Ask about this productRelated genes to: IL1b protein
- Gene:
- IL1B NIH gene
- Name:
- interleukin 1 beta
- Previous symbol:
- -
- Synonyms:
- IL1F2, IL-1B, IL1-BETA
- Chromosome:
- 2q14.1
- Locus Type:
- gene with protein product
- Date approved:
- 1989-03-31
- Date modifiied:
- 2016-10-05
Related products to: IL1b protein
Related articles to: IL1b protein
- The gasdermin (GSDM) family of proteins has emerged as the central executioner of pyroptosis, a form of inflammatory cell death characterized by plasma membrane rupture and the release of pro-inflammatory cytokines such as interleukin-1β (IL-1β), IL-18 and high mobility group protein B1 (HMGB1). Emerging evidence indicates that GSDMs exert diverse functions in health and various disease contexts, which can be either dependent on or independent of pyroptosis, including facilitating mucus secretion, regulating bone resorption, and modulating mitochondrial metabolism. This review provides a comprehensive overview of the GSDM family, detailing the molecular mechanisms of activation, regulation, pore formation, cell rupture and membrane repair. We explored the extensive crosstalk between GSDMs and other cell death modalities, including apoptosis, necroptosis, NETosis, and PANoptosis. Furthermore, we systematically discuss GSDMs' 'double-edged sword' roles in diverse pathologies, ranging from host defense in infectious diseases and chronic inflammation in autoimmune disorders to their complex, context-dependent function in cancer progression and immunity. Finally, we evaluate emerging therapeutic strategies, encompassing small-molecule inhibitors such as disulfiram (DSF), necrosulfonamide (NSA) and dimethyl fumarate (DMF), as well as novel material-based delivery systems. Collectively, these advances underscore the therapeutic potential of targeting GSDMs for precise clinical intervention to treat both inflammatory and non-inflammatory diseases, as well as to enhance cancer immunotherapy. - Source: PubMed
Publication date: 2026/10/02
Xu WeilvLiu ShiyangYu ZexuShi JinhuangYang YangShi Fushan - The morphological and molecular genetic characteristics of wound healing were investigated in male Wistar rats with high and low hypoxia tolerance (HT and HS rats, respectively). A full-thickness skin wound (diameter 16 mm) was inflicted in the interscapular region. On day 11 after wound infliction (proliferation phase), histological examination and morphometric analysis of the wound tissue were performed. The expression of the Hif1a, Epas1, Vegf, Nfkb, Il1b, Il6, Il10, Tnfa, and Tgfb genes in intact skin and in the wound granulation tissue was assessed by PCR, and the serum levels of HIF-1α, IL-1β, IL-6, and IL-10 were detected by ELISA. On day 11 of wound healing, reparative processes were more pronounced in HT animals, manifesting as a significantly smaller wound area compared to HS rats. The ratio of collagen fiber types on day 11 of wound healing in HT and HS rats did not differ significantly. Compared to HT rats, HS animals demonstrated higher expression of the Il6 and Tgfb genes in the granulation tissue, and higher serum levels of IL-6 protein. These data should be considered when conducting studies using animals with different hypoxia tolerance. - Source: PubMed
Publication date: 2026/10/01
Dzhalilova D ShTsvetkov I SKirillova M VMelnikova E AMkhitarov V ADiatroptova M AMakarova O V - PM causes multifaceted detrimental effects on human health. Alveolar type II epithelial (AT-II) cells serve critical function in PM-induced airway inflammation. However, the mechanism remains unclear. - Source: PubMed
Publication date: 2026/09/16
Jin YanZhao YunWei ShihuiChen XingyuZhu KeXiong JuanQi RongbinZhang WenLai TianwenCao Chao - Goblet cell hyperplasia (GCH) is a hallmark of chronic obstructive pulmonary disease (COPD) and contributes to morbidity and mortality. We investigated the cellular and molecular origins of GCH in COPD using single-cell RNA sequencing (scRNA-seq), spatial transcriptomics, and in vitro models. We identified "basal-to-goblet transitional cells" (BGTC) which are transcriptionally and physically located between basal and goblet cells and are characterized by expression of clade B serpins. In vitro studies indicate that inflammatory cytokines, including IL-1β, stimulate basal-to-goblet differentiation through a intermediate and overexpression induces differentiation of airway basal cells into -producing inflammatory goblet cells. In addition, we identified a subset of "goblet-variant basal cells" from lungs of COPD patients that express goblet cell and inflammatory genes ex vivo. Together, these results indicate clade B serpins contribute to altered epithelial differentiation and inflammatory signaling in COPD and support therapeutic targeting of clade B serpins to reduce GCH. - Source: PubMed
Publication date: 2026/09/22
Tufenkjian Tiffany SBlackburn Jessica BNichols David SVasquez AlfredoShaver Ciara MWare Lorraine BBlackwell Timothy SRichmond Bradley W - Macrophages are major contributors to inflammatory responses in acute kidney injury (AKI) and rapidly alter their gene expression through epigenetic regulation. This study focused on ASXL1, a chromatin modifier regulating histone marks consisting of H3K27me3 (repressive) and H3K4me3 (activating) in M1 macrophages. We found that ASXL1-positive M1 macrophages were significantly increased in the unilateral ischemia-reperfusion injury kidneys of male mice in the acute phase. In cultured M1 macrophages, RNA sequencing revealed that Asxl1 knockdown upregulated inflammatory response genes such as Il6 and Il1b. Conversely, the expression of anti-apoptotic genes Csf3 and Lcn2 was suppressed, and pathways related to interleukin-17 signaling and Fcγ receptor-dependent phagocytosis were downregulated. In co-culture experiments, Asxl1 silencing in M1 macrophages induced more severe apoptosis and reduced proliferation of mouse renal cortical tubular cells. Mechanistically, chromatin immunoprecipitation analysis demonstrated that Asxl1 knockdown significantly decreased H3K27me3 levels at the Il6 and Il1b promoter regions and H3K4me3 levels at the Csf3 and Lcn2 promoter regions in M1 macrophages. These findings indicate that ASXL1 suppresses excessive inflammatory cytokine expression and preserves anti-apoptotic activity through histone modifications, while maintaining phagocytic capacity in M1 macrophages. ASXL1 in M1 macrophages thus attenuates inflammatory activation and macrophage-mediated renal tubular cell damage in AKI. - Source: PubMed
Ogura YoshiyasuSugasawa TakehitoNangaku MasaomiMimura Imari