This communication reports on a possible distinct role of HMGB1 protein. Biophysical studies revealed that HMGB1 binds and stabilizes the G-quadruplex of the KRAS promoter element that is responsible for most of the transcriptional activity. Biological data showed that inhibition of HMGB1 increases KRAS expression. These results suggest that HMGB1 could play a role in the gene transcriptional regulation via the functional recognition of the G-quadruplex.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6234227 | PMC |
| http://dx.doi.org/10.1039/c8cc03614d | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
A novel bioassay reflecting response to immune checkpoint inhibitor therapy in non-small cell lung cancer with malignant pleural effusion.
Transl Lung Cancer Res
December 2024
Division of Pulmonary Medicine, Department of Medicine, Jichi Medical University Hospital, Shimotsuke, Tochigi, Japan.
Background: Immune checkpoint inhibitor (ICI) therapy has prolonged the survival of a proportion of patients with advanced non-small cell lung cancer (NSCLC). Histological quantification of programmed cell death-ligand 1 (PD-L1) in tumors is a widely adopted marker for predicting the efficacy of ICI treatment. However, its use in patients with malignant pleural effusion (MPE) is occasionally challenging because of the difficulty of tissue sampling.
View Article and Find Full Text PDF[Mechanism of chrysophanol in inhibiting ox-LDL-induced macrophage foaminess through NF-κB/HMGB1-PI3K/Akt/mTOR pathway].
Zhongguo Zhong Yao Za Zhi
December 2024
School of Basic Medical Sciences, Guangzhou University of Chinese Medicine Guangzhou 511400, China.
The aim of this study was to investigate the underlying mechanism of chrysophanol(Chr) in reducing inflammation and foam cell formation induced by oxidized low-density lipoprotein(ox-LDL) and to investigate the targets and pathways related to effects of Chr on coronary atherosclerosis, providing a theoretical basis for the development of new clinical drugs. RAW264.7 macrophages were cultured in vitro, and after determining the appropriate concentrations of Chr and ox-LDL for treating RAW264.
View Article and Find Full Text PDFInhibition of RIPK1-driven necroptosis ameliorates inflammatory hyperalgesia caused by lipopolysaccharide: involvement of TLR-, NLRP3-, and caspase-11-mediated signaling pathways.
Cell Mol Biol (Noisy-le-grand)
January 2025
Department of Pharmacology, Faculty of Pharmacy, Mersin University, Mersin, Türkiye.
Article Synopsis
- Recent research indicates that blocking the RIPK1/RIPK3/MLKL necrosome can help reduce inflammatory pain linked to conditions like demyelination in the central nervous system.
- This study tests necrostatin-1s (Nec-1s), a specific RIPK1 inhibitor, on LPS-induced inflammatory pain in male mice, assessing pain sensitivity through hot plate tests and examining related protein changes.
- Results show that Nec-1s not only prevents LPS-induced pain relief but also reverses the activation of key proteins and signals involved in inflammation and demyelination, suggesting that RIPK1 inhibitors could be a promising treatment for managing inflammatory pain.
Hydroxysafflor yellow A attenuates the inflammatory response in cerebral ischemia-reperfusion injured mice by regulating microglia polarization per SIRT1-mediated HMGB1/NF-κB signaling pathway.
Int Immunopharmacol
January 2025
Department of Pharmacy, Anhui University of Chinese Medicine, Hefei, China; Anhui Province Key Laboratory of Traditional Chinese Medicine Decoction Pieces of New Manufacturing Technology, Bozhou 236000, China. Electronic address:
Background: Hydroxysafflor yellow A (HSYA), an active component isolated from Carthamus tinctorius L., has demonstrated potent protective effects against cerebral ischaemia/reperfusion (I/R) injury. Microglial polarisation plays a crucial role in I/R.
View Article and Find Full Text PDFRoles of the Receptor for Advanced Glycation End Products and Its Ligands in the Pathogenesis of Alzheimer's Disease.
Int J Mol Sci
January 2025
School of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu 611137, China.
The Receptor for Advanced Glycation End Products (RAGE), part of the immunoglobulin superfamily, plays a significant role in various essential functions under both normal and pathological conditions, especially in the progression of Alzheimer's disease (AD). RAGE engages with several damage-associated molecular patterns (DAMPs), including advanced glycation end products (AGEs), beta-amyloid peptide (Aβ), high mobility group box 1 (HMGB1), and S100 calcium-binding proteins. This interaction impairs the brain's ability to clear Aβ, resulting in increased Aβ accumulation, neuronal injury, and mitochondrial dysfunction.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!