ArticleAmerican journal of translational research2020
hTBK1-c.978T>A mutation promotes the ferroptosis in NSC-34 cells via mediation of KEAP1/NRF2/p62 signaling.
Article in American journal of translational research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Iron homeostasis and ferroptosis in muscle diseases and disorders: mechanisms and therapeutic prospects.Bone research · 2025Review
- The Underestimated Role of Iron in Frontotemporal Dementia: A Narrative Review.International journal of molecular sciences · 2024Review
- Ferroptosis and Neurodegenerative Diseases: Insights into the Regulatory Roles of SLC7A11.Cellular and molecular neurobiology · 2023Review
- Melatonin Induces Autophagy in Amyotrophic Lateral Sclerosis Mice via Upregulation of SIRT1.Molecular neurobiology · 2022Article
- The Protective Effect of Edaravone on TDP-43 Plus Oxidative Stress-Induced Neurotoxicity in Neuronal Cells: Analysis of Its Neuroprotective Mechanisms Using RNA Sequencing.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Role and mechanism of ferroptosis in neurological diseases.Molecular metabolism · 2022Review
- Mechanisms of Ferroptosis and Emerging Links to the Pathology of Neurodegenerative Diseases.Frontiers in aging neuroscience · 2022Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAmyotrophic lateral sclerosis (ALS) can result in the dysfunction of upper and lower motor neurons. A previous study has indicated that TBK1 mutation (hTBK1-c.978T>A) is involved in progression of ALS. However, the mechanism by which TBK1 mutation mediates the progression of ALS remains unclear.
methodsNSC-34 cells with hTBK1-c.978T>A mutation (TBK1 mutation status) was used to mimic ALS
resultshTBK1-c.978T>A mutation significantly inhibited the proliferation of NSC-34 cells via inducing cell ferroptosis, while the effect of TBK1 mutation was notably reversed by Ferrostatin-1 or p62 siRNA. Meanwhile, hTBK1-c.978T>A mutation significantly increased the expression of KEAP1 in NSC-34 cells, while this phenomenon was partially reversed by p62 knockdown.
conclusionhTBK1-c.978T>A mutation promoted promotes the ferroptosis in NSC-34 cells via regulation of KEAP1/NRF2/p62 signaling. Thus, hTBK1-c.978T>A mutation may serve as a possible target for the treatment of ALS.
Indexed as
Identifiers
33312375PMC7724361W3111387282What OpenQuestion holds
Registered trials
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