ArticleNucleic acids research1998
NF-kappaB mediated transcriptional activation is enhanced by the architectural factor HMGI-C.
Article in Nucleic acids research, 1998. 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, 60 citations in OpenAlex.
- O-GlcNAcylation of High Mobility Group Box 1 (HMGB1) Alters Its DNA Binding and DNA Damage Processing Activities.Journal of the American Chemical Society · 2021Article
- Review
- Amplified HMGA2 promotes cell growth by regulating Akt pathway in AML.Journal of cancer research and clinical oncology · 2016Article
- Computational Detection of Stage-Specific Transcription Factor Clusters during Heart Development.Frontiers in genetics · 2016Article
- Correlated expression of HMGA2 and PLAG1 in thyroid tumors, uterine leiomyomas and experimental models.PloS one · 2014Article
- FGF18 as a prognostic and therapeutic biomarker in ovarian cancer.The Journal of clinical investigation · 2013Article
- Liposarcoma: molecular genetics and therapeutics.Sarcoma · 2011Article
- DNA bending by the mammalian high-mobility group protein AT hook 2.Biochemistry · 2010Article
- Transcriptional activity of the murine retinol-binding protein gene is regulated by a multiprotein complex containing HMGA1, p54 nrb/NonO, protein-associated splicing factor (PSF) and steroidogenic factor 1 (SF1)/liver receptor homologue 1 (LRH-1).The international journal of biochemistry & cell biology · 2009Article
- Cellular senescence and chromatin organisation.British journal of cancer · 2007Review
- Transcriptional activation of the cyclin A gene by the architectural transcription factor HMGA2.Molecular and cellular biology · 2003Article
- An increased high-mobility group A2 expression level is associated with malignant phenotype in pancreatic exocrine tissue.British journal of cancer · 2003Article
- Expression of high-mobility-group-protein HMGI-C mRNA in the peripheral blood is an independent poor prognostic indicator for survival in metastatic breast cancer.British journal of cancer · 2003Article
- NF-kappa B-dependent assembly of an enhanceosome-like complex on the promoter region of apoptosis inhibitor Bfl-1/A1.Molecular and cellular biology · 2003Article
- Design and characterization of decoy oligonucleotides containing locked nucleic acids.Nucleic acids research · 2002Article
- Expression of the stress-associated protein p8 is a requisite for tumor development.International journal of gastrointestinal cancer · 2002Review
- Onset of natural killer cell lymphomas in transgenic mice carrying a truncated HMGI-C gene by the chronic stimulation of the IL-2 and IL-15 pathway.Proceedings of the National Academy of Sciences of the United States of America · 2001Article
- Transforming growth factor beta-1 enhances Smad transcriptional activity through activation of p8 gene expression.The Biochemical journal · 2001Article
- Structural changes induced by binding of the high-mobility group I protein to a mouse satellite DNA sequence.Biophysical journal · 2000Article
- Dual function of the epithelial specific ets transcription factor, ELF3, in modulating differentiation.Oncogene · 2000Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High mobility group I proteins (HMGI, HMGY and HMGI-C) are a family of low molecular mass non-histone nuclear proteins which constitute an important component of the active chromatin structure. Two members of this family, HMGI and HMGY, have been demonstrated to contribute to the transcriptional regulation of several promoters by interacting with the DNA and with different transcription factors. On the contrary, very little is known about the third member, HMGI-C, which plays an important role during embryonic growth and in the process of cell transformation, its gene being rearranged in a large number of mesenchimal tumors. In this paper we show for the first time that HMGI-C is also able to function as architectural factor, enhancing the activity of a transcription factor, NF-kappaB, through the PRDII element of the beta-interferon enhancer. Moreover we show that this enhancement is absolutely dependent on the binding of HMGI-C to its target sequence. The demonstration that HMGI-C is able to modulate transcription is thus an important initial step in the identification of genes regulated by this factor.
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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.