Rescuing defective vesicular trafficking protects against alpha-synuclein toxicity in cellular and animal models of Parkinson's disease.

Hilal A. Lashuel, Harald Hirling

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

Studies in yeast are providing critical insights into the mechanisms of neurodegeneration in Parkinson's disease (PD). A recent study shows that disruption of vesicular trafficking between the endoplasmic reticulum (ER) and the Golgi, caused by the overexpression and/or aggregation of alpha-synuclein, is linked to degeneration of dopamine neurons. Overexpression of proteins that are known to enhance ER-to-Golgi transport rescue defective trafficking in yeast, worm, fly, and cellular models of PD.

Original languageEnglish
Pages (from-to)420-424
Number of pages5
JournalACS Chemical Biology
Volume1
Issue number7
DOIs
Publication statusPublished - 22 Aug 2006
Externally publishedYes

Fingerprint

alpha-Synuclein
Endoplasmic Reticulum
Yeast
Parkinson Disease
Toxicity
Animals
Animal Models
Yeasts
Dopaminergic Neurons
Diptera
Neurons
Dopamine
Agglomeration
Proteins

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Rescuing defective vesicular trafficking protects against alpha-synuclein toxicity in cellular and animal models of Parkinson's disease. / Lashuel, Hilal A.; Hirling, Harald.

In: ACS Chemical Biology, Vol. 1, No. 7, 22.08.2006, p. 420-424.

Research output: Contribution to journalArticle

@article{786868dcdda04ed893b6868e3351a295,
title = "Rescuing defective vesicular trafficking protects against alpha-synuclein toxicity in cellular and animal models of Parkinson's disease.",
abstract = "Studies in yeast are providing critical insights into the mechanisms of neurodegeneration in Parkinson's disease (PD). A recent study shows that disruption of vesicular trafficking between the endoplasmic reticulum (ER) and the Golgi, caused by the overexpression and/or aggregation of alpha-synuclein, is linked to degeneration of dopamine neurons. Overexpression of proteins that are known to enhance ER-to-Golgi transport rescue defective trafficking in yeast, worm, fly, and cellular models of PD.",
author = "Lashuel, {Hilal A.} and Harald Hirling",
year = "2006",
month = "8",
day = "22",
doi = "10.1021/cb600331e",
language = "English",
volume = "1",
pages = "420--424",
journal = "ACS Chemical Biology",
issn = "1554-8929",
publisher = "American Chemical Society",
number = "7",

}

TY - JOUR

T1 - Rescuing defective vesicular trafficking protects against alpha-synuclein toxicity in cellular and animal models of Parkinson's disease.

AU - Lashuel, Hilal A.

AU - Hirling, Harald

PY - 2006/8/22

Y1 - 2006/8/22

N2 - Studies in yeast are providing critical insights into the mechanisms of neurodegeneration in Parkinson's disease (PD). A recent study shows that disruption of vesicular trafficking between the endoplasmic reticulum (ER) and the Golgi, caused by the overexpression and/or aggregation of alpha-synuclein, is linked to degeneration of dopamine neurons. Overexpression of proteins that are known to enhance ER-to-Golgi transport rescue defective trafficking in yeast, worm, fly, and cellular models of PD.

AB - Studies in yeast are providing critical insights into the mechanisms of neurodegeneration in Parkinson's disease (PD). A recent study shows that disruption of vesicular trafficking between the endoplasmic reticulum (ER) and the Golgi, caused by the overexpression and/or aggregation of alpha-synuclein, is linked to degeneration of dopamine neurons. Overexpression of proteins that are known to enhance ER-to-Golgi transport rescue defective trafficking in yeast, worm, fly, and cellular models of PD.

UR - http://www.scopus.com/inward/record.url?scp=39049190040&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=39049190040&partnerID=8YFLogxK

U2 - 10.1021/cb600331e

DO - 10.1021/cb600331e

M3 - Article

VL - 1

SP - 420

EP - 424

JO - ACS Chemical Biology

JF - ACS Chemical Biology

SN - 1554-8929

IS - 7

ER -