ArticleCell communication and signaling : CCS2025
The E3 ubiquitin ligase MARCH2 controls TNF-α mediated inflammation by autoubiquitination.
Article in Cell communication and signaling : CCS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 4 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.
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
4 citing papers in PubMed.
- Correction: The E3 ubiquitin ligase MARCH2 controls TNF-α mediated inflammation by autoubiquitination.Cell communication and signaling : CCS · 2026Article
- The regulatory role of post-translational modifications in the pathogenesis of ulcerative colitis.Molecular biology reports · 2026Review
- The plasticity and metabolic reprogramming of macrophage in ulcerative colitis.Frontiers in immunology · 2026Review
- Review
Corrections and comments
- Erratum issued
Authors and funding
12 authors.
Funding
Abstract
backgroundRegulation of the nuclear factor-kappa B (NF-kB) signaling pathway is a major host homeostatic mechanism for controlling hyper-inflammation or chronic inflammation. Despite extensive research, the regulatory factors of NF-kB signaling required to preserve homeostasis and control inflammatory disorders are not fully understood. Moreover, the role of MARCH2 in chronic inflammation models and the regulation of MARCH2 activation remain to be elucidated.
methodsWe monitored disease severity and mortality in MARCH2
resultHere, we report that MARCH2
conclusionOur results indicate that MARCH2 plays a critical role in regulating NEMO/IKKγ under the inflammatory and resting conditions, thereby suppressing excessive or unexpected inflammatory responses. Our findings here not only demonstrate a biological role of MARCH2 in inflammatory signaling pathways but also provide a novel insight in the underlying mechanism.
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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.