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

Loss of PINK1 enhances neurodegeneration in a mouse model of Parkinson's disease triggered by mitochondrial stress

23 Oct 2013

Abstract excerpt

Parkinson's disease (PD) shows a complex etiology, where both genetic and environmental factors contribute to initiation and advance of pathology. Mitochondrial dysfunction and mutation of genes implicated in mitochondria quality control are recognized contributors to etiopathology and progression of PD. Here we report the development and characterization of a genetic mouse model of PD with a combined etiology...

Read the complete abstract on PubMed

Topics

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

Share to Endoplasmic Reticulum Stress and Disease
Share to Neurological diseases and metabolism
Share to Parkinson's Disease Mechanisms and Treatments

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 24161480
DOI: 10.1016/j.neuropharm.2013.10.009

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Loss of PINK1 enhances neurodegeneration in a mouse model of Parkinson's disease triggered by mitochondrial stressPMID 24161480Read ↗

Activation of the mitochondrial unfolded protein response promotes longevity and dopamine neuron survival in Parkinson's disease models.Semantic proximity Read ↗

Oxidative Stress in Genetic Mouse Models of Parkinson’s DiseaseSemantic proximity Read ↗

Inactivation of Pink1 Gene in Vivo Sensitizes Dopamine-producing Neurons to 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and Can Be Rescued by Autosomal Recessive Parkinson Disease Genes, Parkin or DJ-1Semantic proximity Read ↗

A subcellular analysis of genetic modulation of PINK1 on mitochondrial alterations, autophagy and cell death.Semantic proximity Read ↗

Selective disruption of Drp1-independent mitophagy and mitolysosome trafficking by an Alzheimer’s disease relevant tau modification in a novelCaenorhabditis elegansmodelSemantic proximity Read ↗

S-Nitrosylation of PINK1 Attenuates PINK1/Parkin-Dependent Mitophagy in hiPSC-Based Parkinson's Disease Models.Semantic proximity Read ↗

TP53INP1 exerts neuroprotection under ageing and Parkinson’s disease-related stress conditionSemantic proximity Read ↗

G2019S-LRRK2 mutation enhances MPTP-linked Parkinsonism in mice.Semantic proximity Read ↗

Mutant PINK1 upregulates tyrosine hydroxylase and dopamine levels, leading to vulnerability of dopaminergic neurons.Semantic proximity Read ↗

Bacterial artificial chromosome transgenic mice expressing a truncated mutant parkin exhibit age-dependent hypokinetic motor deficits, dopaminergic neuron degeneration, and accumulation of proteinase K-resistant alpha-synuclein.Semantic proximity Read ↗

Mitofusin-mediated ER stress triggers neurodegeneration in pink1/parkin models of Parkinson's disease.Semantic proximity Read ↗

Stress-induced phospho-ubiquitin formation causes parkin degradationSemantic proximity Read ↗

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