Kinase activity is required for the toxic effects of mutant LRRK2/dardarin
Top Cited Papers
- 1 August 2006
- journal article
- Published by Elsevier in Neurobiology of Disease
- Vol. 23 (2) , 329-341
- https://doi.org/10.1016/j.nbd.2006.04.001
Abstract
No abstract availableKeywords
This publication has 28 references indexed in Scilit:
- How genetics research in Parkinson's disease is enhancing understanding of the common idiopathic forms of the diseaseCurrent Opinion in Neurology, 2005
- THE BIOCHEMISTRY OF PARKINSON'S DISEASEAnnual Review of Biochemistry, 2005
- An LRRK2 mutation as a cause for the parkinsonism in the original PARK8 familyAnnals of Neurology, 2005
- Presenilin function and γ‐secretase activityJournal of Neurochemistry, 2005
- Mutations in PTEN-induced putative kinase 1 associated with recessive parkinsonism have differential effects on protein stabilityProceedings of the National Academy of Sciences, 2005
- LRRK2 mutations and ParkinsonismThe Lancet, 2005
- Inclusion body formation reduces levels of mutant huntingtin and the risk of neuronal deathNature, 2004
- Roc, a Ras/GTPase domain in complex proteinsBiochimica et Biophysica Acta (BBA) - Molecular Cell Research, 2003
- Intracellular clusterin causes juxtanuclear aggregate formation and mitochondrial alterationJournal of Cell Science, 2003
- A new locus for Parkinson's disease (PARK8) maps to chromosome 12p11.2–q13.1Annals of Neurology, 2002