Deletion of lrrk2 causes early developmental abnormalities and age-dependent increase of monoamine catabolism in the zebrafish brain.
LRRK2 gain-of-function is considered a major cause of Parkinson's disease (PD) in humans. However, pathogenicity of LRRK2 loss-of-function in animal models is controversial. Here we show that deletion of the entire zebrafish lrrk2 locus elicits a pleomorphic transient brain phenotype in materna...
Saved in:
Main Authors: | Stefano Suzzi, Reiner Ahrendt, Stefan Hans, Svetlana A Semenova, Avinash Chekuru, Paul Wirsching, Volker Kroehne, Saygın Bilican, Shady Sayed, Sylke Winkler, Sandra Spieß, Anja Machate, Jan Kaslin, Pertti Panula, Michael Brand |
---|---|
Format: | article |
Language: | EN |
Published: |
Public Library of Science (PLoS)
2021
|
Subjects: | |
Online Access: | https://doaj.org/article/66a7d68b5aa74d34a2b220b852048894 |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Similar Items
-
LRRK2 kinase activity is dependent on LRRK2 GTP binding capacity but independent of LRRK2 GTP binding.
by: Jean-Marc Taymans, et al.
Published: (2011) -
Storage of neural histamine and histaminergic neurotransmission is VMAT2 dependent in the zebrafish
by: Henri A. J. Puttonen, et al.
Published: (2017) -
Cryo-EM analysis of homodimeric full-length LRRK2 and LRRK1 protein complexes
by: Kushal Sejwal, et al.
Published: (2017) -
The dual-gate lumen model of renal monoamine transport
by: Marty Hinz, et al.
Published: (2010) -
Understanding LRRK2 kinase activity in preclinical models and human subjects through quantitative analysis of LRRK2 and pT73 Rab10
by: Xiang Wang, et al.
Published: (2021)