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MCBG 3 > Cell Cycle III (Sept. 16 - Schultz) > Flashcards

Cell Cycle III (Sept. 16 - Schultz) Flashcards

1
Q

What are RTKs?

A

Receptor tyrosine kinases

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2
Q

Describe the activation of receptor tyrosine kinases

A

Normal RTKs dimerize in response to a ligand signal. Te two kinase domains cross phosphorylate each other and become activated

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3
Q

Describe how the receptor tyrosine kinases can broadcast signals

A

Downstream targeting occurs via intracellular signaling proteins bind to phosphorylated tyrosine.

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4
Q

Explain the process called dominant-negative regulation

A

Excess of mutant RTK receptors will block signaling by the normal receptors - will inhibit activation of other downstream targets

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5
Q

What is Grb2?

A

It is an intracellular signaling protein that binds to RTK and specifically binds to Ras-GEF

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6
Q

Describe the structure of intracellular signaling molecules. What are the two domains that they contain?

A

Sh2 and Sh3 binding domains

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7
Q

Describe the specificity of Sh2 binding with phosphorylated tyrosine kinases

A

Specificity of Sh2 binding domain is determined by the distinct binding site for a particular amino acid side chain. (Plug design - flanking AA sequences determine binding)

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8
Q

In Grb-2, the Sh3 domain binds Ras-GEF because of its ability to bind this particular motif structure…

A

Polyproline helix

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9
Q

What molecule is activated by Sh3 binding of Grb-2 via polyproline helix binding

A

Ras-GEF

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10
Q

What is the function of Ras-GEF

A

Ras-GEF is an exchange factor that activates RAS by exchanging RAS-GDP to RAS-GTP

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11
Q

What would happen if the RAS-GAP failed?

A

No hydrolysis of RAS-GTP -> continued activation of downstream targets. No GTPase activity.

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12
Q

Explain the downstream targets that are affected starting from the binding of an extracellular ligand…all the way to the promotion of S-phase of the cell cycle

A
  1. Extracellular ligand binds to RTK
  2. RTK dimers associate and cross-phosphorylate
  3. SH2 portion of GRB2 binds to RTK and SH3 portion of GB2 binds to RAS-GEF
  4. RAS-GEF activates RAS-GDP -> RAS-GTP
  5. RAS-GTP activates MAPKKK (RAF)
  6. MAPKK (MEK)
  7. MAPK (ERK)
  8. MAPK (Mitogen activating protein kinase) leads to activation of certain gene regulatory proteins (myc, Jun-Fos, Ets)
  9. Myc activates “delayed-response” genes
  10. G1-Cdk activity is increased
  11. G1-Cdk phosphorylates active Rb protein
  12. Rb protein (inactivated by phosphorylation) release active E2F
  13. Upregulation of G1/S-phase cyclins
  14. Active S-Cdk
  15. DNA synthesis
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13
Q

What types of factor would promote activation of RAS?

A

Mitogen or growth factors

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14
Q

What is the difference between a c-SRC kinase and a RTK

A

c-SRC kinases are attached to cytoplasmic side of plasma membrane, but contain no extracellular domain. Upon activation of a nearby ligand receptor, they will associate with the receptor and undergo a conformation change to the active form

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15
Q

Define happloid-sufficiency in terms of tumor-suppressor genes

A

Tumor supressor genes act in recessive manner -> require loss of both copies of gene in order to cause excessive cell proliferation.
One copy of TSG is SUFFICIENT to produce enough elements to suppress cancer and have NORMAL cell proliferation

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16
Q

In contrast to happloid-sufficiency in tumor-supressor genes, what happens when there is a single proto-oncogene

A

They act in a DOMINANT fashion. One mutation is enough to produce cascade of uncontrolled cell proliferation

17
Q

What is a proto-oncogene?

A

They are normal genes that can cause excessive cell proliferation through either mutation or over expression.

18
Q

Describe the 4 stages of programmed cell death (apoptosis)

A
  1. Decision to die or live
  2. Death
  3. Engulfment through phagocytosis
  4. Degredation of cellular materials
19
Q

What is the difference between apoptotic cell death versus necrotic cell death?

A

Apoptosis:

  1. Controlled auto digestion of contents rather than rapid swelling and lysis
  2. Non-inflammatory response
  3. Characteristic skeletal disruptions, eventual cell shrinkage, and membrane “blabbing”
  4. Loss of mitochondria function
  5. Degradation of DNA into nucelosomal fragments
20
Q

In general, describe what occurs to elicit a cell to die…

A
  • Death decision box is activated by factors whether to commit to apoptosis
  • Recruits and activates caspases (proteases)
  • Uptake by phagocytic cells and degradation
21
Q

How to caspases work as the executioner of cells?

A
  • hydrolyze peptide bonds and degrade contents of cells

- work through cascade activation (positive feedback loop)

22
Q

What are factors that contribute to the death signal?

A

TNF alpha/Fas factors
Growth Factor withdrawal
DNA damage/stimulation of P53

23
Q 
The following inhibits the signal which causes activation of caspases
A) TNF alpha
B) Akt
C) Bcl-2
D) CrmA
E) All of the above
A

(C)

24
Q

Where in the cell does the intrinsic signal to undergo apoptosis originate from?

A

Mitochondria

25
Q

How can T-cells skip the regulatory pathway of apoptosis and contribute to cell death?

A

T-cells can secrete granzyme B - bypasses the Life or death decision center and can cause increase caspase cascade

26
Q 
Which of the following when activated are tumor suppressor proteins?
A) EFIIB
B) P53
C) granzyme b
D) Smac/Diablo
E) Bcl-2
A

B) P53 recognizes DNA damage and promotes apoptosis
C) granzyme B promotes caspase activity and promotes apoptosis
D) Smac/Diablo is an inhibitor of an inhibitor of caspases. Its activation causes less XIAP to be produced which leads to MORE caspase activity

27
Q

List diseases associated with inhibition of apoptosis

A
  1. Cancer
  2. Autoimmune disorders
  3. Viral infections
28
Q

List diseases associated with increased apoptosis

A
  1. AIDS
  2. Neurodegenerative disorders
  3. Ischemic injury
29
Q

How can ischemic injury lead to increased apoptosis?

A

Reprofusion of blood (restoring blood flow to ischemic areas after blockage is removed) may cause inflammation and oxidative damage. Free radical release of these damaged cells may interact with redox signaling causing increase in apoptosis.

30
Q

What are FAS ligands?

A

Transmembrane proteins (part of TNF family) which induce apoptosis when binding to receptors.

31
Q

How can viral genes act as inhibitors of apoptosis?

A

Baculovirus p35 and Cowpox virus CrmA work too inhibit caspase activity in cells and stop apoptosis -> increased cell proliferations

32
Q

How can Epstein Barr virus cause cancer?

A

Acts as a Bcl-2 homolog and inhibits caspase activation -> inhibition of apoptosis

MCBG 3 (9 decks)

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