ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2026
UBE2L6 drives ulcerative colitis progression by promoting BIRC2 degradation and activating non-canonical NF-κB signalling.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 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
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPost-translational modifications (PTMs) have been increasingly recognized as important regulators of ulcerative colitis (UC) progression. However, the specific PTM type and key enzyme driving UC remain largely undefined.
methodsGenes related to 21 PTM types were intersected with differentially expressed genes (DEGs) in UC and screened using 113 machine learning algorithms. Functional validation was performed in lipopolysaccharide (LPS) stimulated NCM460 and HT29 cells. Immunoprecipitation-mass spectrometry (IP-MS) combined with data-independent acquisition (DIA) proteomics was used to identify downstream targets and pathways.
resultsUBE2L6 was identified as a key PTM-related gene in UC. In LPS stimulated intestinal epithelial cells, UBE2L6 downregulation was found to markedly attenuate inflammatory responses and barrier dysfunction. BIRC2 was identified as a downstream target of UBE2L6, and the non-canonical NF-κB pathway was determined to be the principal signalling axis involved. Mechanistically, UBE2L6 was shown to facilitate the transfer of K48 linked ubiquitin chains to BIRC2, thereby promoting BIRC2 autoubiquitination and degradation. Consequently, NIK degradation was impaired, leading to NIK accumulation, enhanced p100 processing to p52, and activation of non-canonical NF-κB signalling.
conclusionsUBE2L6 promotes UC progression through BIRC2 degradation-dependent activation of the non-canonical NF-κB pathway and may serve as a potential therapeutic target in UC.
Indexed as
Identifiers
42786362What 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.