Cell Bio Exam 3

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  1. What is autophagy?
    this process is used to dispose of parts of the cell’s own organelles. A used organelle is enclosed by a double membrane of unknown origin, creating an autophagosome, which then fuses with a lysosome.
  2. What is receptor-mediated endocytosis?
    Receptor-mediated endocytosis (RME), also called clathrin-dependent endocytosis, is a process by which cells internalize molecules (endocytosis) by the inward budding of plasma membrane vesicles containing proteins with receptor sites specific to the molecules being internalized.
  3. Fc receptors
    In phagocytosis, when antibodies coat foreign bodies, their coat exposes the Fc region. This region is recognized by special Fc receptors that are located on the surface of macrophages and neutrophils.
  4. What causes Hurler Syndrome?
    A genetic disorder caused by a deficiency of alpha-L-iduronidase, an enzyme responsible for the degradation of heparan sulfate and dermatan sulfate.
  5. What happens to a patient with Hurler Syndrome?
    • - buildup of glycosaminoglycans
    • - enlargement of spleen and liver
    • - mental retardation
    • - faulty degradation of connective tissue, CNS, heart valve flexibility
    • - death occurring around 10 years of age
  6. What does M. tuberculosis do to avoid being killed?
    • prevents the fusion between the phagosome with the lysosome
    • lives in the phagosome, so it goes undetected
    • stops the acidification and maturation of lysosomes (pH 6.4)
  7. Triskelion
    • makes up a clathrin coat
    • each triskelion is composed of 3 clathrin heavy chains and 3 clathrin light chains
    • assemble into a basketlike convex framework of hexagons and pentagons to form coated pits on membranes
  8. Composition of an LDL molecule
    • Each particle consists of a surface monolayer of phospholipids and cholesterol,
    • a core of cholesterol-fatty acid esters,
    • and one molecule of the protein Apo B.
    • Each LDL particle contains a core of about 1500 cholesterol molecules.
    • A large protein called apolipoprotein B-100 organizes the particle and mediates the specific binding of LDL to cell-surface LDL receptors.
  9. Development of atherosclerosis plaque
    • 1. Some of the endothelial cells may detach from the lining of the tube, exposing muscle fibers.
    • 2. LDL may stick to the exposed opening.
    • 3. Macrophages migrate to the tube and try to eat up the LDL, but become overwhelmed and die, becoming foam cells.
    • 4. More macrophages arrive, further blocking the artery.
  10. What is the difference between a stable and unstable atherosclerotic plaque?
    • Stable plaques are rich in extracellular matrix and smooth muscle cells,
    • while unstable plaques are rich in macrophages and foam cells, and likely to be ruptured.
  11. How do statins reduce cholesterol levels?
    • By inhibiting HMG-CoA reductase, statins block the pathway for synthesizing cholesterol in the liver.
    • This is significant because most circulating cholesterol comes from internal manufacture rather than the diet.
    • When the liver can no longer produce cholesterol, levels of cholesterol in the blood will fall.
  12. V-SNARE
    • made out of synaptobrevin, an alpha-helical transmembrane protein
    • is attached to the synaptic vesicle
  13. T-SNARE
    • made up of syntaxin, is also an alpha-helical transmembrane protein
    • t-SNARE strands are attached to the target membrane
  14. Snap25
    • contributes 2 alpha-helices that are attached by a loop.
    • Snap 25 is a peripheral membrane protein.
  15. How do SNAREs function in vesicle docking?
    • These SNAREs catalyze membrane fusion by using the energy that is freed when the interacting helices wrap around each other to pull the membranes together, while squeezing out water molecules from the interface.
    • Lipid molecules in the two interacting bilayers then flow between the membranes to form a connecting membrane.
  16. Rab proteins, what are they and when are they active?
    • highly conserved proteins that direct the vesicle to specific spots on the correct target membrane.
    • function on transport vesicles, on target membranes, or both.
    • cycle between GDP-bound and GTP-bound states.
