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Chapter 17
Vesicular Traffics, Secretion, and Endocytosis
SNARE : SNAP Receptor
SNAP : Soluble NSF Attached Protein
NSF : N-ethylmaleimide (NEM)- Sensitive Factor
COP I : Coat Complex I (Coat Protein)
COP II : Coat Complex II
GGAs : Golgi-associated γ-Adaptin homologues,
Arf-binding
ARF : ADP-ribosylating Factor
VAMP : vesicle-associated membrane protein ( v-SNARE)
Main Content:
1. Techniques for studying the secretory pathway
2. Molecular mechanisms of vesicular traffic
3. Early stages of the secretory pathway
4. Later stages of the secretory pathway
5. Receptor-mediated endocytosis and the sorting of
the internalized proteins
6. Synaptic vesicle function and formation
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Proteins are first transported from ER to Trans-Golgi Network (TGN), and then, transported further via three separate pathways:
1. Constitutive secretion : to the plasma membrane
2. Regulated secretion : stored as secretory vesicle, and
released with stimulus
3. From TGN to late endosomes and then lysosomes
Molecular Mechanisms of Vesicular Traffic
Donor
Vesicle Formation
Budding
Docking
FusionWith Acceptor
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Coat Assembly and Disassembly
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How do vesicles select /recruit correct cargo proteins?
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Docking and Fusion of Transport
Vesicle with its Target Membrane
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(Summary)Molecular mechanisms of vesicular traffic
1. Three types of transport vesicles : COP I, COP II and clatherin
2. Polymerization of cytosolic coat proteins to form a coat for the vesicle
3. Pinch off & release vesicle, decoating→move →docking→fusion
The coat proteins for either constitutive or regulated
vesicles are unknown
Regulated Secretion:
1. trans-Golgi network → bud out→store in a special vesicle, and release by a special stimulus
2. A common mechanism appears to sort regulated proteins. These proteins selectively aggregate together , and withchromogranin A, chromogranin B and secretogranin II before their incorporation into the vesicles.
Proteolytical Processing ofsecretory proteins
Proproteins→ Proteins
Occurs after the secretoryvesicles budded from the TGN
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Receptor-Mediated Endocytosis and
the Sorting of Internalized Proteins
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Type II Familial Hypercholesterolemia
1.normal binding between LDL and LDL receptor, but, no internalization
causes: no interaction between LDL receptor and
clathrin/AP2 coated pits, due to the lack of
sorting sequence
NPXY (Asn, Pro, X, Tyr)
2. In some patients: LDL receptor is normal, but AP2 gene defect, which cannot recognize NPXY