TNF receptor –> death domain –> caspases –> apoptosis OR

kinase signalling pway –> necrosis –> recruits alarmins and immune cells (inflammation)

viruses have many ways to avoid apoptosis! body does necrosis and recruitsimmune cells

induced by infection!

49
Q

MLKL

A

pseudokinase

kinase signalling pway induced by TNFalpha

inserts into membrane and punctures holes so membrane ruptures- TNFalpha induced necrosis

Exam 2 (8 decks)

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