BCL6 is a transcriptional repressor whose deregulated expression plays a key role in diffuse large B-cell lymphomas (DLBCLs). BCL6 expression characterizes one of the two main subtypes (GC type) of DLBCL, while the other (ABC type) is recognized by increased NFkappaB activation. The mechanistic basis of this distinction remains unclear and the BCL6 targets have been only partially explored. Here we describe how NFkappaB activity is increased after BCL6 silencing by shRNA in DLBCL cells, leading us to propose that BCL6 represses NFkappaB activity. We also demonstrate that this repression is brought about by a mechanism involving protein-protein interaction between BCL6 and NFkappaB members, both in vitro and in vivo. Analysis of a series of DLBCLs shows a negative correlation between the expression of NFkappaB target genes and BCL6. This combined approach using silenced cells and a series of human DLBCL samples leads us to a better understanding of the role of BCL6 as an NFkappaB regulator in B-cells.
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http://dx.doi.org/10.1002/path.2279 | DOI Listing |
Stem Cell Res Ther
January 2025
Department of Neurosurgery, The First Medical Centre, Chinese PLA General Hospital, Beijing, 100853, China.
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View Article and Find Full Text PDFBiochim Biophys Acta Mol Basis Dis
January 2025
State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, China; Department of Cariology and Endodontology, School & Hospital of Stomatology, Wuhan University, China. Electronic address:
BRCA1/BRCA2-containing complex subunit 3 (BRCC3) has been proved to exert pro-inflammatory effect in various inflammatory diseases through different mechanisms, but its involvement in pulpitis remains unclear. This study aims to investigate the regulatory role and mechanisms of BRCC3 in modulating dental pulp cell inflammation and pulpitis progression. The expression of BRCC3 was observed to be elevated in human/mouse pulpitis samples and lipopolysaccharide-stimulated human dental pulp cells (hDPCs).
View Article and Find Full Text PDFEur J Pharmacol
January 2025
Pharmacology & Environmental Toxicology, Environmental Studies & Research Institute (ESRI), University of Sadat City, Sadat City 32897, Menoufia, Egypt. Electronic address:
Liver damage is one of the most severe side effects of valproic acid (VPA) therapy. Research indicates that PPAR-α prevents Wnt3a/β-catenin-induced PGC-1α dysregulation, which is linked to liver injury. Although PPAR-α activation has hepatoprotective effects, its role in preventing VPA-induced liver injury remains unclear.
View Article and Find Full Text PDFCell Signal
January 2025
Department of Orthopedics, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, 107 Yanjiang West Road, Guangzhou 510120, PR China. Electronic address:
Intervertebral disc degeneration (IVDD) is a leading cause of low back pain, primarily driven by inflammatory processes within the disc, particularly involving the infiltration and activity of macrophages. High Mobility Group Box 1 (HMGB1) has been identified as a crucial mediator in this inflammatory cascade, yet its precise role in macrophage-induced disc degeneration remains unclear. In this study, we employed a combination of in vivo and in vitro models, including genetically engineered mice with macrophage-specific overexpression of HMGB1, a rat model of IVDD, and cultured macrophages and nucleus pulposus cells (NPCs), to elucidate the role of HMGB1 in IVDD.
View Article and Find Full Text PDFJ Biol Chem
January 2025
Department of Cellular and Molecular Physiology, Penn State College of Medicine, Hershey, Pennsylvania 17033. Electronic address:
Increasing evidence supports the role of an augmented immune response in the early development and progression of renal complications caused by diabetes. We recently demonstrated that podocyte-specific expression of stress response protein regulated in development and DNA damage response 1 (REDD1) contributes to activation of the pro-inflammatory transcription factor NF-κB in the kidney of diabetic mice. The studies here were designed to define the specific signaling events whereby REDD1 promotes NF-κB activation in the context of diabetic nephropathy.
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