Article
Apolipoprotein B100 exit from the endoplasmic reticulum (ER) is COPII-dependent, and its lipidation to very low density lipoprotein occurs post-ER.
The Journal of biological chemistry - 28 Nov 2003
Gusarova Viktoria, Brodsky Jeffrey L, Fisher Edward A
Abstract excerpt
Hepatic apolipoprotein B100 (apoB100) associates with lipids to form dense lipoprotein particles in the endoplasmic reticulum (ER) and is further lipidated to very low density lipoproteins (VLDL). Because the VLDL diameter can exceed 200 nm, classical ER-derived vesicles may be unable to accommodate VLDLs. Using hepatic membranes and cytosol to reconstitute ER budding, apoB100-containing vesicles sedimented...
Topics
- Animals
- Apolipoprotein B-100
- Apolipoproteins B
- Blotting, Western
- COP-Coated Vesicles
- Cell Line
- Cell Membrane
- Cell-Free System
- Centrifugation, Density Gradient
- Cytosol
- Endoplasmic Reticulum
- Fluorescent Antibody Technique, Indirect
- GTPase-Activating Proteins