ArticleFEBS open bio2014
The levels of RAC3 expression are up regulated by TNF in the inflammatory response.
Article in FEBS open bio, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Critical Roles of SRC-3 in the Development and Progression of Breast Cancer, Rendering It a Prospective Clinical Target.Cancers · 2023Review
- NCoA3 upregulation in breast cancer‑associated adipocytes elicits an inflammatory profile.Oncology reports · 2023Article
- NFrontiers in immunology · 2022Article
- Functional relationship between CFTR and RAC3 expression for maintaining cancer cell stemness in human colorectal cancer.Cellular oncology (Dordrecht, Netherlands) · 2021Article
- High RAC3 expression levels are required for induction and maintaining of cancer cell stemness.Oncotarget · 2018Article
- The inflammatory cytokine TNF contributes with RAC3-induced malignant transformation.EXCLI journal · 2018Article
- Humanin inhibits apoptosis in pituitary tumor cells through several signaling pathways including NF-κB activation.Journal of cell communication and signaling · 2017Article
- HSP90AB1: Helping the good and the bad.Gene · 2016Review
- RAC3 more than a nuclear receptor coactivator: a key inhibitor of senescence that is downregulated in aging.Cell death & disease · 2015Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
RAC3 is a coactivator of glucocorticoid receptor and nuclear factor-κB (NF-κB) that is usually over-expressed in tumors and which also has important functions in the immune system. We investigated the role of the inflammatory response in the control of RAC3 expression levels in vivo and in vitro. We found that inflammation regulates RAC3 levels. In mice, sub-lethal doses of lipopolysaccharide induce the increase of RAC3 in spleen and the administration of the synthetic anti-inflammatory glucocorticoid dexamethasone has a similar effect. However, the simultaneous treatment with both stimuli is mutually antagonistic. In vitro stimulation of the HEK293 cell line with tumor necrosis factor (TNF), one of the cytokines induced by lipopolysaccharide, also increases the levels of RAC3 mRNA and protein, which correlates with an enhanced transcription dependent on the RAC3 gene promoter. We found that binding of the transcription factor NF-κB to the RAC3 gene promoter could be responsible for these effects. Our results suggest that increase of RAC3 during the inflammatory response could be a molecular mechanism involved in the control of sensitivity to both pro- and anti-inflammatory stimuli in order to maintain the normal healthy course of the immune response.
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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.