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Exam 2 (PARP) > Endosome- Lysosome System and Cell Digestion > Flashcards

Endosome- Lysosome System and Cell Digestion Flashcards

1
Q

Accumulation of GM2

A

Tay-Sachs Disease

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2
Q

In vivo, whole areas of tissue are affected. Necrosis or apoptosis.

A

Necrosis

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3
Q
  1. Treatment for Gaucher Disease
A
  1. Enzyme replacement therapy- successful in alleviating non CNS symptoms
  2. Administer correct enzyme which has been engineered to be endocytosed by macrophages
  3. Enzymes delivered to lysosomes- breakdown of glucosylceramide
  4. Doesn’t work on types 2 and 3
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4
Q

Treatment of Tay- Sachs Disease

A
  1. ERT has been unsuccessful
  2. The blood-brain barrier makes access difficult
  3. Neurons are not phagocytic
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5
Q

Gene symbol: GNPTAB

A

Mucolipidosis IIa/B (I- Cell Disease)

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6
Q

Transcytosis is crucial to maintaining cell __________

A

Polarity

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7
Q

_____________ is an anti-apoptotic protein which inhibits release of _______ from mitochondria

A

Bcl-2; Cytochrome c

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8
Q

Is LDL good or bad cholesterol?

A

Bad

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9
Q

Vesicular trafficking delivers contents of _______________ to target organelles.

A

Vesicle

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10
Q

In this type of cell death, the process is rapid and uses intracellular enzymes, and leaves no trace

A

Apoptosis

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11
Q

During _______, apoptosis removes webs between fingers and toes or neurons which make the wrong connections

A

Morphogenesis

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12
Q

Transcytosis (IgA) pathway

A
  1. IgA dimerizes
  2. IgA dimers bind to IgA receptor
  3. IgA and receptor complex internalized
  4. Clathrin coated vesicles forms
  5. Clathrin coat falls off
  6. Early endosome fuses with CRE
  7. IgA and receptor “recycled” to apical membrane
  8. Receptor clipped by enzyme to release IgA molecules
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13
Q

How does the H+ ATPase pump impact lysosomes?

A

It helps to maintain a low pH by pushing H+ ions into the lysosome

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14
Q

What are some come symptoms of lysosomal storage disorders?

A

Neuropathies, kidney disease, bone malformations, muscle diseases, and general failure to thrive

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15
Q

Mucolipidosis IIa/B (I- Cell Disease)

A

Adds mannose-6-phosphate to lysosomal enzymes

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16
Q

Cellular swelling. Necrosis or apoptosis

A

Necrosis

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17
Q

Some intermediates in fatty acid oxidation act as ____________ molecules

A

Signaling

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18
Q

Mutations of p53 protein are common in what type of disease?

A

Cancer

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19
Q

Cell is phagocytosed, no tissue reaction. Necrosis or apoptosis.

A

Apoptosis

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20
Q

Trafficking of Lysosomal Hydrolases (Pathway)

A
  1. Manose 6-phosphate moiety added to hydrolases in Golgi
  2. Enzymes partitioned into clathrin coated vesicles by M6P receptor
  3. Clathrin Coated vesicles bud off trans Golgi network and fuse with late endosomes
  4. At lower pH, hydrolases dissociate from the M6P receptors
  5. Empty receptors are recycled to the Golgi for further rounds of transport
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21
Q

What happens in necrosis?

A
  1. Cellular contents spill into the surrounding tissues
  2. Inflammation develops
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22
Q

What process takes place in internal apoptosis?

A

Release of cytochrome c activates a caspase cascade

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23
Q

LDL Endocytosis PATHWAY

A
  1. LDL binds to its receptor
  2. LDL and receptor are internalized
  3. Clathrin coated vesicles forms
  4. Clathrin coat falls off
  5. Early endosome fuses with the Sorting Early Endosome
  6. LDL dissociates from its receptor
  7. LDL traffiscked to Late Endosome and lysosome
  8. LDL receptor recycled back to plasma membrane
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24
Q

DNA fragmentation is random. Necrosis or apoptosis.

