ArticleThe EMBO journal2002
Signaling disrupts mSin3A binding to the Mad1-like Sin3-interacting domain of TIEG2, an Sp1-like repressor.
Article in The EMBO journal, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 56 citations in OpenAlex.
- PrPStem cell reports · 2026Article
- Review
- Upregulating sirtuin 6 ameliorates glycolysis, EMT and distant metastasis of pancreatic adenocarcinoma with krüppel-like factor 10 deficiency.Experimental & molecular medicine · 2021Article
- The Distinct Roles of Transcriptional Factor KLF11 in Normal Cell Growth Regulation and Cancer as a Mediator of TGF-β Signaling Pathway.International journal of molecular sciences · 2020Review
- The potential of targeting Sin3B and its associated complexes for cancer therapy.Expert opinion on therapeutic targets · 2017Review
- Differential coupling of KLF10 to Sin3-HDAC and PCAF regulates the inducibility of the FOXP3 gene.American journal of physiology. Regulatory, integrative and comparative physiology · 2014Article
- Molecular mechanisms of the suppression of axon regeneration by KLF transcription factors.Neural regeneration research · 2014Review
- Single and combinatorial chromatin coupling events underlies the function of transcript factor Krüppel-like factor 11 in the regulation of gene networks.BMC molecular biology · 2014Article
- Article
- A functional family-wide screening of SP/KLF proteins identifies a subset of suppressors of KRAS-mediated cell growth.The Biochemical journal · 2011Article
- Krüppel-like factor KLF9 regulates PPARγ transactivation at the middle stage of adipogenesis.Cell death and differentiation · 2011Article
- Distinct role of Kruppel-like factor 11 in the regulation of prostaglandin E2 biosynthesis.The Journal of biological chemistry · 2010Article
- NFAT-induced histone acetylation relay switch promotes c-Myc-dependent growth in pancreatic cancer cells.Gastroenterology · 2010Article
- Protein kinase Calpha-induced derepression of the human luteinizing hormone receptor gene transcription through ERK-mediated release of HDAC1/Sin3A repressor complex from Sp1 sites.Molecular endocrinology (Baltimore, Md.) · 2008Article
- Human Krüppel-like factor 11 inhibits human proinsulin promoter activity in pancreatic beta cells.Diabetologia · 2007Article
- Kruppel-like transcription factor 13 regulates T lymphocyte survival in vivo.Journal of immunology (Baltimore, Md. : 1950) · 2007Article
- Identification and analysis of cabut orthologs in invertebrates and vertebrates.Development genes and evolution · 2007Article
- Mnt transcriptional repressor is functionally regulated during cell cycle progression.Oncogene · 2005Article
- The family feud: turning off Sp1 by Sp1-like KLF proteins.The Biochemical journal · 2005Review
- Sin3: a flexible regulator of global gene expression and genome stability.Current genetics · 2005Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
Abstract
A Sin3-interacting domain (SID) originally described in Mad proteins is necessary for both transcriptional repression and growth suppression by these transcription factors. We recently reported that a structurally and functionally related Mad1-like SID is also present in five Sp1-like repressor proteins (TIEG1, TIEG2, BTEB1, BTEB3 and BTEB4), demonstrating that SID-mSin3A interactions have a wider functional impact on transcriptional repression. SID-mSin3A interaction is necessary for the anti-proliferative function of Mad, TIEG and BTEB proteins. It remains to be established, however, whether the SID-mSin3A interaction is constitutive or regulated. Here, we describe that the Mad1-like SID domain of the Sp1-like repressor TIEG2 is inhibited by the epidermal growth factor (EGF)-Ras-MEK1-ERK2 signaling pathway, via phosphorylation of four serine/threonine sites adjacent to the SID. This phenomenon disrupts the SID-mSin3A interaction and thereby inhibits TIEG2's repression activity. Thus, these results show for the first time that the repression of a SID-containing protein is regulated by signaling rather than functioning in a constitutive manner, extending our understanding of how the function of SID-containing repressors may be controlled.
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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.