Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Combined Knockout of Lrrk2 and Rab29 Does Not Result in Behavioral Abnormalities in vivo.

Journal of Parkinson's disease - 1 Jan 2021

Mazza Melissa Conti, Nguyen Victoria, Beilina Alexandra, Karakoleva Ema, Coyle Michael, Ding Jinhui, Bishop Christopher, Cookson Mark R

Abstract excerpt

BACKGROUND: Coding mutations in the LRRK2 gene, encoding for a large protein kinase, have been shown to cause familial Parkinson's disease (PD). The immediate biological consequence of LRRK2 mutations is to increase kinase activity, suggesting that inhibition of this enzyme might be useful therapeutically to slow disease progression. Genome-wide association studies have identified the chromosomal loci around...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Corpus Striatum
Share to Genome-Wide Association Study

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Leucine-Rich Repeat Serine-Threonine Protein Kinase-2

Share to Mice, Knockout

Share to Mutation

Share to Parkinson Disease

Source

Open in PubMed Open full text

Identifiers

PMID: 33523017
DOI: 10.3233/JPD-202172
PMCID: PMC9272729

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Combined Knockout of Lrrk2 and Rab29 Does Not Result in Behavioral Abnormalities in vivo.PMID 33523017Read ↗

Combined knockout of <i>Lrrk2</i> and <i>Rab29</i> does not result in behavioral abnormalities <i>in vivo</i>Semantic proximity Read ↗

LRRK2 mouse models: dissecting the behavior, striatal neurochemistry and neurophysiology of PD pathogenesis.Semantic proximity Read ↗

LRRK2 knockout mice have an intact dopaminergic system but display alterations in exploratory and motor co-ordination behaviors.Semantic proximity Read ↗

Enhanced striatal dopamine transmission and motor performance with LRRK2 overexpression in mice is eliminated by familial Parkinson's disease mutation G2019S.Semantic proximity Read ↗

LRRK2 at Striatal Synapses: Cell-Type Specificity and Mechanistic Insights.Semantic proximity Read ↗

Genetic LRRK2 models of Parkinson's disease: Dissecting the pathogenic pathway and exploring clinical applications.Semantic proximity Read ↗

Cell autonomous role of leucine-rich repeat kinase in protection of dopaminergic neuron survivalSemantic proximity Read ↗

Behavioral Deficits and Striatal DA Signaling in LRRK2 p.G2019S Transgenic Rats: A Multimodal Investigation Including PET NeuroimagingSemantic proximity Read ↗

Modeling Parkinson’s disease in LRRK2 rodentsSemantic proximity Read ↗

Dopaminergic Neurodegeneration Induced by Parkinson’s Disease-Linked G2019S LRRK2 is Dependent on Kinase and GTPase ActivitySemantic proximity Read ↗

Robust kinase- and age-dependent dopaminergic and norepinephrine neurodegeneration in LRRK2 G2019S transgenic mice.Semantic proximity Read ↗

Dopaminergic neurodegeneration induced by Parkinson's disease-linked G2019S LRRK2 is dependent on kinase and GTPase activity.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.