A

Necrosis

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25
Q

Lysosomal delivery and degradation of intracellular organelles

A

Autophagy

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26
Q

Though these macromolecules cannot be oxidized by mitochondria, they can be oxidized by peroxisomes.

A

Long chain fatty acids

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27
Q

Peroxisomes play a major role in ___________metabolism in the cell

A

Lipid

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28
Q

Symptoms of Tay Sachs Disease

A
  1. Hypotonia
  2. Decreased muscle strength and spasticity leading to ataxia and paralysis
  3. Startle response
  4. Blindness
  5. Deafness
  6. Cognitive decline
  7. Infantile: fatal in childhood
  8. Juvenile: onset between 2 and 10
  9. Adult- onset in 30s or 40s
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29
Q

Ligands and receptors have different fates depending on the ____________ and trafficking route inside the cell.

A

Receptor

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30
Q

Early Endosome marker

A

Rab 5

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31
Q

Are all members of the Bcl-2 family anti-apoptotic?

A

No, some are pro-apoptotic

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32
Q

Types of endocytosis that is non-selective

A
  1. Phagocytosis
  2. Pinocytosis
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33
Q

What is vesicular trafficking?

A

A basic cellular process in which membrane- bound carriers bud off the donor compartment and fuse with the receipt one.

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34
Q

What is autophagy used for?

A
  1. Organelle removal and turnover
  2. A source of nutrient during “starvation”
  3. Degradation of long-lived, aggregated or misfolded proteins
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35
Q

Lysosome marker

A

LAMP1, LAMP2, LAMP3

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36
Q

Peroxisomes contain a variety of _________ enzymes, including catalase.

A

Oxidative

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37
Q

Fast recycling marker

A

Rab 4

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38
Q

Gene symbol GBA

A

Gaucher Disease

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39
Q

A chloride channel protein is mutated in ______

A

Cystic fibrosis

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40
Q

Cells with DNA damage are monitored by what protein?

A

P53

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41
Q

Trafficking of Lysosomal Hydrolases Pathway

A
  1. Mannose-6-phospahate moiety added to hydrolases in cis Golgi.
  2. Enzymes partitioned into clathrin coated vesicles by M6P receptor in trans golgi
  3. CCVs bud off trans golgi network and fuse with late endosomes
  4. At lower pH, hydrolases disscoiate from the M6P receptors
  5. Empty receptors are recycled to the Golgi for further rounds of transport.
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42
Q

Enzymes found in lysosomes

A
  1. Nucleases
  2. Proteases
  3. Glycosidases
  4. Lipase
  5. Phosphatases
  6. Sulfatases
  7. Phospholipases
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43
Q

In transferrin endocytosis, the ligand is ________ and the receptor is _________.

A

Recycled; recycled

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44
Q

Gene symbol: HEXA

A

Tay-Sachs Disease

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45
Q

Oxidation produces __________ as a by-product.

A

Hydrogen peroxide

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46
Q

Which cell types would lipofuscin granules accumulate in?

A

Heart muscle, neurons, retina

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47
Q

Late endosome pH

A

5.5

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48
Q

Before vesicle can be off loaded, v-snare must bind to ____________.

A

t-snare

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49
Q

Enzyme reaction for Gaucher Disease

A

Glucosylceramide + H20 -> Ceramide +Glucose

50
Q

Internally or externally induced. Necrosis or apoptosis.

A

Apoptosis

51
Q

In LDL endocytosis, the ligand is __________ and the receptor is ___________.

A

Degraded; recycled

52
Q

What process takes place in external apoptosis?

A

Fas ligands bind to Fas receptors on the cell surface to activate a caspase cascade

53
Q

Can peroxisomes divide?

A

Yes

54
Q

Defective protein of Gaucher Disease

A

Glucocerebrosidase (GCase)

55
Q

Defective protein in Tay-Sachs Disease

A

beta-N-acetylhexosaminidase (a- subunit)

56
Q

Where might lysosome related organelles be found?

A

Melanocytes

T-lymphocytes

Platelets

57
Q

The lysosome must be uncoated to _________ with the late endosome

A

Fuse

58
Q

What is the process of macro-autophagy in starvation conditions?

