ArticleThe EMBO journal2026
GTPase Rab11b and effector Rab11-FIP2 promote NLRP3 stability during inflammasome priming.
Article in The EMBO journal, 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
13 authors.
Funding
Abstract
Membrane trafficking through the trans-Golgi network has been shown to guide activation of the NLRP3 inflammasome. Rab11 GTPases and their effector Rab11-FIP2 regulate endosomal trafficking and retrograde transport. Here, we demonstrate that Rab11b and Rab11-FIP2 contribute to NLRP3 and pro-IL-1β stabilization during the inflammasome priming phase, which is followed by inflammasome activation. We show Rab11-FIP2 to promote TAK1 phosphorylation and TAK1-mediated activation of IKKβ, a process controlling NLRP3 translocation to the trans-Golgi network. Human NLRP3 and Rab11-FIP2 bind each other via their phosphatidylinositol-4 phosphate (PI4P)-binding domains KMKK and N-terminal C2 domain, respectively. We also provide evidence indicating that Rab11-FIP2 stabilizes NLRP3 on early endosomes, which is important for ASC speck formation. These findings provide insights into the mechanisms controlling stability and intracellular trafficking of NLRP3 in human macrophages.
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.