Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Biochem 1502 > Cell Cycle and Cancer > Flashcards

Cell Cycle and Cancer Flashcards

1
Q

G1 checkpoint checks for

A

Favorable environment and DNA damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

G2 checkpoint checks for

A

DNA replication complete, chromosomes intact

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What cells are permanently in G0 and are unable to replicate

A

neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Senescence

A

decrease in the proliferative capacity with age, irreversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

If a cell can be activated by external agents to enter cell cycle, it is called

A

quiescent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

A cell that has not committed to cell cycle “specialized resting state” is known to be in…

A

G0

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

chemotherapeutic agents target rapidly dividing cells and are only effective on tumors with a high percentage of replicating cells

A

cell cycle specific

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which chemotherapeutic drugs are useful against low percentage replicating cells?

A

b. Cell cycle non-specific

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

3 classes of cell cycle specific chemotherapeutics

A

antimetabolites, antibiotics, mitotic spindle poisons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Antimetabolites

A

inhibit purine or pyrimidine precursors or compete with them for incorporation into DNA/RNA. Effects S-PHASE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Examples of Antimetabolites

A

Methotrexate, 5-flurouracil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Methotrexate

A

inhibits thymidine synthesis by inhibiting regeneration of tetra-folate for normal folate metabolism – starving cells of folate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q
  1. 5-Flurouracil
A

irreversibly binds dUMP preventing synthesis of Thymidylate and preventing DNA biosynthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Anticancer antibiotics

A

Cell cycle specific and non-specific, but Bleomycin causes cells to accumulate in G2 PHASE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Examples of Anticancer antibiotic

A

Bleomycin (G2 PHASE SECIFIC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Examples of Mitotic Spindle Poisons

A

Vincristine, Vinblastine (Vinca alkaloids), and Taxol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Mitotic Spindle Poisons

A

M-PHASE SPECIFIC: (Vinca alkaloids) block mitosis by binding to tubulin, disrupting the spindle apparatus and causing depolymerization. Taxol causes stabalization of MTs and prevents disassembly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Taxol

A

Mitotic Spindle Poisons - causes stabalization of MTs and prevents disassembly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Vincristine, Vinblastine (Vinca alkaloids)

A

Mitotic Spindle Poisons - block mitosis by binding to tubulin, disrupting the spindle apparatus and causing depolymerization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What non-malignant cells are effects by chemotherapy?

A

hair follicles, none marrow, GI tract epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

2 types of cell cycle regulation

A

cascade of protein phosphorylation (cyclin-CDK), checkpoints

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Cyclin

A

cell cycle regulators that cycle due to synthesis and degradation during the cell cycle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What causes degradation of cyclin?

A

ubiquitin tagged proteosomal pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

CDK

A

constant concentration, but enzyme activity changes throughout cell cycle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What 4 things regulate CDK

A

a. Association with cyclins
b. Phosphorylation at stimulatory sites
c. Phosphorylation at inhibitory sites
d. Binding to CDK inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Association of CDK-cyclin complex causes

A

phosphorylation of the CDK protein which is then active to add phosphate groups to its target proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

CDK necessary for S-phase transition

A

CDK2, triggers DNA replication machinery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

CDK necessary for M phase transition

A

CDK1; triggers mitosis machinery, MTs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What Cyclin-CDK complex is required for passage through R point?

A

Cyclin D + CDK4/6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What Cyclin-CDK complex is required for G1/S-phase transition?

A

Cyclin E + CDK2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What Cyclin-CDK complex is required for S/G2-phase transition?

A

Cyclin A + CDK2/1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What Cyclin-CDK complex is required for G2/M-phase transition?

A

Cyclin B + CDK1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Retinoblastoma

A

regulates G1 checkpoint and inhibits cell cycle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

In early G1, Rb is…

A

underphosphorylated, which allows it to bind and “hold back” TFs required for G1/S transition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Increasing concentration of D/CDK4-6 causes..

A

Hyperphosphorylation of Rb, resulting in release of TFs and activation of genes necessary for S-phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What activates Cyclin D1?

A

MAP-kinase cascade by growth factors

37
Q

What TFs ae inhibited by Rb?

A

E2F and DP1

38
Q

p53

A

tumor suppressor gene that detects DNA damage and determines progression of cell cycle

39
Q

p53 is a TF for what gene?

A

it can turn on transcription of CDK inhibitor p21 (CIP) which will halt cell cycle in G1 phase to allow time for DNA damage repair

40
Q

What does p53 do if damage is irreparable?

A

triggers apoptosis

41
Q

3 p53 functions:

A

regulates genes involved in cell cycle control, arrest the cell during DNA damage, and commits a cell to apoptosis if necessary

42
Q

tumor suppressor genes

A

proteins involved in checkpoint control

43
Q

Most common mutation in cancer

A

p53

44
Q

HPV 16 and 18 and their viral proteins E6 and E7

A

Bind p53 and Rb respectively and cause loss of function

45
Q

Mutations in p53 commonly occur in which domain?

A

The DNA binding domain, meaning it cannot bind to the promotor of CDKi/p21/CIP

46
Q

During apoptosis, cleavage of what proteins allows cell to begin shrinking?

A

Lamins and actin filaments

47
Q

During apoptosis, the cell shrinks, chromatin breaks down and nucleus and cell fragment and are removed by?