A
  1. Rag-GTPase becomes GDP bound and no longer associated with the lysosome membrane.
  2. mTORC1 is dephosphorylated and dissociates from Rag-GTPases
  3. TFEB is dephosphorylated and translocates to the nucleus
  4. TFEB turns on the transciption of the genese needed for autophagy and lysosome biogenesis
  5. Macro-autophagy occurs
  6. Nutrients are generated, and Rag-GTPases return to GTP bound form
59
Q

Vesicular sorting is ___________ specific

A

Cargo

60
Q

Regulates normal growth and differentiation

A

Epidermal Growth Factor (EGFR)

61
Q

In vivo: individual cells appear affected. Apoptosis or necrosis

A

Apoptosis

62
Q

In this type of endocytosis only what gets bound to the receptor will be engulfed.

A

RME

63
Q

Externally induced only. Necrosis or apoptosis.

A

Necrosis

64
Q

_____________- tagged cytoplasmic and nuclear proteins are destroyed by proteasomes.

A

Ubiquitin

65
Q

Autophagy and Neuro-degeneration disorders

A

Parkinson’s

Huntington’s

ALS

66
Q

Catalase converts ________ to ________.

A

H2O2; H2O

67
Q

Once dissociated from transferrin, where does the Fe++ go?

A

The cytoplasm

68
Q

Cellular defect of Mucolipidosis IIa/B (I-Cell Disease)

A
  1. Lysosomal enzymes are secreted instead of being delivered to lysosomes
  2. Many substances accumulate in lysosomes making inclusion bodies
  3. Not all cells are affected. There are other ways for enzymes to get to the enzyme
69
Q

Slow recycling marker

A

Rab 11

70
Q

What is the importance of the ubiquitin tag?

A

It notifies the cell that the tagged molecule needs to be degraded

71
Q

What diseases are caused by protein aggregates?

A

Alzheimer’s or Huntington’s

72
Q

What shape are peroxisomes?

A

Spherical

73
Q

Activation of ________ triggers apoptosis

A

Caspases

74
Q

______________ transport lipids around the body through the blood.

A

Lipoproteins

75
Q

Cell ingestion of material from outside of the cell is called _____________.

A

Endocytosis

76
Q

___________ is caused by damage and leads to cell swelling and rupture

A

Necrosis

77
Q

Late endosome marker

A

Rab 7

78
Q

Proteosome degradation inactivates the ________

A

Cyclin-Cdk complex

79
Q

____________ have a lysosomal storage disorder

A

1/5000th

80
Q

How many molecules can transferrin carry at one time?

A

Up to two

81
Q

EGFR Endocytosis Pathway

A
  1. Ligand binds to EGFR and receptor dimerizes
  2. Ubiquitin binds to the receptor
  3. EGFR complex internalized
  4. Clathrin coated vesicles form
  5. Clathrin coat falls off
  6. Early endosome fuses with the sorting early endosome
  7. EGFR complex trafficked to lysosome through the late endosome
  8. Entire EGFR complex digested by the lysosome
  9. EGF signaling cascade turned off
82
Q

Ladder like DNA fragmentation. Apoptosis or necrosis

A

Apoptosis

83
Q

Some viruses are able to inhibit apoptosis by making a __________ like protein.

A

Bcl-2

84
Q

In starvation conditions, ________ is no longer associated with the lysosome membrane.

A

Rag-GTPase

85
Q

Symptoms of I-Cell Disease

A
  1. Failure to thrive
  2. Developmental delays
  3. Abnormal skeletal development
  4. Restricted joint movement
  5. Hepatosplenomegaly
  6. Fatal in early childhood
86
Q

An autophagosome is a spherical structure with ___________ membranes.

A

Double layered

87
Q

_________ are required for plasmalogen synthesis.

A

Peroxisomes

88
Q

pH of lysosome

A

4.5

89
Q

Treatment for I- Cell Disease

A
  1. Enzyme replacement therapy has been unsuccessful
  2. Gene therapy is a possible therapy
  3. Transporting enzymes to the Golgi
90
Q

Early endosome pH

A

6.5

91
Q

What does p53 trigger?

