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

<i>Drosophila</i> CHIP protects against mitochondrial dysfunction by acting downstream of Pink1 in parallel with Parkin

4 Aug 2017

Abstract excerpt

ABSTRACT Mitochondrial kinase PTEN‐induced putative kinase 1 (PINK1) and E3 ubiquitin ligase Parkin function in a common pathway to regulate mitochondrial homeostasis contributing to the pathogenesis of Parkinson disease. The carboxyl terminus of Hsc70‐interacting protein (CHIP) acts as a heat shock protein 70/heat shock protein 90 cochaperone to mediate protein folding or as an E3 ubiquitin ligase to target...

Read the complete abstract on PubMed

Topics

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

Share to Autophagy in Disease and Therapy
Share to Mitochondrial Function and Pathology
Share to Parkinson's Disease Mechanisms and Treatments

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 28778978
DOI: 10.1096/fj.201700011r

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

<i>Drosophila</i> CHIP protects against mitochondrial dysfunction by acting downstream of Pink1 in parallel with ParkinPMID 28778978Read ↗

Disease-associated mutations in C-terminus of HSP70 interacting protein (CHIP) impair its ability to negatively regulate mitophagy.Semantic proximity Read ↗

Parkin, PINK1, and DJ-1 form a ubiquitin E3 ligase complex promoting unfolded protein degradationSemantic proximity Read ↗

The complex I subunit NDUFA10 selectively rescues Drosophila pink1 mutants through a mechanism independent of mitophagy.Semantic proximity Read ↗

DJ-1 is critical for mitochondrial function and rescues PINK1 loss of function.Semantic proximity Read ↗

CHIP deficiency decreases longevity, with accelerated aging phenotypes accompanied by altered protein quality control.Semantic proximity Read ↗

Ubp2 modulates DJ-1-mediated redox-dependent mitochondrial dynamics in <i>Saccharomyces cerevisiae</i>Semantic proximity Read ↗

Autophagy inhibition rescues structural and functional defects caused by the loss of mitochondrial chaperone <i>Hsc70-5/mortalin</i> in <i>Drosophila</i>Semantic proximity Read ↗

Mitochondrial pathology and muscle and dopaminergic neuron degeneration caused by inactivation of Drosophila Pink1 is rescued by ParkinSemantic proximity Read ↗

CHIP Is Associated with Parkin, a Gene Responsible for Familial Parkinson's Disease, and Enhances Its Ubiquitin Ligase ActivitySemantic proximity Read ↗

Overexpressed PERK suppresses the neurodegenerative phenotypes in PINK1B9 flies by enhancing mitochondrial function.Semantic proximity Read ↗

The STING pathway does not contribute to <i>Pink1/parkin</i> phenotypes in <i>Drosophila</i>Semantic proximity Read ↗

Deficiency in MICOS component Chchd3 Compromises Drosophila Heart Function via mitophagy, ROS and ER StressSemantic proximity Read ↗

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