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Flashcards in Cell Cycle Deck (70):
1

G1

growth phase before DNA synthesis

2

G2

second growth period that's before cell division

3

M phase

cell division

4

G1/S checkpoint

start or restriction point. cell tells if conditions are faborable for division

5

G2/M chekcpoint

make sure all DNA has been replicated and the environment is still favorable for division

6

metaphase/anaphase transition point

all chromosomes are evalutated to ensure that they are attached to mitotic spindle

7

DNA damage checkpoint

functions throughout the cell cycle, detects damage ti DBA

8

CDKs

enzymes that help progress through the cell cycle

9

M phase Cyclin/CDK complexs

Cyclin A/CDK1
Cyclin B/CDK1

10

Mid G1 cyclin/CDK complexes

cyclin D/CDK4
Cyclin D/ CDK6

11

late G1 cyclin.CDK complexes

Cyclin E/CDK2

12

S cylin CDK compelx

cyclin A/CDK2

13

how are cyclins degraded

ubiquitin-dependent proteolysis

14

how is cyclin B ubiquinited

anaphase promoting complex

15

mitogenic signals

tissue-specific growth factors
required to stimulate cell growth and dvision

16

what phase are most differentiated cell in

G0

17

in general what do interactions between cell and ECM do

promote cell division

18

in general what do interactions between neighboring cells do

inhibit cell division

19

contract inhibition

two neighboring cells contact each other and inhibit cell dibision

20

early-response genes

genes transcribed within a few minutes of addition of gorwth factor to a cell in G0

21

what is a key player amoung the early-response genes

transcription factor c-FOs

22

function of c-fos

stimulate transcripition of delayed response genes

23

what do the recceptors for gorwth facotors contain

intrinsic tyrosine kinase activitry

24

what does ligand binding to receptors for growth factors tirgger

recpetor dimerixation, autophosphorylation of tyrosine residues within the recpetor

25

how do most growth factors stimulate transcription of the gene encording c-fos

MAP kinase cascade

26

how does MAP kinase cascade start

GRB2 binds to phosphotyrosine residues within the activated receptor.

27

what happesn after GRB2 bindws

binds to SOs, brining it into the cell membrane

28

what happens when Sos is in the cell membrane

activates Ras

29

what does active Ras do

activates Raf

30

what does activated Raf do

activate MAP kinase kinase

31

what does MAP kinase kinase do

activate MAP kinase

32

what does MAP kinase do

stimulate c-Fos transcirption

33

what happens after the cell passes the restrition point

it can go through the S, G2, M phases of cell cycle in the absense of growth factors

34

what is the key target for cycline D-CDK4/6 compelx

retinoblastoma protein (RB)

35

fucntion of Rb

binds to E2F proteins

36

functino of E2F proteins

transcription factors, stimulate transciriiption of cyclin E and cyclin A and CDK2.

37

when E2F is bound to Rb how does it function

as a repressor instead of activator

38

when cyclin E-CDK2 is present, Rb phosporylation because what

independt of cyclin D-CDK4.6

39

INK4

growth inhibitory factors taht compete with cyclin D for binding to CDK4/6

40

p27KIP1

small protein that forms a compelx with cyclin A-CDK2,

41

what is the most important driver of events leading up to mitosis

CDK1

42

when is cyclin A present

from early S phase

43

when does cyclin B synthesisi ahppen

late in S phase, incrases through G2

44

when is the peak levle of cyclin B

metaphase of mitosis

45

the cyclin/CDK1 complexes are held in an inactivate state until when

DNA replication is completed

46

what triggers activation of anaphase promoting complex

appropriate arrangement of chromosomes and attachment to mitotic spindle in metaphase

47

how does protein dephosphorylation affect the effects of cyclin/CDK1 actiity

reverse

48

ATM

detects replication forks, activates another kinase that preents dephosphorylation and activation of cyclin/CDK1 complexes needed to enter mitosis

49

when is ATM active

as long as replication forks are present

50

what is anaphase depend ont

association of all chromosomes with the spindle

51

what activates ATR

DNA damage caused by UV light and certain drugs

52

activation of ATM/ATR does what

inhbiits phosphateaases tha tnormally dephosphorylate and activate cycline/CDK2 and cyclin/CDK1 compelxes

53

activation of ATM/ATR results in phosphorylation of waht protein

p53

54

p53

transcritpion factor that is normally unsable

55

importnat traget of p53`

p21CIP1.

56

p21CIP1

inhbitior of cyclin-dpeendent kinases.

57

what specifically does p21CIP1 inhibit

cylin/CDK1 and cycline/CDK2

58

what caues ataxia-telangiectasisa

muations in protein kianse ATM

59

symptoms of ataxia telangeita

susceptivle to infection (especially chronic lung)
increases risk for leukemia, lymphoma, sensitive to radiation exposure

60

what produces TNF

macropahses

61

waht produces Fas ligands

natural killer cells, cytotoxic T lymphocytes

62

proapoptotic proteins

PUMA, BID, BAX (BCL-2 family)

63

BCL-2

antiapoptotic protein. inhibits BAX

64

BAX

can form a channel in the mitochondrial outer membran

65

function of PUMA and BID

stimulate BAX

66

when stimualtes BAX allows the release of waht

cytochrome c

67

what happens when cytochorome c enters cytoplasm

binds to Apaf-1

68

what happens after cytochrome c binds to Apaf-1

makes apoptosomes

69

function of apoptosome

recruite, activate caspase 9

70

functino of caspase 9

activates caspase 3 (excustioner caspases)