A

DNA REPAIR OR APOPTOSIS

92
Q

Transferrin Endocytosis

A
  1. Fe3+- transferrin bound to receptor
  2. Transferrin complex is internalized
  3. Clathrin coated vesicle forms
  4. Clathrin coat falls off
  5. Early endosome fuses with Sorting Early Endosome
  6. Fe3+ dissociates from transferrin
  7. Fe 3+ transported to cytoplasm for use in metabolism
  8. Transferrin and receptor recycled back to plasma membrane
  9. Transferrin dissociates from receptor
93
Q

Cellular condensation/ shrinking. Necrosis or apoptosis

A

Apoptosis

94
Q

Membrane remains intact until the cytoplasm pinches off because of blebbing. Necrosis or Apoptosis

A

Apoptosis

95
Q

What is the major phospholipid in myelin?

A

Plasmalogen

96
Q

Accumulation of Glucosylceramise

A

Gaucher Disease

97
Q

What type of proteins are digested by proteasomes?

A
  1. Misfolded
  2. Short-lived
  3. Abnormal
  4. Unneeded proteins
98
Q

Plasma glycoproteins that transports iron

A

Transferrin

99
Q

_______ is cellular suicide

A

Apoptosis

100
Q

After leaving the Golgi, the vesicle either goes to the ___________ or ____________.

A

Lysosome; plasma membrane

101
Q

Symptoms of Type 1 Gaucher Disease

A
  1. Non-neuropathic Gaucher Disease
  2. Most common
  3. Hepatosplenomegaly because macrophages cannot completely digest aged RBC
  4. Anemia, thrombocytopenia, lung disease, and bone abnormalities
102
Q

Lysosomal storage disorders result in the accumulation of a ___________ in the lysosome.

A

Substrate

103
Q

What is the major degradative compartment in eukaryotic cells?

A

Lysosome

104
Q

Proteasomes digest __________ proteins

A

Misfolded

105
Q

Lysosome enzymes are made in the ____________, then transferred to the ____________, which then becomes a lysosome.

A

ER; endosome

106
Q

Lysosome size

A

0.5-1.0 µm

107
Q

Lysosomal storage disorders usually result in a __________ defect in a single lysosomal enzyme.

A

Genetic

108
Q

Receptor- Mediated Endocytosis Steps

A
  1. Ligands bind receptors at cell surface
  2. Ligand-bound receptors cluster in clathrin- coated pits
  3. Coated pits form coated vesicles
  4. Receptors and ligands go to early endosomes
109
Q

What is the difference between lysosomes and lysosome related organelles?

A

Lysosome relate organelles are cell specific

110
Q

Endosome turns into_________

A

Lysosome

111
Q

__________diseases can be caused by misfolded proteins.

A

Prion

112
Q

Endosomes are also known as _____________

A

Multi-vesicular bodies

113
Q

Types of endocytosis

A
  1. Phagocytosis
  2. Pinocytosis
  3. Receptor- mediated endocytosis (RME)
114
Q

Are lysosomes heterogeneous or homogeneous ?

A

Heterogeneous

115
Q

ATP depleted. Necrosis or apoptosis.

A

Necrosis

116
Q

Lysosome and Neuro-degeneration disorders

A

Gaucher’s Disorder

Alzheimer’s Disease

117
Q

Symptoms of Type 2 Gaucher Disease

A
  1. Neuropathic forms
  2. Type 1 symptoms, abnormal eye movements, seizures, and brain damage
  3. Type 2 is lethal in infancy
  4. Type is slower progressing
118
Q

Which type of cell death requires ATP?

A

Apoptosis

119
Q

Enzyme reaction Tay- Sachs Disease

A

GM2->GM3

120
Q

Transcytosis occurs in __________ cells

A

Epithelial cells

121
Q

3 steps to Autophagy

A
  1. Initiation
  2. Elongation and Closure
  3. Degradation
122
Q

End products of lysosomal digestion

A

Lipofuscin granules

Exam 2 (PARP) (17 decks)

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