    • In their GDP-bound state, they are inactive and bound to another protein that keeps them soluble in the cytosol.
    • In their GTP-bound state, they are active and tightly associated with the membrane of an organelle or transport vesicle.
  17. Rab effectors
    • these structures vary greatly.
    • Some are motor proteins that propel vesicles along to their target membrane,
    • while others are tethering proteins that have long threadlike domains that serve as “fishing lines.” (located on the target membrane.
  18. What kind of defects are seen in the receptors of familial hypercholesterolemias?
    • receptor may not be produced
    • receptor may be underproduced
    • LDL doesn't bind to receptors
    • if the LDL does bind, it doesn't internalize the LDL
  19. Pinocytosis
    • takes in extracellular fluids
    • non-specific unlike receptor-mediated endocytosis
    • requires ATP
    • generates very small vesicles
  20. How do syphilis cells evade the immune system?
    • treponema pallidum
    • hides from phagocytes by coating its surface with fibronectin, which is produced naturally by the body - wound healing
  21. How do legionella pneuomophila cells evade the immune system?
    • Legionella is phagocytosed by lung macrophages
    • the phagosome is fused with the rough ER instead of being delivered to the lysosome.
    • the Legionella proliferate inside the phagosome.
  22. What degrades:
    • cathepsin
    • collagenase
    • acid ribonuclease
  23. Describe the process by which iron gets taken into the cell.
    • Iron gets attached to a signaling glycoprotein called transferrin.
    • The transferrin with iron will bind to transferrin receptors on the cell surface and enter the cell via receptor-mediated endocytosis.
    • The vesicle is delivered to the early endosome which has a slightly lower pH, causing iron to fall off the transferrin.
    • Iron is retained in the cell, while transferrin gets recycled back to the membrane.
  24. Vesicle Transport Model
    Cargo proteins get delivered to the 1st layer of the cisternae and move in sequence, while the layers of the Golgi and its enzymes remain held in place.
  25. Lamellan Maturation Model
    • the Golgi is a dynamic structure where the cisternae themselves move.
    • The vesicles that arrive from the ER fuse with one another to become a cis Golgi network.
    • Then, it would push the next layers back.
    • Budding COPI-vesicles would collect the appropriate enzymes and carry them back to the earlier cisterna where they function.
  26. What was the Pulse-Chase technique?
    • Slice cells.
    • Put slices in container with necessary amino acids.
    • At 0 min, add radioactive 3H leucine.
    • At 3 min, add nonradioactive leucine to dilute solution.
    • Fix tissue to a slide.
    • Cover slide with silver bromide photographic emulsion solution.
    • The silver in the solution will interact with the photons emitted by the decay of the radioactive leucine.
  27. What were the results of the Pulse-Chase?
    3, 10, 30, 2 hrs
    • 3 min: proteins were found on rough ER.
    • 10 min: found in cytoplasmic area between ER and Golgi Apparatus.
    • 30-60 min: found in the Golgi.
    • 2 hrs: found in the apical region of the acinar cell, where they’re supposed to be.
  28. What are the characteristics of the signal peptide?
    • 6-15 amino acids long
    • made up of mostly hydrophobic side chains because it needs to be able to get into the membrane.
  29. Describe the process of protein translocation into the ER.
    • SRP attaches to the signal peptide of a growing peptide coming out of a ribosome
    • It halts translation and delivers the ribosome and peptide being translated to an SRP receptor on the rER membrane.
    • The receptor brings the ribosome close to and allows it to attach to the protein translocator on the rER membrane.
    • The signal peptide is then threaded through the pore of the protein translocator and curves around to go to the seam of the protein translocator and the peptide is allowed to continue translation and is “dumped” into the lumen of the rER through the protein translocator.
  30. Where do COPI-coated vesicles bud from?
    bud from Golgi compartments
  31. Where do COPII-coated vesicles bud from?
    the ER
Card Set:
Cell Bio Exam 3
2011-11-21 05:19:07
cell bio endocytosis transport

Cellular Transport Systems
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