ArticleGenes & development2004
A nuclear isoform of the focal adhesion LIM-domain protein Trip6 integrates activating and repressing signals at AP-1- and NF-kappaB-regulated promoters.
Article in Genes & development, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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.
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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
49 citing papers in PubMed, 117 citations in OpenAlex.
- HIF1-driven TDP-43 stabilizes TRIP6 mRNA to drive angiogenesis and colorectal cancer progression under hypoxia.Translational oncology · 2026Article
- The FcRn from gene to protein and function: comparison between species.Frontiers in immunology · 2025Review
- Mena regulates nesprin-2 to control actin-nuclear lamina associations, trans-nuclear membrane signalling and gene expression.Nature communications · 2023Article
- Article
- Characterisation of a nucleo-adhesome.Nature communications · 2022Article
- A chemical probe for BAG1 targets androgen receptor-positive prostate cancer through oxidative stress signaling pathway.iScience · 2022Article
- TRIP6 promotes inflammatory damage via the activation of TRAF6 signaling in a murine model of DSS-induced colitis.Journal of inflammation (London, England) · 2022Article
- The LIM domain protein nTRIP6 modulates the dynamics of myogenic differentiation.Scientific reports · 2021Article
- Anti-oncogene PTPN13 inactivation by hepatitis B virus X protein counteracts IGF2BP1 to promote hepatocellular carcinoma progression.Oncogene · 2021Article
- TRIP6 regulates the proliferation, migration, invasion and apoptosis of osteosarcoma cells by activating the NF-κB signaling pathway.Experimental and therapeutic medicine · 2020Article
- Inflammatory Signaling in Hypertension: Regulation of Adrenal Catecholamine Biosynthesis.Frontiers in endocrinology · 2018Review
- The tumor-associated YB-1 protein: new player in the circadian control of cell proliferation.Oncotarget · 2017Article
- Review
- The LIM domain protein nTRIP6 acts as a co-repressor for the transcription factor MEF2C in myoblasts.Scientific reports · 2016Article
- The Interactome of the Glucocorticoid Receptor and Its Influence on the Actions of Glucocorticoids in Combatting Inflammatory and Infectious Diseases.Microbiology and molecular biology reviews : MMBR · 2016Review
- The conserved LIM domain-containing focal adhesion protein ZYX-1 regulates synapse maintenance in Caenorhabditis elegans.Development (Cambridge, England) · 2014Article
- The LIM domain protein nTRIP6 recruits the mediator complex to AP-1-regulated promoters.PloS one · 2014Article
- Functional crosstalk of PGC-1 coactivators and inflammation in skeletal muscle pathophysiology.Seminars in immunopathology · 2014Review
- Selective modulation of the glucocorticoid receptor can distinguish between transrepression of NF-κB and AP-1.Cellular and molecular life sciences : CMLS · 2014Article
- Nuclear receptors in inflammation control: repression by GR and beyond.Molecular and cellular endocrinology · 2013Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glucocorticoid receptor (GR)-mediated transrepression of the transcription factors AP-1 and NF-kappaB, responsible for most of the anti-inflammatory effects of glucocorticoids, is initiated by the tethering of GR to the promoters of target genes. We report that this tethering is mediated by a nuclear isoform of the focal adhesion LIM domain protein Trip6. Trip6 functions as a coactivator for both AP-1 and NF-kappaB. As shown by chromatin immunoprecipitation, Trip6 is recruited to the promoters of target genes together with AP-1 or NF-kappaB. In the presence of glucocorticoids, GR joins the Trip6 complex. Reducing the level of Trip6 by RNA interference or abolishing its interaction with GR by dominant-negative mutation eliminates transrepression. We propose that GR tethering to the target promoter through Trip6 forms the basis of transrepression, and that Trip6 exerts its nuclear functions by acting as a molecular platform, enabling target promoters to integrate activating or repressing signals.
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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.