ArticleGlia2026
The ZNF148-ZEB1-AS1-IGF2BP2-NOD2 Axis Drives Microglial Antipneumococcal Immunity in Bacterial Meningitis.
Article in Glia, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- RNA-binding proteins: a comprehensive review of multifaceted regulatory mechanisms in neuroinflammation and implications in the pathogenesis of neurological disorders.Journal of neuroinflammation · 2026Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Streptococcus pneumoniae (Spn) meningitis remains a lethal central nervous system (CNS) infection with limited therapies. This study identifies the lncRNA ZEB1-AS1 as a central coordinator of microglial immunity against Spn through a multi-tiered regulatory cascade. Transcriptomic analysis revealed Spn-induced ZEB1-AS1 upregulation in human microglia, driven by ZNF148, which directly binds its promoter. Functional interrogation demonstrated that ZEB1-AS1 knockdown impairs bacterial clearance and pro-inflammatory cytokine production (IL-1β, IL-6, TNF-α, p < 0.01), while its overexpression amplifies these responses. Crucially, ZEB1-AS1 recruits the m6A reader IGF2BP2 to stabilize NOD2 mRNA in cytoplasmic complexes, extending transcript stability. This molecular scaffolding enables NOD2-dependent antimicrobial functions, as evidenced by rescue experiments in which IGF2BP2 overexpression reversed ZEB1-AS1 deficiency phenotypes. In vivo, microglial manipulation of the murine homolog Zeb1-os1 regulated cerebral Spn burdens, NOD2 expression, and infection-induced cognitive outcomes in both directions. The tripartite ZEB1-AS1/IGF2BP2/NOD2 interaction was validated by RNA pulldown and co-immunoprecipitation, establishing a linear pathway from ZNF148-mediated transcriptional activation to IGF2BP2-dependent mRNA stabilization. Collectively, this ZNF148 to ZEB1-AS1 to IGF2BP2 to NOD2 axis bridges the gap between transcriptional and post-transcriptional immune regulation, proposing IGF2BP2's RNA-binding domain as a therapeutic target against drug-resistant Spn meningitis.
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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.