IL1B & A2M Protein Protein Interaction Antibody Pair
- Known as:
- IL1B & A2M Protein Protein Interaction Antibody Pair
- Catalog number:
- DI0035
- Product Quantity:
- 1 Set
- Category:
- -
- Supplier:
- Abno
- Gene target:
- IL1B & A2M Protein Interaction Antibody Pair
Related genes to: IL1B & A2M Protein Protein Interaction Antibody Pair
- Gene:
- CASP1 NIH gene
- Name:
- caspase 1
- Previous symbol:
- IL1BC
- Synonyms:
- ICE
- Chromosome:
- 11q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-05-07
- Date modifiied:
- 2016-10-05
- 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 & A2M Protein Protein Interaction Antibody Pair
Related articles to: IL1B & A2M Protein Protein Interaction Antibody Pair
- Neuroinflammation plays an important role in the pathobiology of Progressive Supranuclear Palsy Syndrome (PSP-S). However, it is not adequately known whether peripheral inflammation correlates to neuroinflammation in PSP-S. This study aimed to examine a link between peripheral and brain inflammation in PSP-S by integrating blood and cerebrospinal fluid (CSF) inflammatory profile and Positron Emission Tomography (PET)-Magnetic Resonance Imaging (MRI) (PET-MRI). - Source: PubMed
Publication date: 2026/07/23
Dey SaikatKumar AishwaryaKumar PardeepKavya Paranthaman VMondal SandipanHolla Vikram VKamble NitishMahale RohanPal Pramod KYadav RaviDebnath Monojit - Fibroblasts are linked to stress responses in a broad number of diseases. Here, we used immortalized mouse embryonic fibroblasts (iMEFs) to elucidate their signaling behavior in response to proinflammatory lipopolysaccharides (LPS) and angiotensin II (Ang-II). To test for the role of the mitochondrial electron transport chain (ETC), iMEFs were cultured in glucose- and galactose-containing media promoting glycolysis and mitochondrial oxidative phosphorylation, respectively. In addition, we used alternative oxidase (AOX), a ubiquinol oxidoreductase that serves as a naturally evolved rescue mechanism in case of ETC disruption. We found that within 24 h of treatment, LPS upregulated a number of proinflammatory genes, namely Tlr4, Il6, Tgfb1, Nlrp3, Casp1, and Il1b; largely, the effect was more pronounced in galactose-containing media and attenuated by AOX. The increase in transcripts resulted partly in elevated cytokine secretion. Twenty-four hours of Ang-II treatment also induced these genes, albeit to a lesser degree and less sensitive to AOX. Cellular oxygen consumption rates (OCRs) were higher in galactose media but remained unaffected by either stimulus. Our results suggest that fibroblasts undergo a similar proinflammatory phenotypic shift in response to different stressors. This response is shaped by ETC activity, which, surprisingly, is not reflected in altered OCRs. - Source: PubMed
Publication date: 2026/08/05
Mühlon Marie MSchenkl ChristinaHarder LukasGiordano LucaVoll Julian MFranke ChristianDudziak DianaDoenst TorstenClaus Ralf ASzibor Marten - Melanoma is an aggressive form of skin cancer characterized by high metastatic potential and increasing incidence and mortality worldwide. Although significant advances have been achieved with immune checkpoint inhibitors and targeted therapies, effective preventive and long-term therapeutic strategies remain limited. Bacillus Calmette-Guérin (BCG), widely used in bladder cancer immunotherapy, exhibits potent immunostimulatory properties and has emerged as a promising platform for recombinant cancer vaccines. Among the candidate antigens, Antigen 85A (Ag85A), derived from Mycobacterium bovis, is notable for its strong immunogenicity and ability to induce robust Th1-mediated cellular immune responses. In this study, recombinant BCG strains overexpressing efficacy was evaluated in melanoma models in vitro and in vivo. Gene expression analysis by RT-qPCR revealed that rBCG-Ag85A induced systemic immune activation, characterized by increased Il1B and Trl4 expression in splenocytes. In tumor tissues, rBCG-Ag85A significantly upregulated genes associated with apoptosis (Bax, Bcl2), oxidative stress (Sod1, Cat), inflammatory and immune signaling pathways (Tlr4, Nfkb, Il12, Il1b, Casp1), and modulation of pathways involved in cellular metabolism (Mtor) indicating enhanced modulation of the tumor microenvironment. Functionally, these molecular and immunological effects were associated with reduced tumor progression, slower tumor growth, and improved survival in B16F10 melanoma-bearing mice. Collectively, these findings demonstrate that rBCG-Ag85A promotes multifaceted antitumor activity through the modulation of apoptosis, inflammation and oxidative stress-related gene expression, highlighting its potential as a promising prophylactic vaccine strategy to prevent cutaneous malignant melanoma and supporting future studies aimed at elucidating the immune cell populations involved and optimizing combinatorial therapeutic approaches. - Source: PubMed
