ArticleInflammation2012
The chromosomal protein HMGN2 mediates the LPS-induced expression of β-defensins in mice.
Article in Inflammation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 15 citations in OpenAlex.
- Deficiency of HMGN2 enhances antibacterial activity of macrophages by promoting H3 histone modification-mediated CD14/iNOS expression.Frontiers in immunology · 2025Article
- Tryptophan promoted β-defensin-2 expressionRSC advances · 2020Article
- HMGN2 regulates non-tuberculous mycobacteria survival via modulation of M1 macrophage polarization.Journal of cellular and molecular medicine · 2019Article
- Increased expression of high-mobility group nucleosomal-binding domain 2 protein in various tumor cell lines.Oncology letters · 2018Article
- Antibacterial mechanism of high-mobility group nucleosomal-binding domain 2 on the Gram-negative bacteria Escherichia coli.Journal of Zhejiang University. Science. B · 2017Article
- Knockdown of HMGN2 increases the internalization of Klebsiella pneumoniae by respiratory epithelial cells through the regulation of α5β1 integrin expression.International journal of molecular medicine · 2016Article
- The modulation of MiR-155 and MiR-23a manipulates Klebsiella pneumoniae Adhesion on Human pulmonary Epithelial cells via Integrin α5β1 Signaling.Scientific reports · 2016Article
- β-Defensin 1 plays a role in acute mucosal defense against Candida albicans.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human β-defensin-2 (HBD-2), an antimicrobial peptide produced by epithelial cells, plays an important role in the body's innate and adaptive immunity. High-mobility group N2 (HMGN2), a member of the HMG superfamily, binds to chromatin to modulate gene transcription. Previously, we have shown that HMGN2 acts as a positive modulator of the signal transduction cascade in the process of inducible human β-defensin expression. In our current study, we found that down-regulation of HMGN2 reduces the expression level of murine β-defensin-3 and -4 (mBD-3 and mBD-4), but not mBD-1 upon LPS stimulation in various tissues of pregnant ICR mice, as well as in embryonic and neonatal lungs and livers at different developmental time points. In the control group, murine HMGN2 expression decreased, while mBD-1 and mBD-4 expression increased slightly during development. In the LPS-treated groups, murine HMGN2 and mBD-1 expression did not change significantly, whereas mBD-3 and mBD-4 expression significantly increased in maternal, embryonic, and neonatal tissues, especially the mBD-3 expression. HMGN2 shRNA interference led to decreased mBD-3 and mBD-4 expression, while mBD-1 expression did not significantly change. These results demonstrate that HMGN2 is a component of the LPS-induced mouse β-defensin response.
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.