Autophagy inhibition promotes defective neosynthesized proteins storage in ALIS, and induces redirection toward proteasome processing and MHCI-restricted presentation.

Wenger, Till

Autophagy inhibition promotes defective neosynthesized proteins storage in ALIS, and induces redirection toward proteasome processing and MHCI-restricted presentation. [electronic resource] - Autophagy Mar 2012 - 350-63 p. digital

Publication Type: Journal Article; Research Support, Non-U.S. Gov't

1554-8635

10.4161/auto.18806 doi


Adaptor Proteins, Signal Transducing--metabolism
Antigen Presentation--drug effects
Autophagy--drug effects
Green Fluorescent Proteins--metabolism
HeLa Cells
Histocompatibility Antigens Class I--immunology
Humans
Inclusion Bodies--drug effects
Intracellular Signaling Peptides and Proteins
Molecular Chaperones--metabolism
NF-E2-Related Factor 2--metabolism
Proteasome Endopeptidase Complex--metabolism
Proteasome Inhibitors--pharmacology
Protein Biosynthesis--drug effects
Protein Folding--drug effects
Protein Processing, Post-Translational--drug effects
Protein Structure, Quaternary
Proteins--metabolism
Proteolysis--drug effects
Puromycin--pharmacology
Recombinant Fusion Proteins--metabolism
Ribosomes--metabolism
Sequestosome-1 Protein
Signal Transduction--drug effects
Substrate Specificity--drug effects
Transcription, Genetic--drug effects
Ubiquitin--metabolism