A

Macrophages

48
Q

What is done by the cell to promote phagocytosis by macrophages?

A

translocation of phosphotidylserine from the inside of the cell to the outer surface

49
Q

Apoptosis in hematopoiesis

A

EPO not only promotes cell division, but it also inhibits apoptosis

50
Q

How does EPO inhibit apoptosis?

A

EPO binds its receptor (tyrosine kinase) on erythroid precursors and induces anti apoptotic molecule (Bcl-XL)

51
Q

Apoptosis and estrogen

A

Estrogen causes apoptosis of osteoclasts to prevent bone resorption, estrogen deprivation in post-menopausal women results in osteoporosis

52
Q

Apoptosis in aging

A

Deregulated apoptosis - apoptosis of irreplaceable cells (neurons, cardiac myocytes), decreased apoptosis of damaged or senescent cells

53
Q

How can cancer cells be resistance to chemotherapy

A

inability to activate apoptosis machinery

54
Q

CNS during acute ischemia or traumatic injury would result in

A

necrotic death at the site of injury, apoptosis may occur at a certain distance from the injury site

55
Q

Chronic neurodegenerative diseases would result in

A

apoptosis

56
Q

Neurodegenerative disease list

A

Huntingtons, Alzheimers, Parkinsons- chronic stroke, brain trauma, spinal cord injury - acute

57
Q

Would the presence of cytokines cause apoptosis?

A

No

58
Q

Would the presence of oxidation cause apoptosis?

A

Yes

59
Q

Activation of apoptosis occurs when

A

a signal is generated from within the cell, substances bind receptors on the cell surface (death receptors)

60
Q

Which two families of proteins mediate apoptosis?

A

Caspases and BCl2

61
Q

Caspases are

A

cysteine aspartate proteases that exist as a proenzyme

62
Q

BCl2 are

A

pro-survival and pro-death factors

63
Q

How do caspases work?

A

they have a proteolytic cysteine that cleaves proteins at an aspartate once signals are received and enzymatic cleavage activates the enzyme

64
Q

Initiator caspase

A

cleave and activate proteins in the caspase cascade to trigger the onset of apoptosis

65
Q

Effector Caspase

A

cleave and destroy critical components of the cell

66
Q

BCL-2 family members that are pro-survival

A

BCL2 and BCL-XL

67
Q

BCL2 family members that are pro-death

A

BAX, BAD, BID, BAK

68
Q

The ratio of what determines the cell’s fate

A

Pro-death and pro-survival BCL2 proteins

69
Q

In neurodegenerative diseases apoptosis is inappropriately

A

ACTIVE

70
Q

In cancer, apoptosis is

A

DECREASED

71
Q

Cytochrome c

A

mediates apoptosis via release fro the mitochondria

72
Q

BH-3

A

A unique domain on PRO-DEATH BCL2 proteins that binds to and INHIBITS pro-survival proteins

73
Q

BCL-2

A

located on mitochondrial membrane, bound to Apaf-1

74
Q

What happens when BCL2 pro death proteins recognize cell stress

A

They bind BCL-2, causing mitochondrial membrane to depolarize and form pores which allow cytochrom c and smac/diable to enter the cytosol

75
Q

Anti-apoptic proteins

A

located within the mitochondria and function to keep the mitochondrial membrane intact

76
Q

Pro-apoptotic proteins

A

located in the cytosol and detect cell stress

77
Q

Cytochrome C

A

located within the Mitochondrial inter membrane space, released when pro-apoptotic proteins bind BCL-2, causes activation of caspase 9

78
Q

When the pro-apoptotic signals bind BCL2, what happend to the mitochondrial membrane

A

it becomes depolarized and pores result, which allow release of cytochrome c and SMAC/DIABLo

79
Q

Apaf-1

A

generally bound to mitochondrail membrane with BCL-2, but when pro-death proteins bind and pores form, it is released and works with cytochrome c to activate caspase 9

80
Q

apoptosome

A

Cytochrome C + Apaf-1, molecules of caspase 9 form a multiprotein complex

81
Q

Caspase 9

A

stress pathway; activates other caspases and leads to proteolytic activity to degrade structural proteins and DNA

82
Q

Smac/DIABLO

A

Also released from mitochondria when pores form, they inactivate a group of anti-apoptotic proteins (IAPs)

83
Q

Tumor necrosis factor

A

integral membrane receptor that binds TNF-alpha and activates the death receptor (extrinsic apoptotic pathway)

84
Q

Fas

A

integral membrane receptor that binds FASL and activates the death receptor (extrinsic apoptotic pathway)

85
Q

TNF and Fas activate

A

death-signaling complex and activation of Caspase 8, which activates other caspases and results in phagocytosis of the cell

86
Q

Caspases 3, 6, 7

A

FINAL EXECUTIONERS, activate proteases and DNases

87
Q

Caspases activate

A

DNases (which work at coils, defined length fragments), proteases that breakdowm structural proteins (laminas), and INHIBIT DNA repair enzymes

88
Q

p53 and apoptosis

A

Increases BAX, increases Fas receptor, and reduces levels of growth factors (IGFBP3)

89
Q

Nucleosomal fragments

A

result from DNase activity since DNases work between the nucleosome complexes

Biochem 1502 (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions