ArticlePloS one2017
The essential and downstream common proteins of amyotrophic lateral sclerosis: A protein-protein interaction network analysis.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Integrative analysis of transcriptomics and drug-target networks identifies SMN1 as a novel biomarker and therapeutic target for amyotrophic lateral sclerosis.Journal, genetic engineering & biotechnology · 2025Article
- Article
- TDP-43 protein interactome informs about perturbed canonical pathways and may help develop personalized medicine approaches for patients with TDP-43 pathology.Drug discovery today · 2023Review
- Integrative Proteome Analysis Revels 3-Hydroxybutyrate Exerts Neuroprotective Effect by Influencing Chromatin Bivalency.International journal of molecular sciences · 2023Article
- A molecular view of amyotrophic lateral sclerosis through the lens of interaction network modules.PloS one · 2022Article
- Biological networks and complexity in early-onset motor neuron diseases.Frontiers in neurology · 2022Article
- A serum microRNA sequence reveals fragile X protein pathology in amyotrophic lateral sclerosis.Brain : a journal of neurology · 2021Article
- Proteinopathies as Hallmarks of Impaired Gene Expression, Proteostasis and Mitochondrial Function in Amyotrophic Lateral Sclerosis.Frontiers in neuroscience · 2021Review
- Excessive Homeostatic Gain in Spinal Motoneurons in a Mouse Model of Amyotrophic Lateral Sclerosis.Scientific reports · 2020Article
- From Multi-Omics Approaches to Precision Medicine in Amyotrophic Lateral Sclerosis.Frontiers in neuroscience · 2020Review
- A network analysis revealed the essential and common downstream proteins related to inguinal hernia.PloS one · 2020Article
- Protein-protein interactions reveal key canonical pathways, upstream regulators, interactome domains, and novel targets in ALS.Scientific reports · 2018Article
- TDP-43 regulates the alternative splicing of hnRNP A1 to yield an aggregation-prone variant in amyotrophic lateral sclerosis.Brain : a journal of neurology · 2018Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Amyotrophic Lateral Sclerosis (ALS) is a devastative neurodegenerative disease characterized by selective loss of motoneurons. While several breakthroughs have been made in identifying ALS genetic defects, the detailed molecular mechanisms are still unclear. These genetic defects involve in numerous biological processes, which converge to a common destiny: motoneuron degeneration. In addition, the common comorbid Frontotemporal Dementia (FTD) further complicates the investigation of ALS etiology. In this study, we aimed to explore the protein-protein interaction network built on known ALS-causative genes to identify essential proteins and common downstream proteins between classical ALS and ALS+FTD (classical ALS + ALS/FTD) groups. The results suggest that classical ALS and ALS+FTD share similar essential protein set (VCP, FUS, TDP-43 and hnRNPA1) but have distinctive functional enrichment profiles. Thus, disruptions to these essential proteins might cause motoneuron susceptible to cellular stresses and eventually vulnerable to proteinopathies. Moreover, we identified a common downstream protein, ubiquitin-C, extensively interconnected with ALS-causative proteins (22 out of 24) which was not linked to ALS previously. Our in silico approach provides the computational background for identifying ALS therapeutic targets, and points out the potential downstream common ground of ALS-causative mutations.
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