BCL3
- Known as:
- BCL3
- Catalog number:
- 002474A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- BCL3
Related genes to: BCL3
- Gene:
- BCL3 NIH gene
- Name:
- BCL3 transcription coactivator
- Previous symbol:
- D19S37, BCL4
- Synonyms:
- -
- Chromosome:
- 19q13.32
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-01-25
Related products to: BCL3
Related articles to: BCL3
- Postoperative cognitive dysfunction (POCD) is a common neurological complication involving the hippocampus, a brain region critical for learning and memory. Circular RNA (circRNA) plays an important role in regulating gene expression. Our objective is to predict and verify a circRNA-miRNA-mRNA network in POCD. - Source: PubMed
Publication date: 2026/09/11
Zhang YajingLu ShujunYu YingYan ZheQi Qingling - Effector CD8+ T cells are key drivers of type 1 diabetes (T1D) pathogenesis, yet questions remain regarding the molecular defects leading to altered cytotoxicity, peripheral tissue phenotype, and receptor specificity. We analyzed human pancreatic lymph nodes (pLNs) using mass cytometry and single-cell RNA-seq (scRNA-seq) with combined T cell receptor (TCR) profiling. Cytometric analysis revealed enrichment of T stem cell memory-like (TSCM-like) cells (CD8+CD45RA+CD27+CD28+CCR7+CXCR3+) in T1D pLNs. scRNA-seq indicated an elevated inflammatory cytokine gene signature (IFITM3, LTB) along with regulators of terminal differentiation (BCL6, BCL3), coupled with downregulation of exhaustion-associated genes (DUSP2, NR4A2, TSC22D3) in CD8+ T cells in T1D pLNs. Immune response enrichment analysis (IREA) indicated IL-15 signaling as a significant driver of these phenotypes. Integrated TCR and transcriptomics analysis revealed a cluster of diverse naive-like CD8+ T cell clones in T1D pLNs. Comparison of pLNs and pancreatic tissue slice isolates indicated sharing of effector CD8+ T cells, with enhanced terminal effector signatures within the pancreas relative to paired pLNs. Multiplex imaging revealed differential localization of T cell factor 1 (TCF1)- and thymocyte selection-associated high mobility group box protein (TOX)-expressing T cells in the pancreas, with islet-proximal TCF1+TOX+ cells displaying a mixture of activation and exhaustion-associated phenotypes. Thus, we provide multimodal cellular profiles enriched in T1D tissues for consideration in therapeutic targeting. - Source: PubMed
Publication date: 2026/09/15
Peters Leeana DSeay Howard RSmith Justin APosgai Amanda LBerkowitz Reed LWasserfall Clive HAtkinson Mark ABacher RhondaBrusko Maigan ABrusko Todd M - Cancer involves abnormal cell proliferation and migration throughout the body. Genetic changes occurring in hereditary breast cancer led to the activation of oncogenes, resulting in gain-of-function effects. This study was designed to conduct a phylogenetic analysis of breast cancer-related oncogenes and tumor suppressor genes families in humans relevant to different species and their potential against breast cancer. - Source: PubMed
Publication date: 2026/08/14
Nazir AmnaAmbreen SadafNawaz Yasir - Toll-like receptors (TLRs) are key sensors of infection and injury, and are critical inducers of inflammation. TLR-induced activation of the NF-κB and MAPK pathways promotes the secretion of mediators of inflammation such as cytokines and chemokines. Control of cytokine production is critically important, as unnecessary inflammatory responses can lead to tissue damage, while insufficient inflammatory responses can lead to susceptibility to infection. Previous studies showed that TLR4 uses distinct NF-κB and MAPK activation properties to discriminate between low and high concentrations of ligand, triggering cytokine production only at ligand concentrations that activate both pathways. The switch-like activation of MAPKs by TLR4 establishes an inflammatory threshold for ligand concentrations that facilitates threat discrimination. Using murine macrophages, we reveal that MAPK activation properties are TLR-specific, and that switch-like MAPK activation is not a general feature of all TLRs. Consequently, certain TLRs do not have an inflammatory threshold of ligand concentration and may not effectively filter signal from noise. The activation properties of the ERK pathway, rather than messenger RNA levels, dictate the patterns of TNFα cytokine secretion for all TLRs examined. We demonstrate that the TLR4 inflammatory threshold can be modulated by costimulation with granulocyte-macrophage colony-stimulating factor in an ERK-dependent manner. We show that deletion of BCL-3 changes the TLR4-induced ERK pathway activation properties from switch-like to gradual and lowers the activation threshold. We reveal that different TLRs have different capacities to discriminate threats based on ligand concentration, and that ERK pathway activation properties can be altered to change the cellular decision to initiate inflammation. - Source: PubMed
Elhadedy NadaAlotaibi AreejMcGarry LynnCarmody Ruaidhrí J - In this study, a reaction pathway for converting the psychoactive compound Δ-THC into the nonpsychoactive cannabidiol (CBD) was proposed. Related cannabinoids, including Δ-THC and cannabinol (CBN), were also examined. The transformation proceeds via two key steps: (i) hydrogen elimination and cyclic ether ring cleavage, and (ii) hydrolysis to form hydroxyl groups, facilitated by boron trichloride (BCl) as a Lewis acid and 2,6-di--butyl-4-methylpyridine as a selective base. Energy calculations indicate that is the rate-determining transition state for Δ-THC, Δ-THC, and CBN, with corresponding activation free energies of 49.4, 50.3, and 54.1 kcal mol, respectively. The overall reaction is highly exergonic (Δ = -33.9 to -32.9 kcal mol), indicating spontaneous conversion under mild conditions. These results provide a foundation for developing efficient and scalable production of nonpsychoactive cannabinoids, supporting the development of safe and commercially viable therapeutic applications. - Source: PubMed
Publication date: 2026/07/10
Kongkaew SirilakParasuk WarapornParasuk Vudhichai