ArticleGenes & genomics2026
Multi-omics profiling uncovers LINC00486-associated lncRNA regulation in human traumatic brain injury.
Article in Genes & genomics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
backgroundTraumatic brain injury (TBI) induces broad molecular changes in the human brain, altering gene expression in diverse neural and glial cells. While the transcriptional effects of TBI on protein-coding genes are well characterized, the roles of long noncoding RNAs (lncRNAs), key regulators of gene expression and chromatin, remain largely unknown.
objectiveOur objective was to identify lncRNAs altered in TBI and explore their potential regulatory functions.
methodsWe applied an integrative multi-omics approach combining single-nucleus RNA sequencing (snRNA-seq), isoform-level transcriptomics, transposable element (TE) annotation, and RNA-binding protein (RBP) interaction analyses. Public snRNA-seq datasets from cortical tissues of 12 TBI patients and 5 controls were analyzed to resolve injury-driven transcriptional signatures. We have performed differential expression analysis on 12,801 human lncRNAs, examined isoform-specific expression with TE content, and explored RBP-lncRNA interactions using CLIP-seq data.
resultsCell-type diversity decreased in TBI, and reactive and progenitor-like states were expanded. We identified 190 upregulated lncRNAs, mainly in glial cells. Among these, LINC00486 emerged as a brain-enriched lncRNA consistently increased after TBI. Isoform analysis showed its dominant brain isoform contains LINEs and LTRs, linking it to regulatory networks associated with endogenous retroelement activation. Functional enrichment connected LINC00486 to neurodevelopment, serotonin metabolism, and neuroinflammatory pathways. CLIP-seq data confirmed its interactions with stress-responsive RBPs such as AGO2 and TARDBP.
conclusionsOur multi-omics analysis identifies LINC00486 as a potential regulator of transcriptional plasticity in TBI. Its TE content and RBP interactions suggest a role in lncRNA-mediated regulatory networks during injury, highlighting possible therapeutic targets in neurotrauma.
Indexed as
Identifiers
41055884What 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.