Evidence map›Paper›PMID 41952619›Full record

ArticleBioscience reports2026

G3BP1 is a SWI/SNF-bound regulator of transcription that modulates activation of STATs.

Natalia Papadopoulos, Niki Sarri, Johan Lennartsson, Carl-Henrik Heldin

Abstract read
In one paragraph

Article in Bioscience reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Natalia PapadopoulosDepartment of Medical Biochemistry and Microbiology, Uppsala University, Sweden.ORCID 0000-0001-5781-5524
Niki SarriDepartment of Medical Biochemistry and Microbiology, Uppsala University, Sweden.
Johan LennartssonDepartment of Pharmaceutical Biosciences, Uppsala University, Sweden.
Carl-Henrik HeldinDepartment of Medical Biochemistry and Microbiology, Uppsala University, Sweden.ORCID 0000-0002-9508-896X

Funding

Swedish Cancer Foundation #222363 Pj03H
6 · The paper itself

Abstract

RAS GTPase-activating protein-binding protein 1 (G3BP1) is a component of the RAS signaling pathway and a phosphorylation-dependent RNA/DNA endoribonuclease that links signal transduction and RNA metabolism. We identified G3BP1 as a nuclear interactor of platelet-derived growth factor receptor-β, forming a complex with BAF155, a component of the SWI/SNF chromatin remodeling complex, as well as with the transcription factor STAT3. Depletion of G3BP1 in human primary fibroblasts AG1523 reduced PDGF-BB-induced activation of STAT3 while increasing mRNA levels of FOS, MYC, and CCND1, which encode proteins involved in growth stimulation. Both STAT1 and cyclin D1 mRNA and protein levels were elevated upon G3BP1 knockdown, identifying G3BP1 as a negative regulator of STAT1 and cyclin D1 expression. G3BP1 depletion did not abolish PDGF-BB-induced proliferation of human primary fibroblasts. Thus, G3BP1 interacts with the SWI/SNF chromatin remodeling complex in the nucleus and regulates cell growth pathways by modulating STAT signaling and transcription of growth-associated genes.

Indexed as

Chromosomal Proteins, Non-HistoneDNA HelicasesRNA Recognition Motif ProteinsSTAT1 Transcription FactorSTAT3 Transcription FactorTranscription FactorsTranscription, GeneticBecaplerminCell ProliferationCells, CulturedChromatin Assembly and DisassemblyCyclin D1FibroblastsGene Expression RegulationHumansPoly-ADP-Ribose Binding ProteinsBecaplerminCCND1 protein, humanChromosomal Proteins, Non-HistoneCyclin D1DNA HelicasesG3BP1 protein, humanPoly-ADP-Ribose Binding ProteinsProto-Oncogene Proteins c-sisRNA HelicasesRNA Recognition Motif ProteinsSMARCA2 protein, humanSTAT1 protein, humanSTAT1 Transcription FactorSTAT3 protein, humanSTAT3 Transcription FactorTranscription Factorscell proliferationchromatin remodelingG3BP1PDGFRbetasignal transducers and activators of transcriptiontranscription factors

Identifiers

PMID41952619
PMCPMC13161325

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Registered trials

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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.