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MCB 2 Block 4 > Cell Cycle > Flashcards

Cell Cycle Flashcards

1
Q

G1 info

A

Period respondent to mitogenic GFs and TGF-B

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2
Q

R point gen

A

In G1 and is point of no return

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3
Q

Interphase

A

Chromosome duplication and consists of G1, S, G2

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4
Q

Prophase

A

Chromo condensation

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5
Q

Prometaphase

A

Nuc envelope breakdown

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6
Q

Metaphase

A

Chromo align at metaphase plate

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7
Q

Anaphase A

A

Chromo movement to poles (Dyenin motor)

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8
Q

Anaphase B

A

Spindle pole seperation

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9
Q

Telophase

A

Nuc envelope reassemble

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10
Q

Cytokinesis

A

Contractile ring forms cleavage furrow

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11
Q

Restriction point

A

Related to presence or deprivation of mitogen. GFs coax G0 to G1. Commital step

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12
Q

G1

A

Synth mRNA and proteins, cell growth size

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13
Q

S

A

DNA replication- duplicate chromosomes, polyploidy same

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14
Q

G2

A

Cell growth

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15
Q

G1 to S

A

after R point. DNA dmg checkpoint for entrance to S

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16
Q

S phase check

A

DNA dmg checkpoint, halted if genome damaged

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17
Q

G2 to M

A

Entrance blocked if DNA rep not complete

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18
Q

M to Anaphase

A

inhibited if chromatids not assembled in mitotic spindles

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19
Q

G1 reg

A

CDK4,6/Cyclin D.

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20
Q

Inducer of S phase

A

SCF = ubiq-protein ligase

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21
Q

S phase role of cyclins

A

S phase cyclin-cdk induces DNA rep

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22
Q

G2 cyclin role

A

M cyclin-cdk induces early mitotic steps = cdk1/Cyclin B

23
Q

M phase reg

A

APC/C and Cdc14 phos = late mitosis

24
Q

Proteins that regulate cell cycle

A

Cyclins and CDK

25
Q

Cyclins

A

regulate cdk activity. Levels are cyclic, rapidly synth and degraded. Bind to activated cdks

26
Q

Cdk

A

Cyclin dependent kinases are proteins which phos other proteins. Dependent on cyclin binding for kinase activity. Constant lvls and act at checkpoints. After use, cyclin is degraded after detached.

27
Q

G1 to R complex

A

Cyclin D-CDK 4,6

28
Q

G1 to S complex

A

Cyclin E-cdk2

29
Q

S to G2 complex

A

Cyclin A-cdk2

30
Q

G2 to M complex

A

Cyclin B- cdk1

31
Q

Draw G1 to S path

A

On paper

32
Q

Cyclin D

A

Only in G1, rqrd for passage through R point. Made at start of G1 by GF, binds and activates CDK4/6. Degraded at end of G1

33
Q

Cyclin E

A

Mid G1: CyclinD/cdk4,6 phos Rb releasing E2f - Cyclin E release and binding to cdk2.

34
Q

DNA dmg and G1

A

Inhibit cyclin D first to stop progression past R point then Cyclin E

35
Q

Normal G1

A

CyclinD/cdk4,6 phos Rb which breaks up pRb-E2F complex. E2F activates genes involved in S phase (DNA poly and cyclin E). CyclinE/Cdk 2 further activate Rb for more E2F (pos feedback)

36
Q

Inhib cell cycle

A

Hypophos of Rb sequesters E2F TF therefore inhibiting cell progression

37
Q

Cdk Inhibitors

A

INK4 (inhibs cdk4) binds and inhibs cyclinD/cdk4 = R point halt = p15 and p16

CIP (cdk inhib protein) family bind and inhibt all cyclin-cdk complexes = p21

38
Q

TGF-B and cell cycle

A

Modulates levels of cdk inhibitors, strongly induces p15 (DNA dmg for p21). important for expression of p15 and p16 = pro-apop.

39
Q

TGF-B pathway

A

TGF-B to TGFB2R dimerizes with and phosphorylates TGFB1 which phosphorylates SMAD2/3 which activate SMAD4 which goes to nuc and complexes with TFs leading to INKs p15 and p16 therefore preventing phos of Rb

40
Q

HNPCC and TGF-B

A

slip and frameshift mutations assoc with TGFBR and assoc with loss of SMADs

41
Q

Pancreatic carcinoma

A

loss of SMAD4 (loss of p15 and p16)

42
Q

p53 general

A

kept at low levels by mdm2 (binds p53 in nucleus and ubiqs it). Excess mdm2 inhibits p53 and is often overexpressed in cancers. DNA dmg induces kinases which phos p53 (kinase = ATM) therefore blocking mdm2 binding therefore it is free from degradation leading to accumulation and transC of p21

43
Q

ATM mutations

A

poor response to gamma radiation

44
Q

p14ARF

A

tumor supp gene. Inhibits mdm2 and leads to p53 accumulation without need of phos. ARF sequesters mdm2 in nucleus. ARF responds to increased levels of E2F (ex: adenovirus, MYC, onceogenes, RAS)

45
Q

Role of p53 and cancers

A

Inhibits oncogene induced transformations, inhbits tumor growth and progression, removes cells with DNA dmg, leads to apoptosis, transC BAX to BID (BAX needs to homodimerize to form pores [inhib by bcl-2= heterodimer] leading to cyt-C leak and apop).

46
Q

G2 to M major

A

Cdk1/Cyclin B (M cyclin = MPF) enables G2 to M. Complex initially activated by phosphorylating CAK (cdk activating kinase). If DNA not completly replicated, signal sent to inhib cdk1/cyclin B.

47
Q

Inhib of G2 to M

A

by Wee1 kinase stops MPF activation by another phos so it wins over CAK

48
Q

Reg of G2 to M

A

Phosphatase Cdc25 activated by phos, removes Wee1 inhibiting phosphate therefore cyclinB/cdk1 active leading to nuc envelope breakdown, chromo condensation and bipolar spindle formation.

49
Q

Nuc envelope breakdown

A

By lamin phosphorylation (MPF induces)

50
Q

Anaphase promoting complex

A

M-cdk prepares duplicated chromosomes for separation: induce spindle form and chromo attach. APC induces chromatid separation at spindle attach checkpoint if everything is lined up.

51
Q

APC activation

A

Activated by cdc20 and M-cdk. APC activates seperase which promotes progression into anaphase by seperating chromatids

52
Q

Spindle attach checkpoint

A

Blocks metaphase-anaphase transition if kinetechores not properly aligned.

53
Q

Kinetechore sensor

A

MAD2, activated if chromo not attached to spindle and division blocked at metaphase. Inhibits APC activation if not attached to kinetechore

MCB 2 Block 4 (10 decks)

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