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

ER-mitochondria contact sites in neurodegeneration: genetic screening approaches to investigate novel disease mechanisms

17 Dec 2020

Abstract excerpt

Mitochondria-ER contact sites (MERCS) are known to underpin many important cellular homoeostatic functions, including mitochondrial quality control, lipid metabolism, calcium homoeostasis, the unfolded protein response and ER stress. These functions are known to be dysregulated in neurodegenerative diseases, including Parkinson's disease (PD), Alzheimer's disease (AD) and amyloid lateral sclerosis (ALS), and the...

Read the complete abstract on PubMed

Topics

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

Share to Alzheimer's disease research and treatments
Share to Endoplasmic Reticulum Stress and Disease
Share to Mitochondrial Function and Pathology

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 33335290
DOI: 10.1038/s41418-020-00705-8

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

ER-mitochondria contact sites in neurodegeneration: genetic screening approaches to investigate novel disease mechanismsPMID 33335290Read ↗

Impaired mitochondrial–endoplasmic reticulum interaction and mitophagy in Miro1-mutant neurons in Parkinson’s diseaseSemantic proximity Read ↗

Decreasing pdzd8-mediated mito–ER contacts improves organismal fitness and mitigates Aβ 42 toxicitySemantic proximity Read ↗

Inter-organellar Communication in Parkinson's and Alzheimer's Disease: Looking Beyond Endoplasmic Reticulum-Mitochondria Contact SitesSemantic proximity Read ↗

Genome-wide CRISPR/Cas9 screen shows that loss of GET4 increases mitochondria-endoplasmic reticulum contact sites and is neuroprotective.Semantic proximity Read ↗

PINK1/Parkin Mediated Mitophagy, Ca2+ Signalling, and ER–Mitochondria Contacts in Parkinson’s DiseaseSemantic proximity Read ↗

Miro1 mutations disrupt cellular calcium homeostasis via dysregulation of mitochondria-ER-contact-sites, rendering iPSC-derived neurons more susceptible to lipid peroxidation.Semantic proximity Read ↗

The Role of Mitochondrial Dysfunction and ER Stress in TDP-43 and C9ORF72 ALSSemantic proximity Read ↗

Parkinson’s genes orchestrate pyroptosis through selective trafficking of mtDNA to leaky lysosomesSemantic proximity Read ↗

Altered MICOS Morphology and Mitochondrial Ion Homeostasis Contribute to Poly(GR) Toxicity Associated with C9-ALS/FTDSemantic proximity Read ↗

Partial loss of MCU mitigates pathology in vivo across a diverse range of neurodegenerative disease modelsSemantic proximity Read ↗

Cellular senescence links mitochondria-ER contacts and agingSemantic proximity Read ↗

The Emerging Role of RHOT1/Miro1 in the Pathogenesis of Parkinson's DiseaseSemantic proximity Read ↗

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