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MCM Quiz2 > Cell Cycle Cell Death > Flashcards

Cell Cycle Cell Death Flashcards

1
Q

What are the cell cycles?

A

M Phase -> G1 phase -> G0 phase -> S phase -> G2 phase

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2
Q

What is the m phase?

A

mitosis

Chromosome duplication/segregation
Cytokinesis- cell division

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3
Q

G1 Phase?

A

RNA & Protein Synthesis / Cell growth

duration between completion of cell division and initiation of DNA replication

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4
Q

G0 Phase

A

No Cell division

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5
Q

S phase

A

synthesis

DNA replication
Histone Synthesis
Centrosome formed
Chromosome duplication

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6
Q

G2 Phase

A

Preparation for Mitosis

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7
Q

Restriction point

A

Discrete time point where errors are checked

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8
Q

Checkpoint-

A

Halts Cell cycle if proper synthesis does not occur

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9
Q

Locations of restriction point?

A

G1 phase (two hours prior to S phase)

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10
Q

Checkpoints?

A

G1 checkpoint,
G2 checkpoint,
Metaphase checkpoint

If growth factor signals are limiting, cells go into G0 →
Makes sure cell doesn’t grow too fast, too much, etc.

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11
Q

Cdk1:Cyclin B, what is it?

A

triggers G 2 → M transition

Cyclin A is synthesized in S and destroyed starting at prometaphase
Cyclins B are synthesized in S/G 2 and destroyed following the completion of chromosome attachment to the spindle

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12
Q

Cdk2: Cyclin A,E

A

Triggers G 1 → S transition

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13
Q

Cdk4, Cdk6: Cyclin D1 –D3

A

Phosphorylation of the retinoblastoma susceptibility protein (pRb) in G 1

Triggers passage of the restriction point and cyclin E synthesis in some cell types

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14
Q

How do Cyclin and CDK become activated?

A

have to be phosphorylated to activate it
-For the complex to be active, therefore, it must be phosphorylated on the first site, but dephosphorylated on the other two sites by the protein phosphatase cdc25

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15
Q

Cdk1:Cyclin B, what does it do?

A

triggers G 2 → M transition

Cyclins B are synthesized in S/G 2 and destroyed following the completion of chromosome attachment to the spindle

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16
Q

Cdk2: Cyclin A,E

A

Triggers G 1 → S transition

Cyclin A is synthesized in S and destroyed starting at prometaphase

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17
Q

Cdk4, Cdk6: Cyclin D1 –D3

A

Phosphorylation of the retinoblastoma susceptibility protein (pRb) in G 1

Triggers passage of the restriction point and cyclin E synthesis in some cell types

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18
Q

Cyclin and CDK come together, how are they activated when they come together?

A

-For the complex to be active, therefore, it must be phosphorylated on the first site, but dephosphorylated on the other two sites by the protein phosphatase cdc25

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19
Q

what do CKI do?

A

keep the balance, cells dont go to the next step prematurely

  • inhibitor binding or phosphorylation interference
  • block actions of CDK
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20
Q

what happens when INK4 binds?

A

twisting of the Cdk upper lobe blocks cyclin binding or interferes with ATP hydrolysis.

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21
Q

When p27 or p21 binds, what happens?

A

a loop insinuates into the upper lobe of the Cdk and blocks ATP binding

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22
Q

what does p21 do?

A

Induced by p53 tumor suppressor. Cell-cycle arrest after DNA damage. Binds PCNA and inhibits DNA synthesis. Promotes cell cycle arrest in senescence and terminal differentiation

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23
Q

what does p27 do?

A

Cell cycle arrest in response to growth suppressers like TGF-β and in contact inhibition and differentiation

24
Q

what does p16 do?

A

Cooperates with the retinoblastoma susceptibility protein (pRb) in growth regulation. Cell-cycle arrest in senescence. Altered in a high percentage of human cancers

25
Q

RAS proteins, what do that do?

A

GTPases that receive signal from catalytic receptors, induct cell proliferation

26
Q

How do cells enter the S phase?

A

Mitogen attaches to receptor, activates MAPK, activates MYC

27
Q

what is the G1/S Transition?

A

E-CDK2 complexes drive pRb hyperphosphorylation

Liberates E2F transcription factors from pRb control

E2F can increase transcription of genes

28
Q

what does cyclin A do during s phase?

A

stabilizes prereplication complex

29
Q

what is the G2/M transition?

A
  • Activation of CDK1/cyclin B at the G 2 /M boundary
  • CDK1/cyclin B translocate to the nucleus
  • Activated anaphase promoting complex (APC) destroy

cdk1 freeing cyclin B for degradation

30
Q

Checkpoints, what are they?

A
  • Cell cycle checkpoints are cellular mechanisms, which control the order and timing of cell cycle phase transitions
  • Checkpoints mostly activated by genotoxic stress mainly DNA damage
31
Q

G1 checkpoint:

A
  • After DNA damage, two parallel checkpoint pathways target the activity of Cyclin/Cdk complexes
  • The slower pathway involves the stabilization of p53 and transcriptional upregulation of p21 which binds and inhibits the Cyclin/Cdk complexes
  • The faster pathway acts via the activation of Chk2 and the inactivation of Cdc25
32
Q

G2 checkpoint:

A
  • After DNA damage induction, two ATM-dependent checkpoint pathways are activated
  • The checkpoint kinases, Chk1/Chk2, target Cdc25 for nuclear export leading to the accumulation of the inactive CyclinB1/Cdk1 complex
  • The lack of activated CyclinB1/Cdk1 interrupts the feedback loops (dotted lines), resulting in G2 arrest
33
Q

Tumors?

