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M2M Exam 3 wk 2 > Autophagy > Flashcards

Autophagy Flashcards

1
Q

Lysosomes function:

A

degrade & recycle macromolecules

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2
Q

Functions for macroautophagy

A
  1. Re-cycle proteins and other macromolecules under conditions of nutrient deprivation- allow recycling of amino acids, nucleotides and fatty acids.
  2. Remove organelles- mitochondria and peroxisomes.
  3. Allow cell survival under stress conditions (growth factor deprivation, hypoxia etc.)
  4. Present antigens to MHC system
  5. Neuro-protection- e.g. remove protein aggregates to prevent neuronal damage in e.g. Huntington’s, Parkinson’s disease etc.
  6. Remove intracellular pathogens
  7. Aging- increased autophagy can extend life in worms and other model organisms
  8. Tumor suppression- e.g. an autophagy gene (Beclin 1) is a haploinsufficient tumor suppressor in mice.
  9. Tumor promotion- e.g. required for progression and (perhaps) metastasis.
  10. Inhibits apoptosis/ cell death but also kills cells. Type II programmed cell death.
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3
Q

autophagy is

A

how stuff is delivered to lysosomes

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4
Q

autophagy recycles proteins and other macromolecules under conditions of

A

under conditions of nutrient deprivation- allow recycling of amino acids, nucleotides and fatty acids.

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5
Q

autophagy removes _____

A

organelles- mitochondria and peroxisomes.

and intra cellular pathogens

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6
Q

autophagy allows cells to

A

survival under stress conditions (growth factor deprivation, hypoxia etc.)

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7
Q

autophagy presents

A

Present antigens to MHC system

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8
Q

autogphagy functions in neuro-protection: examples

A

e.g. remove protein aggregates to prevent neuronal damage in e.g. Huntington’s, Parkinson’s disease etc.

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9
Q

autophagy and aging:

A

increased autophagy can extend life in worms and other model organisms

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10
Q

autophagy and tumor suppression

A

e.g. an autophagy gene (Beclin 1) is a haploinsufficient tumor suppressor in mice.

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11
Q

autophagy and tumor promotion

A

e.g. required for progression and (perhaps) metastasis.

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12
Q

autophagy inhibits

A

apoptosis/ cell death but also kills cells. Type II programmed cell death.

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13
Q

autophagy is induced during times of

A

nutrient stress

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14
Q

Atg genes

A

regulate autophagy

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15
Q

autophagic process

A
  1. induction
  2. vesiiclenucleation
  3. vesicle expansion
  4. cargo targeting
  5. veiscle closure
  6. vesicle fusion with endosome
  7. vesicle fusions with lyosome
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16
Q

induction

A

nutrient starvation, growth factor–mediated starvation exposure to chemo drugs, like rapamycin

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17
Q

vesicle nucleation also called

A

phagophore

18
Q

vesicle expansion also called

A

also called omegasome

19
Q

examples of cargo targeting

A

LC3II and p62

20
Q

when vesicle closure occurs, it is called

A

autophagosome

21
Q

when the vesicle fuses with the endosome, called

A

amphisome

22
Q

when the vesicles fuses with the lysosome, it is then called

A

autolysosome

23
Q

What regulates autogphagy?

A
  1. amino acids ad other nutrients
  2. growth factors
  3. lipids
  4. everything that regulated the PI3 kinase pathway
  5. Multiple protein kinases
  6. tumor suppressor proteins like p53, positive and negative regulation
  7. mutated oncogenes like Ras (positive and negative regulation
24
Q

Autophagy signaling often converges on the

A

mTOR pathway

25
Q

Beclin-1 interacts with Bcl-xL via

A

a BH3 domain

26
Q

The BH3 mimetic _____ and disrupts the ______

A

ABT 737

Beclin-1-Bcl-xl interaction

27
Q

Some examples of anti-cancer agents that have been proposed to work by inducing autophagic cell death

A
  1. mTOR inhibitors
  2. Topoisomerase inhibitors
  3. Arsenic
  4. Radiation
  5. Vitamin D analogs
  6. Oncolytic viruses
  7. DNA alkylating agents
  8. HDAC inhibitors
  9. TRAIL
28
Q

______ inhibitors induced caspase-independent, autophagic cell death

A

HDAC

29
Q

knockout of autophagy can prevent

A

cell death

30
Q

autophagic cell death is associated with formation of

A

autophagic vesicles

31
Q

Autophagy is a

A

highly regulated process and likely important in many physiological and pathological processes.

32
Q

Autophagy is Intimately associated with

A

apoptosis & cell death

33
Q

autophagy can

A

kill cells or protect cells against nutrient deprivation induced stress, neurodegeneration and anti cancer agents

34
Q

Macroautophagy

A
  • form a double membrane vesicle that captures cytosolic components/organelles. Then fuse with lysosome where hydrolases degrade contents of autophagosome.
35
Q

Chaperone-mediated–

A

recognition of specific proteins that contain a specific recognition sequence (based on amino acid sequence KFERQ). Direct binding and delivery to lysosome.

36
Q

Describe process of macroautophagy.

A
  1. Activate a PI3K complex that allows nucleation of a membrane that will eventually form autophagosome.
  2. Regulation of protein conjugation events to extend membrane.
  3. Randomly capture, or specifically deliver cargo to the extending autophagosome, then join the membranes to close the vesicle.
  4. Fuse with lysosome.
  5. Recycle amino acids and other macromolecular precursors.
37
Q

Describe rationale behind autophagy’s protective action against neurodegeneration.

A
  1. Aggregate-prone proteins (e.g. those with expanded stretches of glutamine residues in diseases like Huntington’s disease) will cause neuronal cell death.
  2. Autophagy degrades the aggregate-prone proteins (perhaps after they have started to form small aggregates).
  3. No toxic stimulus, no neuronal cell death.
38
Q

Identify mechanisms by which apoptosis induction and autophagy are connected.

A 
Many proteins - e.g. Bcl-2 - that regulate apoptosis/ cell death, also control autophagy--remember, this could create problems in interpreting results of therapeutic interventions designed to target these proteins.  
Apoptotic proteases (caspases) can cleave essential autophagy regulators inactivating them and therefore blocking the process of autophagy.  
In some cases, -e.g. with starvation-induced cell death, it is easy to see why autophagy would protect– it provides essential nutrients at least in the short term.  
In others, e.g. stress-induced cell death from chemotherapy etc. its less clear why autophagy would be protective.
39
Q

Many proteins - e.g. _____ - that regulate apoptosis/ cell death, also control __________

A

Bcl-2

autophagy–remember, this could create problems in interpreting results of therapeutic interventions designed to target these proteins.

40
Q

Apoptotic proteases (caspases) can _______.

A

cleave essential autophagy regulators inactivating them and therefore blocking the process of autophagy

41
Q

In some cases, -e.g. with starvation-induced cell death, it is easy to see why autophagy would protect– _______

A

it provides essential nutrients at least in the short term.

In others, e.g. stress-induced cell death from chemotherapy etc. its less clear why autophagy would be protective.

M2M Exam 3 wk 2 (11 decks)

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