ArticleCell death discovery2023
Dysregulation of a lncRNA within the TNFRSF10A locus activates cell death pathways.
Article in Cell death discovery, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 12 citations in OpenAlex.
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- Proteomics signatures associated with cognitive trajectories: evidence from the English Longitudinal Study of Ageing.medRxiv : the preprint server for health sciences · 2026Article
- Epigenome-wide exploratory study of blood DNA methylation and markers of physical performance indicates subtle differences across levels of cardiovascular fitness.Frontiers in physiology · 2026Article
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- High Glucose-induced transcriptomic changes in human trabecular meshwork cells.Molecular biology reports · 2025Article
- Therapeutic targets for age-related macular degeneration: proteome-wide Mendelian randomization and colocalization analyses.Frontiers in neurology · 2024Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
TNFRSF10A (tumor necrosis factor receptor superfamily member 10A) encodes a cell surface receptor protein involved in apoptotic, necroptotic, and inflammatory pathways. Dysregulation of TNFRSF10A has been implicated in sensitization to apoptosis and to the development of multiple diseases, yet little is known of the AC100861.1 long noncoding RNA (lncRNA) that lies head-to-head with TNFRSF10A. Given its genomic positioning, we sought to investigate the function of AC100861.1, focusing on its potential relationship with TNFRSF10A and the role it may play in death receptor signaling. Using knockdown and overexpression strategies, we probed cell viability and examined transcript and protein-level changes in key genes involved in apoptosis, necroptosis, and inflammation. Decreased cell viability was observed upon TNFRSF10A overexpression, regardless of whether the cells were subjected to the chemical stressor tunicamycin. Similarly, overexpression of AC100861.1 led to increased cell death, with a further increase observed under conditions of cellular stress. Knockdown of TNFRSF10A increased cell death only when the cells were stressed, and AC100861.1 knockdown exhibited no effect on cell death. Neither knockdown nor overexpression of either of these genes greatly affected the expression of the other. Manipulating AC100861.1, however, led to marked changes in the expression of genes involved in necroptosis and inflammatory cell-signaling pathways. Additionally, RNA fluorescence in situ hybridization (RNA-FISH) revealed that the AC100861.1 transcript is localized primarily to the cytoplasm. Together, these data suggest that AC100861.1 may have a role in regulating necroptotic and inflammatory signaling pathways and that this function is separate from changes in TNFRSF10A expression. Given the importance of this genomic locus for cell survival, these data provide insight into the function of a poorly understood lncRNA with potential implications regarding disease pathology and treatment.
Identifiers
What OpenQuestion 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 OpenQuestion graph.