A

Space occupying lesions that may or may not be neoplasms

34
Q

Neoplasm?

A

relatively autonomous abnormal growth with abnormal gene regulation, 2 types: benign and malignant

35
Q

Cancer

A

Malignant neoplasm (can produce metastasis)

36
Q

Metastasis

A

Secondary growth of cancer at different - location from primary neoplasm

37
Q

How to name cancer?

A
  1. Differentiation state (epithelial, non epithelial, etc)
  2. embryonic origin
  3. benign or malignant
38
Q

what are the three steps of cancer?

A

initiation, promotion, progression

39
Q

initiation of cancer?

A
  • irreversible
  • chemicals,radiation, viruses
  • oncogenes can be activated
  • inactivation of tumor suppressor gene
40
Q

promotion of cancer?

A
  • reversible in early stages
  • threshold exists
  • inhibition of cell death in affected cells
  • chromosomal changes
  • tumor to neoplasms
  • CLONAL EXPANSION, promoting gene activation
41
Q

.progression of cancer?

A

continuing change of unstable karyotype

42
Q

what are oncogenes

A

drive growth, enhanced expression leads to unregulated growth

43
Q

what are Tumor Suppressors?

A
  • can inhibit cell division, loss of these leads to cell growth
  • mostly recessive
  • In carcinogenesis: inactivating mutations, deletions, loss of expression

-p53,rb, p16I,p14ARF

44
Q

p16I, what is it?

A

tumor suppressor gene, inactivation of the INK4a locus on human chromosome 9p21 in human cancers

45
Q

Rb, what is it?

A

tumor suppressor gene, retinoblastoma if inactivated?

46
Q

Hallmarks of cancer?

A
  • Acquire self-sufficiency of growth signals
  • Become insensitive to growth inhibitory signals
  • Evade cell death
  • Acquire limitless replicative potential
  • Angiogenesis
47
Q

tumor microenvironment? components?

A

tissue environment in which cancer cells exists, that include normal cells, secretory factors, and the extracellular matrix

  • Cellular components such as immune cells, fibroblasts, blood vessel cells , EMT cells
  • secretory factors
  • extracellular matrix: proteins + proteogycans
  • promotes therapy resistance + cancer growth
48
Q

Chemotherapy, what does it do?

A

Utilizes: alkylating agents, incalcating agent, antimetabolites

cell damage

49
Q

Radiation therapy , what does it do?

A
  • Direct deposition of energy to break DNA bonds
  • Hydrolysis of water to produce powerful damaging free radicals

cell and DNA damage

50
Q

surgery on cancer?

A

just cut it out

51
Q

DNA – Immunotherapy what does it do?

A

receptor based treatment

52
Q

When does cell death occur?

A

Cell death occurs when they loss of large amounts of genetic material due to DNA damage as they divide reaching a critical level of genomic instability

53
Q

what is Necrosis? what happens?

A

uncontrolled form of cell death

  • swelling cell membrane
  • organelle swelling
  • degradation of DNA
  • failure of normal cell pathways
  • Ca2+ overload, mitochondria uncoupling, ROS production
  • inflammation
  • in all cells
54
Q

what is Apoptosis? what happens?

A
  • Cell membrane: membrane blebbing and eventually fragmentation
  • Cytoplasm: Fragmentation and shrinkage
  • Nucleus : Chromatin condensation and degradation
  • Cell membrane loses its asymmetry, and phosphatidylserine becomes exposed
  • no inflammation
  • hematopoietic cells
  • ATM senses changes, P53, CD95
  • Bax and Bak form pores on membrane, activated by Bcl2
55
Q

what is Autophagy? what happens?

A
  • Process responsible for degrading longlived proteins and cytoplasm organelles, the products of which are recycled to generate macromolecules and ATP so as to maintain cellular homeostasis
  • Cell membrane: membrane blebbing
  • Cytoplasm: accumulation of two-membrane autophagic vacuoles
  • Nucleus : Partial chromatin condensation
  • no inflammation
  • all cells
56
Q

what is Mitotic Catastrophe? what happens?

A
  • Mitotic catastrophe is defined as a type of cell death that is caused by aberrant mitosis.
  • Cell membrane: No change
  • Cytoplasm: larger cytoplasm with the formation of giant cell.
  • nuclear fragmentation. Premature chromosome condensation
  • no inflammation
  • all cells
57
Q

what is Senescence? what happens?

A
  • Permanent cell cycle arrest, reproductive death
  • Cell membrane: No change
  • Cytoplasm: Flattening and increased granularity
  • Nucleus : Distinct heterochromatic structure
  • Inflammation
  • all cells
  • p53-p21
  • p16-rb pathways

MCM Quiz2 (10 decks)

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