ReviewCell death and differentiation2026
HECT ubiquitin ligases as regulators of inflammatory signalling.
Review in Cell death and differentiation, 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.
- E3 Ubiquitin Ligases in MASH-Associated Liver Fibrosis: Mechanisms and Therapeutic Opportunities.Liver international : official journal of the International Association for the Study of the Liver · 2026Review
- Targeting E3 Ubiquitin Ligases in Post-Traumatic Osteoarthritis: Therapeutic Opportunities and Pharmacological Perspectives.Pharmaceutics · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Ubiquitination is a versatile post-translational modification that regulates protein stability, localisation and signalling. By modifying a wide range of substrates, ubiquitination controls key physiological processes, including inflammatory responses, which are the focus of this article. Precise regulation of inflammatory signalling is essential, as insufficient activation compromises host defence while sustained signalling contributes to chronic inflammation, autoimmunity and degenerative disease. Within the ubiquitin system, E3 ligases confer substrate specificity and influence ubiquitin chain topology, thereby directing downstream protein fate and signalling outcomes. HECT family E3 ligases form transient E3~ubiquitin thioester intermediates that enable controlled ubiquitin transfer to target proteins. Through this activity, they regulate the strength and duration of inflammatory signalling pathways. In this review, we discuss HECT E3 ubiquitin ligases involved in inflammation and how their ubiquitin-modifying functions influence immune signalling and inflammatory disease progression.
Identifiers
41957124What 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.