Publication date: 2026/08/05
Lanius Suzana LemkePacheco Bruna SilveiraSousa Fernanda Severo SabedraNeto Amilton Clair Pinto SeixasScholl Nicole RamosCardozo Stella Julli FariasEhlert Maria EduardaFerreira Valentina GessingerCollares Tiago VeirasBorsuk SibeleDellagostin OdirBohn Thais Larre OliveiraSeixas Fabiana Kömmling - Breast cancer is one of the most prevalent malignancies among women worldwide; its incidence and mortality are expected to increase annually. Cancer is composed not only malignant cells but also a complex and dynamic network of interacting stromal cells, specifically immune cells, which contribute to tumor development and progression. Increasing evidence highlights the critical role of tumor-associated macrophages (TAMs) and their inflammasome-driven signaling pathways in tumor progression and therapeutic resistance. Curcumin, a natural compound with anti-carcinogenic potential, has a role in the regulation of cancer development and progression. However, its specific effects on inflammasome activation in TAMs within the tumor microenvironment (TME) remain insufficiently characterized. THP-1 monocytes differentiated into macrophages acquire the TAM-like phenotype when treated with conditioned media from breast cancer cells. Our present study aimed to investigate the effects of curcumin on inflammasome activation in macrophages induced by breast cancer-derived conditioned media. Breast cancer-derived conditioned medium stimulation induced manifestation of a pro-inflammatory TAM-like phenotype, characterized by increased interleukin (IL)-1β secretion and upregulation of NOD-like receptor protein 3 (NLRP3), caspase-1, and IL-1β. Curcumin pretreatment significantly reduced IL-1β secretion as well as NLRP3 protein levels. Moreover, it also suppressed and mRNA expression. In conclusion, curcumin attenuates tumor-induced inflammasome activation, highlighting its potential to modulate TME-driven breast cancer progression via the NLRP3/caspase-1/IL-1β axis. - Source: PubMed
Publication date: 2026/07/02
Kunchana KhwandowJarisarapurin WattanasedJang Jeong-HoonWattanapitayakul SuvaraSurh Young-Joon - Osteoarthritis (OA) is a prevalent degenerative joint disease characterized by progressive cartilage destruction. Emerging evidence suggests that chondrocyte pyroptosis, a pro-inflammatory programmed cell death pathway, contributes to OA pathogenesis. However, the molecular mechanisms underlying pyroptosis in OA and potential therapeutic interventions remain incompletely understood. Bulk RNA-seq datasets (GSE114007 and GSE254844) were analyzed to identify differentially expressed genes (DEGs) and co-expression modules via DESeq2 and WGCNA. Shared key DEGs (SKDEGs) were subjected to GO and KEGG enrichment analyses to reveal relevant pathways. Pyroptosis-related DEGs (PRDEGs) were intersected with SKDEGs and used for drug prediction in EnrichR. Predicted compounds were further examined for potential targets using TCMSP, HIT, and SwissTargetPrediction databases to identify hub genes. Single-cell RNA-seq data (GSE169454) were analyzed to determine the cellular localization, differential expression, and pathway activity of hub genes. Finally, in vitro experiments with primary human normal and OA chondrocytes were performed to validate the effects of the identified compound on cell proliferation and pyroptosis. Analysis of bulk RNA-seq data identified 146 SKDEGs, with pyroptosis emerging as the most significantly enriched pathway. Six PRDEGs were identified, and curcumin was predicted as a key therapeutic compound. Intersection of curcumin targets with PRDEGs revealed four hub genes (CASP1, IL1B, IL18, NLRP3), all upregulated in OA. Single-cell analysis confirmed that these hub genes were predominantly expressed in OA-associated chondrocyte subtypes, with increased pathway activity and expression along pseudotime trajectories. In vitro, curcumin (10 µM) promoted chondrocyte proliferation and significantly suppressed the mRNA and protein expression of the hub genes, indicating inhibition of pyroptosis. Chondrocyte pyroptosis is a critical contributor to OA progression, and curcumin can alleviate OA by targeting pyroptosis-related pathways. This integrative study provides mechanistic insights and a potential therapeutic strategy for OA. - Source: PubMed
Publication date: 2026/07/20
Huang JuanZhang ChiHe QingchuanChen YuanChen RuyanYang Shibin