ReviewCell death and differentiation2021
ER-mitochondria contact sites in neurodegeneration: genetic screening approaches to investigate novel disease mechanisms.
Review in Cell death and differentiation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 93 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
93 citing papers in PubMed.
- Ion-GPS nanocapsules activate calcium-permeable gates in inflammatory microglia for nerve function recovery.Bioactive materials · 2026Article
- Inter-Organelle Membrane Contact Sites as Physiological Regulatory Hubs in the Brain: From Neurons to Glial Cells.Biomolecules · 2026Review
- Mitoxyperiosis: A Novel Mitochondria-Driven Cell Death Mechanism in Immunometabolic Stress.Cell biology international · 2026Review
- GRP75 sustains CD8Cell death and differentiation · 2026Article
- ERO1a fosters glioblastoma aggressiveness and metabolic flexibility by regulating mitochondria-associated membrane dynamics.Nature cell biology · 2026Article
- Alzheimer's Disease and MERC Dysfunction: Integrating Mechanisms, Biomarkers, and Therapeutic Strategies.Molecular neurobiology · 2026Review
- Cell Structure Segmentation in TEM Images of Murine Skin Melanoma Cells by Deep Learning Model.Journal of imaging · 2026Article
- Excessive ER-mitochondria coupling: A DRP1-driven mechanism underlying mitochondrial dysfunction and impaired autophagy in stress-induced depression-like behavior in mice.Redox biology · 2026Article
- Natural photosynthetic system for restoring homeostasis of animal organelle interaction network.Nature communications · 2026Article
- Parkinson's disease-associated PLA2G6 protects IP3R1 protein to control ER-mitochondria tethering and CaNature communications · 2026Article
- Filamin A phosphorylation at S2152: a molecular switch fueling cancer and neurodegeneration.Cell communication and signaling : CCS · 2026Review
- Maternal High-Fat Diet Worsens Necrotizing Enterocolitis via Effects on Mitochondrial Function in Newborn Mice.Cellular and molecular gastroenterology and hepatology · 2026Article
- Parkin Deficiency Impairs ER-Mitochondria Associations and calcium homeostasis via IP3R-Grp75-VDAC1 Complex.International journal of biological sciences · 2026Article
- ACSL5 programs fatty acid metabolism and mitochondrial fitness to sustain pathogenic T cells and exacerbate Sjögren's syndrome.International journal of biological sciences · 2026Article
- CRISPR-based functional genomic screening in neurodegeneration: mechanistic insights into AD, PD, and ALS.Frontiers in aging neuroscience · 2026Review
- Mitochondria-ER contact sites in neurological disorders.Animal cells and systems · 2026Review
- RHOA regulates mitochondria-ER contact sites through modulation of the VAPB/PTPIP51 tether.Nature communications · 2025Article
- Endoplasmic reticulum-mediated organelle crosstalk in kidney disease.Nature reviews. Nephrology · 2025Review
- Article
- Glucose restriction induces degeneration of neurons with mitochondrial DNA depletion by altering ER-mitochondria calcium transfer.Molecular psychiatry · 2025Article
33 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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 number of disease-related proteins and genes being associated with MERCS is increasing. However, many details regarding MERCS and their role in neurodegenerative diseases remain unknown. In this review, we aim to summarise the current knowledge regarding the structure and function of MERCS, and to update the field on current research in PD, AD and ALS. Furthermore, we will evaluate high-throughput screening techniques, including RNAi vs CRISPR/Cas9, pooled vs arrayed formats and how these could be combined with current techniques to visualise MERCS. We will consider the advantages and disadvantages of each technique and how it can be utilised to uncover novel protein pathways involved in MERCS dysfunction in neurodegenerative diseases.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.