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
- A549 cells are widely used as an in vitro model of alveolar type II (ATII) epithelial cells; however, their phenotype and metabolic state are highly sensitive to culture conditions, cell density, and the duration of static, non-passaged cultivation. Here, we examined how prolonged static culture affects lipid metabolism, mitochondrial bioenergetics, and viability in A549 cells. A549 cultures were maintained without passaging for up to 25 days in DMEM or Ham's F-12 and analyzed using lipid secretion assays, targeted lipidomics, [C]-acetate incorporation, Seahorse bioenergetic profiling, and transcriptional analysis of stress-associated markers. Several surfactant-associated readouts were highest during early culture, peaking on day 7, as evidenced by elevated expression of and SP-A and maximal secretion of surfactant-associated phospholipids. With prolonged cultivation and increasing culture density, cellular phosphatidylglycerol levels declined progressively and became nearly undetectable by day 25, accompanied by reduced anabolic lipid metabolism, lower oxygen consumption, and impaired glycolytic activity. These changes coincided with increased reactive oxygen species, elevated intracellular Ca levels, and increased expression of stress-associated transcripts, including , , and . Later stages were also associated with reduced mitochondrial respiration and decreased viability. Collectively, our findings show that prolonged static culture is associated with metabolic remodeling and reduced bioenergetic capacity in A549 cells. - Source: PubMed
Publication date: 2026/04/10
Ďurišová IvanaŠofranková LuciaKvasnička AlešBaláž MiroslavFábryová IvanaFriedecký DavidBalážová Mária - Innate immune and interferon-induced responses to in vivo nasal infection with rhinovirus (RV)16 in healthy subjects are accelerated by low-dose dietary supplementation with carrot-derived pectic polysaccharide rhamnogalacturonan-I (cRG-I), together with reduced duration and severity of symptoms. We aimed to further identify temporal mRNA responses by nasal epithelial cells (NEC) after RV16 infection, and to assess the effect of cRG-I supplementation. NECs were obtained prior to (day(d)-55) and after 8-weeks (d-1) of supplementation (0, 0.3, 1.5 g/d), and on d3, d6, d9 and d13 after exposure to 100 TCID50 RV16. Transcriptome data were generated and analysed with the R2: Genomics Analysis and Visualization platform (https://r2.amc.nl). RV16 infection reduced expression of genes related to oxidative phosphorylation (d3), induced gene expression by interferon (d6-9), and reduced expression of cilia-related genes (d13). cRG-I changed these responses. At low-dose, gene expression of important transcription factors and effector molecules (IRF4, IRF8, RFX3, IL-1B, CASP1) was enhanced markedly earlier (d3-6). At high-dose, cRG-I induced expression of inflammasome-related genes already after 8-weeks supplementation. cRG-I, in a dose-dependent manner, significantly affected the sequence and intensity of genes that regulate pathways involved in anti-viral responses and epithelial repair. This may underlie the reduced duration and severity of symptoms. - Source: PubMed
Mol JasperVolckmann RichardRavi AbilashRavanetti LaraCalame WimMcKay SueAlbers RuudKoster JanLutter René - Periosteal regeneration requires tissue engineering strategies that simultaneously support osteogenesis, angiogenesis, and immunomodulation. In this study, fibroin/sulfated alginate (F/sA) composite membranes loaded with exosomes derived from human adipose-derived stem cells (hADSCs) treated with pure, 4 mol% B-doped, and 4 mol% B and 8 mol% Zn-doped hydroxyapatite (HA) were developed for periosteal tissue engineering. It was hypothesized that incorporation of sA and HA-conditioned exosomes enhances osteoimmunomodulation while preserving scaffold integrity. F/sA membranes with varying sulfated alginate content (0-20 wt%) were fabricated and characterized. Increasing sulfated alginate content enhanced water uptake and degradation while reducing tensile strength and Young's modulus. A 95 : 5 F/sA ratio was identified as optimal exosome delivery composition, exhibiting the highest hADSC viability and reducing IL1B and CASP1 levels in THP-1 macrophages ( < 0.05). It was also found that exosomes isolated from pure and doped HA-treated hADSCs showed treatment-dependent alterations in the cargo. The 8 mol% B-doped HA group significantly increased exosome yield, while all HA treatments reduced protein/particle and DNA/particle ratios. Doped HA treatments significantly increased RNA/particle ratio ( < 0.05). Exosome-loaded F/sA membranes enhanced early cell attachment and proliferation and significantly promoted osteogenic differentiation of hADSCs, increasing , , and expression. Immunomodulatory effects were observed for all exosome groups, except for the 4 mol% B and 8 mol% Zn-doped HA groups, which significantly increased expression. Overall, this study demonstrates that HA doping modulates exosomal composition in a dopant-dependent manner and that exosome-functionalized F/sA membranes constitute a multifunctional periosteal substitute with tunable properties. - Source: PubMed
Publication date: 2026/04/16
Akbaba SemaTuracli Karaguven Senem OzgeEvis ZaferTezcaner Ayşen - Inflammation is a key feature in breast cancer progression, with neutrophil extracellular traps (NETs) playing an important role. NETs are DNA-based structures released by neutrophils that can promote tumor adhesion, invasion, and immune evasion. Another crucial mechanism is the inflammasome, a multiprotein complex that drives inflammation through cytokine release. Both mechanisms are present in tumors and may act synergistically. In this study, we evaluated how isolated NETs modulate the NLRP3 inflammasome in a human breast cancer model. Exposure of MDA-MB-231 cells to NETs increased the expression of , , and . Blocking IL-1R with Anakinra reduced expression, while inhibition of the P2X7 receptor with A740003 decreased and . ELISA confirmed that NETs stimulate IL-1β release, which was reduced by MCC950, Anakinra, and A740003. Functionally, NETs accelerated tumor cell migration, and this effect was inhibited by MCC950 and Anakinra. Bioinformatics analysis of TCGA breast cancer samples showed differential inflammasome gene expression among subtypes and a positive correlation between inflammasome components and NET-related genes. These findings highlight the interplay between inflammatory and immune mechanisms in breast cancer progression and may support the development of new therapeutic strategies. - Source: PubMed
Publication date: 2026/02/27
Silva Alexander Gonçalves daPereira EvellynAlmeida Vitor HPinto Laryssa DSouza Juliana LTilli Tatiana MCoutinho-Silva RobsonMedei EmilianoKonig SandraMonteiro Robson Q - The nucleotide-binding oligomerization domain (NOD)-like receptor pyrin domain-containing 3 (NLRP3) inflammasome is a signalling hub associated with the pathogenesis of neuroinflammatory conditions such as multiple sclerosis (MS). NLRP3 inflammasome activation requires interplay between pathogen-/damage-associated molecular patterns and other soluble factors, which initiates inflammation to promote the secretion of the cytokine, interleukin (IL)-1β. - Source: PubMed
Publication date: 2026/02/06
Otálora-Alcaraz AlmudenaSun Melody CuiHofman NicoleCostelloe LisaKearney HughPrenderville Jack ADowner Eric J