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A lipid-based model for the creation of an escape hatch from the endoplasmic reticulum
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A lipid-based model for the creation of an escape hatch from the endoplasmic reticulum
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Journal Article
A lipid-based model for the creation of an escape hatch from the endoplasmic reticulum
2007
Overview
Ditch the 'dislocon'?
A protein channel has been hypothesized as a component of the endoplasmic reticulum (ER) to account for the fact that misfolded proteins and non-enveloped viruses can pass through the ER into the cytoplasm. Der1 protein in yeast and the Derlins in other eukaryotes are examples of protein types that might function in such a dislocation channel or 'dislocon'. But Hidde Ploegh, writing in our occasional Hypothesis series, suggests an alternative mechanism that might do the job without the need for a protein-based channel. Instead, an escape hatch triggered by lipid rearrangement would allow both proteins and viruses to traverse the ER.
Lipids are not encoded by a DNA template and therefore cannot be mutated, knocked out or knocked down. This by no means renders them impotent from a cell biological perspective. Here I propose a model for the involvement of lipid rearrangements in the execution of crucial steps in (glyco)protein quality control.
Publisher
Nature Publishing Group UK,Nature Publishing,Nature Publishing Group
Subject
/ Biological and medical sciences
/ DNA
/ Endoplasmic Reticulum - chemistry
/ Endoplasmic Reticulum - metabolism
/ Endoplasmic Reticulum - virology
/ Fundamental and applied biological sciences. Psychology
/ Hatches
/ Humanities and Social Sciences
/ Lipids
/ Membrane and intracellular transports
/ Molecular and cellular biology
/ Mutation
/ Science
