ArticleJournal of molecular biology2016
The HMGB1 C-Terminal Tail Regulates DNA Bending.
Article in Journal of molecular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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.
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
22 citing papers in PubMed, 40 citations in OpenAlex.
- Counteraction of HMGB1 at ss-dsDNA junctions maintains liquidity of protamine-DNA co-condensates.Nature communications · 2026Article
- HMGB1 Assists in Overcoming Cisplatin Resistance in Chemoresistant Human Ovarian Cancer Cells.Molecular carcinogenesis · 2026Article
- Counteraction of HMGB1 at ss-dsDNA junctions maintains liquidity of protamine-DNA co-condensates.bioRxiv : the preprint server for biology · 2026Article
- HMGB1 as an emerging key modulator of bone remodeling: a narrative review.Stem cell research & therapy · 2025Review
- ROS anchor PAMPs-mediated extracellular HMGB1 self-association and its dimerization enhances pro-inflammatory signaling.Redox biology · 2025Article
- MaPom1, a Dual-Specificity Tyrosine Phosphorylation-Regulated Kinase, Positively Regulates Thermal and UV-B Tolerance inInternational journal of molecular sciences · 2024Article
- Adenovirus protein VII binds the A-box of HMGB1 to repress interferon responses.PLoS pathogens · 2023Article
- The role of circulating cell-free DNA as an inflammatory mediator after stroke.Seminars in immunopathology · 2023Review
- Review
- Targeting HMGB1 for the treatment of sepsis and sepsis-induced organ injury.Acta pharmacologica Sinica · 2022Review
- Article
- Targeting HMGB1: An available Therapeutic Strategy for Breast Cancer Therapy.International journal of biological sciences · 2022Review
- Interactions of HMGB Proteins with the Genome and the Impact on Disease.Biomolecules · 2021Review
- HMGB1 coordinates SASP-related chromatin folding and RNA homeostasis on the path to senescence.Molecular systems biology · 2021Article
- The role of high mobility group protein B3 (HMGB3) in tumor proliferation and drug resistance.Molecular and cellular biochemistry · 2021Review
- Targeting Chromosomal Architectural HMGB Proteins Could Be the Next Frontier in Cancer Therapy.Cancer research · 2020Review
- Loss of High-Mobility Group Box 1 (HMGB1) Protein in Rods Accelerates Rod Photoreceptor Degeneration After Retinal Detachment.Investigative ophthalmology & visual science · 2020Article
- Novel biomarkers for risk stratification of Barrett's oesophagus associated neoplastic progression-epithelial HMGB1 expression and stromal lymphocytic phenotype.British journal of cancer · 2020Article
- Cleavage of HMGB1 by Proteolytic Enzymes Associated with Inflammatory Conditions.Frontiers in immunology · 2020Article
- The acidic tail of HMGB1 regulates its secondary structure and conformational flexibility: A circular dichroism and molecular dynamics simulation study.Computational and structural biotechnology journal · 2020Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
High mobility group box protein 1 (HMGB1) is an architectural protein that facilitates the formation of protein-DNA assemblies involved in transcription, recombination, DNA repair, and chromatin remodeling. Important to its function is the ability of HMGB1 to bend DNA non-sequence specifically. HMGB1 contains two HMG boxes that bind and bend DNA (the A box and the B box) and a C-terminal acidic tail. We investigated how these domains contribute to DNA bending by HMGB1 using single-molecule fluorescence resonance energy transfer (FRET), which enabled us to resolve heterogeneous populations of bent and unbent DNA. We found that full-length (FL) HMGB1 bent DNA more than the individual A and B boxes. Removing the C-terminal tail resulted in a protein that bent DNA to a greater extent than the FL protein. These data suggest that the A and B boxes simultaneously bind DNA in the absence of the C-terminal tail, but the tail modulates DNA binding and bending by one of the HMG boxes in the FL protein. Indeed, a construct composed of the B box and the C-terminal tail only bent DNA at higher protein concentrations. Moreover, in the context of the FL protein, mutating the A box such that it could not bend DNA resulted in a protein that bent DNA similar to a single HMG box and only at higher protein concentrations. We propose a model in which the HMGB1 C-terminal tail serves as an intramolecular damper that modulates the interaction of the B box with DNA.
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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.