ArticleMolecular and cellular biology1997
Intra- and intermolecular cooperative binding of high-mobility-group protein I(Y) to the beta-interferon promoter.
Article in Molecular and cellular biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
41 citing papers in PubMed, 118 citations in OpenAlex.
- HMGA2 directly mediates chromatin condensation in association with neuronal fate regulation.Nature communications · 2023Article
- The acidic domain of Hmga2 and the domain's linker region are critical for driving self-renewal of hematopoietic stem cell.International journal of hematology · 2022Article
- AP-1 subunits converge promiscuously at enhancers to potentiate transcription.Genome research · 2021Article
- Genome reading by the NF-κB transcription factors.Nucleic acids research · 2019Review
- Cross-talk among HMGA1 and FoxO1 in control of nuclear insulin signaling.Scientific reports · 2018Article
- Protein Cofactors Are Essential for High-Affinity DNA Binding by the Nuclear Factor κB RelA Subunit.Biochemistry · 2018Article
- Anti-Transcription Factor RNA Aptamers as Potential Therapeutics.Nucleic acid therapeutics · 2016Review
- RNA-Mediated Regulation of HMGA1 Function.Biomolecules · 2015Review
- HMGB1 in health and disease.Molecular aspects of medicine · 2014Review
- The Wnt/β-catenin/T-cell factor 4 pathway up-regulates high-mobility group A1 expression in colon cancer.Cell biochemistry and function · 2013Article
- Characterization of the Stoichiometry of HMGA1/DNA Complexes.The open biochemistry journal · 2013Article
- High-mobility-group a-like CarD binds to a DNA site optimized for affinity and position and to RNA polymerase to regulate a light-inducible promoter in Myxococcus xanthus.Journal of bacteriology · 2013Article
- Core promoter-selective function of HMGA1 and Mediator in Initiator-dependent transcription.Genes & development · 2011Article
- Evolution and diversity of secretome genes in the apicomplexan parasite Theileria annulata.BMC genomics · 2010Article
- Origins of specificity in protein-DNA recognition.Annual review of biochemistry · 2010Review
- Functional equivalence of HMGA- and histone H1-like domains in a bacterial transcriptional factor.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- The dynamics of HMG protein-chromatin interactions in living cells.Biochemistry and cell biology = Biochimie et biologie cellulaire · 2009Review
- A dimer-specific function of the transcription factor NFATp.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Inhibition of high-mobility-group A2 protein binding to DNA by netropsin: a biosensor-surface plasmon resonance assay.Analytical biochemistry · 2008Article
- Homeodomain-interacting protein kinase-2 (HIPK2) phosphorylates HMGA1a at Ser-35, Thr-52, and Thr-77 and modulates its DNA binding affinity.Journal of proteome research · 2007Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The mammalian high-mobility-group protein I(Y) [HMG I(Y)], while not a typical transcriptional activator, is required for the expression of many eukaryotic genes. HMG I(Y) appears to recruit and stabilize complexes of transcriptional activators through protein-DNA and protein-protein interactions. The protein binds to the minor groove of DNA via three short basic repeats, preferring tracts of adenines and thymines arranged on the same face of the DNA helix. However, the mode by which these three basic repeats function together to recognize HMG I(Y) binding sites has remained unclear. Here, using deletion mutants of HMG I(Y), DNase I footprinting, methylation interference, and in vivo transcriptional assays, we have characterized the binding of HMG I(Y) to the model beta-interferon enhancer. We show that two molecules of HMG I(Y) bind to the enhancer in a highly cooperative fashion, each molecule using a distinct pair of basic repeats to recognize the tandem AT-rich regions of the binding sites. We have also characterized the function of each basic repeat, showing that only the central repeat accounts for specific DNA binding and that the presence of a second repeat bound to an adjacent AT-rich region results in intramolecular cooperativity in binding. Surprisingly, the carboxyl-terminal acidic tail of HMG I(Y) is also important for specific binding in the context of the full-length protein. Our results present a detailed examination of HMG I(Y) binding in an important biological context, which can be extended not only to HMG I(Y) binding in other systems but also to the binding mode of many other proteins containing homologous basic repeats, which have been conserved from bacteria to humans.
Indexed as
Identifiers
What OpenQuestion holds
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.