ArticleGenes to cells : devoted to molecular & cellular mechanisms2026
Cancer-Associated STAT3 Mutations Maintain ES Cell Self-Renewal Through Phosphorylation-Independent Mechanisms.
Article in Genes to cells : devoted to molecular & cellular mechanisms, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Cancer-Associated STAT3 Mutations Maintain ES Cell Self-Renewal Through Phosphorylation-Independent Mechanisms.Genes to cells : devoted to molecular & cellular mechanisms · 2026Article
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
Signal transducer and activator of transcription 3 (STAT3) is essential for embryonic stem (ES) cell self-renewal, and its mutations are found in various human diseases. In this study, we investigated the effects of disease-associated STAT3 mutations (Y640F and G656insF) on ES cell properties. These mutations maintained ES cell self-renewal in the absence of LIF and MEK/GSK3 inhibitors. Although these mutants exhibited enhanced transcriptional activity, their phosphorylation status remained unchanged after LIF stimulation. Importantly, these mutations functioned independently of endogenous STAT3, as demonstrated in STAT3 knockout ES cells. Our findings reveal that disease-associated STAT3 mutations can maintain stem cell properties through phosphorylation-independent mechanisms, providing insights into how these mutations might regulate stem cell functions in both developmental and pathological contexts.
Indexed as
Identifiers
What 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.