Membrane Trafficking Flashcards Preview

MCD - Metabolism > Membrane Trafficking > Flashcards

Flashcards in Membrane Trafficking Deck (15):
1

Explain exocytosis

A mechanism for secreting intracellular materials using ATP.

2

Explain endocytosis

A mechanism for importing extracellular materials using ATP.

3

Define constitutive secretion

Steady stream of vesicles that bud from the trans Golgi network and fuse with plasma membrane to release its contents. Used by all cells

4

Define regulated secretion

Products are concentrated and stored in secretory vesicles until an extracellular signal stimulates their secretion. Only used by specialised cells

5

Summarise exocytosis pathway including cellular locations for secreted protein

1) Synthesis (ribosomes on rough ER)
2) Post-translational modifications (lumen of rough ER)
3) Exocytosis (vesicles containing protein move from trans face of Golgi app. to cell membrane)

6

Which important type of molecule do Low Density Lipoproteins contain?

Cholesterol

7

Summarise the process of receptor-mediated endocytosis

1) LDL receptors are activated by binding of LDLs
2) LDLs cluster to form a clathrin coated pit
3) Invaginates to form a clathrin coated vesicle
4) Vesicle becomes uncoated and fuses with an early endosome, LDL receptors recycled to cell membrane
5) Endosome fused with lysosome to release the cholesterol
6) Lysosome releases free cholesterol into intracellular space and now contains endocytosed hydrolytic enzymes.

8

Explain pinocytosis

Ingestion of fluid into a cell via budding of small vesicles from cell membrane

9

Phagocytosis

Ingestion or engulfing of solid molecules into phagosomes e.g. microbes uptaken for destruction.

10

Summarise the molecular mechanism of vesicular transport within cells

1) Cargo sorting in lumen and vesicle formation in donor membrane
2) Vesicle movement, involving microtubules and actin (in cytoskeleton)
3) Vesicle tethering/docking via an acceptor compartment membrane (protein) (protein mediated tethering)
4) Vesicle fusion with acceptor membrane and release of cargo

11

Diseases associated with membrane trafficking failure

Cystic Fibrosis
Robinow Syndrome
Familial Hypercholesteraemia

12

Explain the mechanisms underlying Cystic Fibrosis

CFTR gene mutation
- CFTR protein doesn't fold normally and is degraded in ER.

13

Explain the mechanisms underlying Robinow Syndrome

Cell surface tyrosine kinase receptor responsible for aspects of cartilage and bone growth mutation.
Mutation causes retention and degradation of the receptor in ER.

14

What is the root cause underlying Familial Hypercholesteraemia?

Excessive LDL levels as unable to store LDL in cells

15

Explain the 5 types of mechanisms underlying Familial Hypercholesteraemia

1) LDL receptor not synthesised
2) LDLR not transported from ER to Golgi properly = low cell surface expression
3) LDLR doesn't bind LDL effectively
4) LDLR:LDL complex doesn't cluster in clathrin-coated pits for receptor mediated endocytosis
5) LDL not released from receptor in endosome and LDLR not recycled back to cell surface