ArticleNucleic acids research2004
RING1 inhibits transactivation of RBP-J by Notch through interaction with LIM protein KyoT2.
Article in Nucleic acids research, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- The impact of Hnrnpl deficiency on transcriptional patterns of developing muscle cells.FEBS open bio · 2026Article
- Article
- Canonical and noncanonical NOTCH signaling in the nongenetic resistance of cancer: distinct and concerted control.Frontiers of medicine · 2025Review
- Exosome-mediated delivery of RBP-J decoy oligodeoxynucleotides ameliorates hepatic fibrosis in mice.Theranostics · 2022Article
- Structurally conserved binding motifs of transcriptional regulators to notch nuclear effector CSL.Experimental biology and medicine (Maywood, N.J.) · 2019Review
- The evolution of transcriptional repressors in the Notch signaling pathway: a computational analysis.Hereditas · 2019Article
- The Pathogenesis and Therapies of Striated Muscle Laminopathies.Frontiers in physiology · 2018Review
- [Inhibitory effect of KyoT2 overexpression on proliferation and migration of airway smooth muscle cells in mice with asthma].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2016Article
- Development of autoantibodies against muscle-specific FHL1 in severe inflammatory myopathies.The Journal of clinical investigation · 2015Article
- The role of Notch receptors in transcriptional regulation.Journal of cellular physiology · 2015Review
- Polycomb group oncogene RING1 is over-expressed in non-small cell lung cancer.Pathology oncology research : POR · 2014Article
- FHL1C induces apoptosis in Notch1-dependent T-ALL cells through an interaction with RBP-J.BMC cancer · 2014Article
- RBPJ, the major transcriptional effector of Notch signaling, remains associated with chromatin throughout mitosis, suggesting a role in mitotic bookmarking.PLoS genetics · 2014Article
- Structure and function of the CSL-KyoT2 corepressor complex: a negative regulator of Notch signaling.Structure (London, England : 1993) · 2014Article
- Notch inhibitors for cancer treatment.Pharmacology & therapeutics · 2013Review
- Dysregulation of FHL1 spliceforms due to an indel mutation produces an Emery-Dreifuss muscular dystrophy plus phenotype.Neurogenetics · 2013Article
- Genes, proteins and complexes: the multifaceted nature of FHL family proteins in diverse tissues.Journal of cellular and molecular medicine · 2010Review
- SLIMMER (FHL1B/KyoT3) interacts with the proapoptotic protein Siva-1 (CD27BP) and delays skeletal myoblast apoptosis.The Journal of biological chemistry · 2009Article
- Notch signaling regulates the FOXP3 promoter through RBP-J- and Hes1-dependent mechanisms.Molecular and cellular biochemistry · 2009Article
- Proteomic identification of FHL1 as the protein mutated in human reducing body myopathy.The Journal of clinical investigation · 2008Article
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6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The DNA-binding protein recombination signal binding protein-Jkappa (RBP-J) mediates transcriptional activation of the Notch intracellular domain (NIC). In the absence of transcriptional activators, RBP-J suppresses transcription by recruiting co-suppressors. KyoT2 is a LIM domain protein that inhibits the RBP-J-mediated transcriptional activation. Here we provide evidence that the polycomb group protein RING1 interacts with the LIM domains of KyoT2 in yeast and mammalian cells. The interaction between KyoT2 and RING1 was detected both in vitro and in vivo. By using a co-immunoprecipitation assay, we also showed that, though RING1 and RBP-J did not associate directly, the two molecules could be co-precipitated simultaneously by KyoT2, probably through the LIM domains and the RBP-J-binding motif of KyoT2, respectively. These results suggested the formation of a three-molecule complex consisting of RBP-J, KyoT2 and RING1 in cells. Moreover, we found that overexpression of RING1 together with KyoT2 in cells inhibited transactivation of RBP-J by NIC. Suppression of the NIC- mediated transactivation of RBP-J by RING1 was abrogated by overexpression of KBP1, a molecule that competed with RING1 for binding to LIM domains of KyoT2, suggesting that suppression of RBP-J by RING1 was dependent on its associating with KyoT2. Taken together, our data suggested that there might be at least two ways of the KyoT2-mediated suppression of RBP-J, namely competition for binding sites with transactivators, and recruitment of suppressors such as RING1.
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