ArticleMolecular cancer2010
The haematopoietic GTPase RhoH modulates IL3 signalling through regulation of STAT activity and IL3 receptor expression.
Article in Molecular cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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
17 citing papers in PubMed, 28 citations in OpenAlex.
- Targeting p16Leukemia · 2025Article
- CellFM: a large-scale foundation model pre-trained on transcriptomics of 100 million human cells.Nature communications · 2025Article
- E3 ubiquitin ligase RNF128 negatively regulates the IL-3/STAT5 signaling pathway by facilitating K27-linked polyubiquitination of IL-3Rα.Cell communication and signaling : CCS · 2024Article
- Molecular basis and current insights of atypical Rho small GTPase in cancer.Molecular biology reports · 2024Review
- Article
- Prognostic prediction of lung adenocarcinoma by integrative analysis of RHOH expression and methylation.The clinical respiratory journal · 2023Article
- RNA sequencing reveals CircRNA expression profiles in chicken embryo fibroblasts infected with velogenic Newcastle disease virus.Frontiers in veterinary science · 2023Article
- Nascent RHOH acts as a molecular brake on actomyosin-mediated effector functions of inflammatory neutrophils.PLoS biology · 2022Article
- MARCH3 negatively regulates IL-3-triggered inflammatory response by mediating K48-linked polyubiquitination and degradation of IL-3Rα.Signal transduction and targeted therapy · 2022Article
- Deletion of murineSmall GTPases · 2022Article
- Bimodal expression ofEJHaem · 2021Article
- Activation of STAT transcription factors by the Rho-family GTPases.Biochemical Society transactions · 2020Review
- Physiological role of Kvβ2 (AKR6) in murine skeletal muscle growth and regulation.Acta physiologica (Oxford, England) · 2018Article
- RhoH participates in a multi-protein complex with the zinc finger protein kaiso that regulates both cytoskeletal structures and chemokine-induced T cells.Small GTPases · 2018Article
- RhoH is a negative regulator of eosinophilopoiesis.Cell death and differentiation · 2016Article
- Correlation between Plasma Interleukin-3, the α/β Globin Ratio, and Globin mRNA Stability.Anemia · 2014Article
- Toxin-induced RhoA activity mediates CCL1-triggered signal transducers and activators of transcription protein signaling.The Journal of biological chemistry · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRhoH is a constitutively active member of the family of Rho GTPases. Its expression is restricted to the haematopoietic lineage, where it serves as a positive regulator for T cell selection and mast cell function and as a negative regulator for growth-related functions in other lineages. Here, we examined the activation of signal transducer and activator of transcription (STAT) proteins in response to stimulation with interleukin 3 (IL3).
resultsUsing the murine IL3-dependent cell line BaF3 we investigated the influence of RhoH protein expression levels on IL3-mediated cellular responses. RhoH overexpressing cells showed lower sensitivity to IL3 and decreased STAT5 activation. SiRNA-mediated repression of RhoH gene expression led to an increase in proliferation and STAT5 activity which correlated with an increased number of IL3 receptor α chain molecules, also known as CD123, expressed at the cell surface. Interestingly, these findings could be reproduced using human THP-1 cells as a model system for acute myeloid leukaemia, where low RhoH levels are known to be an unfavourable prognostic marker. Overexpression of RhoH on the other hand caused an induction of STAT1 activity and western blot analysis revealed that activated STAT1 is phosphorylated on Tyr701. STAT1 is known to induce apoptosis or cell cycle arrest and we detected an upregulation of cyclin-dependent kinase inhibitors (CDKI) p21Cip1 and p27Kip1 in RhoH overexpressing BaF3 cells.
conclusionsWe propose that RhoH functions as a negative regulator for IL3-induced signals through modulation of the JAK-STAT pathway. High levels of RhoH allow the IL3-dependent activation of STAT1 causing decreased proliferation through upregulation of p21Cip1 and p27Kip1. Low RhoH levels on the other hand led to an upregulation of IL3-dependent cell growth, STAT5 activity and an increase of CD123 surface expression, linking RhoH to a CD123/STAT5 phenotype that has been described in AML patients.
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.