ArticleInflammation2026
Inhibition of SPI1 by ADAP Regulates S100A8/A9 Signaling in Macrophages to Control the Development of Colitis.
Article in Inflammation, 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
Although the immune adaptor protein ADAP (adhesion and degranulation adaptor protein) plays a critical role in regulating macrophage inflammatory responses, its impact on intestinal inflammation remains elusive. This study reveals that ADAP-deficient mice have increased susceptibility to dextran sulfate sodium (DSS)-induced colitis and intestinal inflammation due to upregulation of S100A8/A9 expression (also known as MRP8 and MRP14, respectively) both in vivo and in vitro. Mechanistically, ADAP promotes proteasomal degradation of the transcription factor SPI1 (SPI-1 proto-oncogene) via the E3 ubiquitin ligase FBXW7 (F-box and WD repeat domain-containing 7)-mediated ubiquitination. ADAP deficiency increases SPI1 expression for transcription of the S100A8/A9 promoter. Blockade of SPI1 effectively prevents colitis-induced S100A8/A9 upregulation in macrophages. Thus, our findings highlight the potential link between ADAP and intestinal inflammation, while also paving the way for therapeutic interventions targeting the ADAP-SPI1-S100A8/A9 signaling axis in inflammatory colitis.
Indexed as
Identifiers
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.