ArticleBMB reports2016
Non-histone protein HMGB1 inhibits the repair of damaged DNA by cisplatin in NIH-3T3 murine fibroblasts.
Article in BMB reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Synergistic Anticancer Activity ofCells · 2026Article
- HMGB1: A Central Node in Cancer Therapy Resistance.International journal of molecular sciences · 2025Review
- Role of Metastasis-Related Genes in Cisplatin Chemoresistance in Gastric Cancer.International journal of molecular sciences · 2019Article
- Interactions of high mobility group box protein 1 (HMGB1) with nucleic acids: Implications in DNA repair and immune responses.DNA repair · 2019Review
- Effect of in vivo post-translational modifications of the HMGB1 protein upon binding to platinated DNA: a molecular simulation study.Nucleic acids research · 2018Article
- 29-kDa FN-f inhibited autophagy through modulating localization of HMGB1 in human articular chondrocytes.BMB reports · 2018Article
- Identification of specifically activated angiogenic molecules in HMGB-1-induced angiogenesis.BMB reports · 2017Article
- Secreted HMGB1 from Wnt activated intestinal cells is required to maintain a crypt progenitor phenotype.Oncotarget · 2016Article
- High Mobility Group B Proteins, Their Partners, and Other Redox Sensors in Ovarian and Prostate Cancer.Oxidative medicine and cellular longevity · 2016Review
- HMGB1 in health and disease.Molecular aspects of medicine · 2014Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The nuclear non-histone protein high mobility group box (HMGB) 1 is known to having an inhibitory effect on the repair of DNA damaged by the antitumor drug cisplatin in vitro. To investigate the role of HMGB1 in living cells, we studied the DNA repair of cisplatin damages in mouse fibroblast cell line, NIH-3T3. We evaluated the effect of the post-synthetic acetylation and C-terminal domain of the protein by overexpression of the parental and mutant GFP fused forms of HMGB1. The results revealed that HMGB1 had also an inhibitory effect on the repair of cisplatin damaged DNA in vivo. The silencing of HMGB1 in NIH-3T3 cells increased the cellular DNA repair potential. The increased levels of repair synthesis could be "rescued" and returned to less than normal levels if the knockdown cells were transfected with plasmids encoding HMGB1 and HMGB1 K2A. In this case, the truncated form of HMGB1 also exhibited a slight inhibitory effect. [BMB Reports 2016; 49(2): 99-104].
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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.