IL-1 beta Monoclonal Antibody (B122), eBioscience/IL-1 beta单克隆抗体（B122）

货号：14-7012-81,14-7012-85

规格：50 µg,500 µg

价格：1455,3663

产品类型：流式抗体

品牌：eBioscience

物种：其它

宿主：Armenian hamster仓鼠

抗体亚型：IgG

克隆号：B122

荧光染料：Alexa Fluor 488

类型:	单抗	同型对照：
浓度：	0.5 mg/mL	用法：	1-4 µg/mL（ELISA)；Assay-Dependent(FN)；Assay-Dependent(Neu)；(Flow)

产品详细信息Description: The B122 antibody reacts with mouse and rat interleukin-1beta (IL-1beta), a 17 kDa factor secreted primarily by monocytes. IL-1 has effects on T-helper cells, inducing IL-2 secretion and expression of IL-2 receptors.Applications Reported: The B122 antibody has been reported for use in cytokine neutralization, immunoblotting (WB), and ELISA. Please refer to Functional Grade purified B122 (cat. 16-7012) for functional assays.Applications Tested: The B122 antibody hasbeen tested as the capture antibody in a sandwich ELISA for analysis of mouse interleukin-1 beta (IL-1 beta) in combination with the biotinylated polyclonal anti-mouse interleukin-1 beta for detection and recombinant mouse IL-1 beta (14-8012) as the standard. A suitable range of concentrations of this antibody for ELISA capture is 1-4 µg/mL. A standard curve consisting of doubling dilutions of the recombinant standard over the range of 2000 pg/mL - 15 pg/mL should be included in each ELISA plate.Purity: Greater than 90%, as determined by SDS-PAGE.Aggregation: Less than 10%, as determined by HPLC.Filtration: 0.2 µm post-manufacturing filtered.靶标信息Interleukin-1 beta (IL-1 beta) is a proinflammatory cytokine expressed by monocytes, macrophages, and dendritic cells. IL-1 beta is synthesized in response to inflammatory stimuli as a 31 kDa inactive pro-form that accumulates in the cytosol. Cleavage of pro-IL-1 beta into the active 17 kDa protein requires the activation of inflammasomes, which are multi-protein complexes that respond to pathogens, stress conditions, and other danger signals. Inflammasome activation triggers the processing of the caspase-1 precursor into its active form, which in turn cleaves pro-IL-1 beta. IL-1 beta lacks a signal sequence peptide for classical ER/Golgi pathway and is secreted alongside caspase-1 via an alternate and incompletely understood mechanism. Although IL-1 beta is most often secreted in its active form, secretion of the uncleaved protein may be detectable under some biological conditions. IL-1 beta signals through two receptors, IL-1RI and IL-1RII, both of which are shared with IL-1 alpha. IL-1 beta activity can be moderated by IL-1 Receptor Antagonist (IL-1RA), a protein produced by many cell types that blocks receptor binding through competitive inhibition. IL-1 beta play an important role in innate host defense by triggering the production of other proinflammatory cytokines in target cells and initiating acute-phase responses to infection and injury. Elevated levels of IL-1 beta have been associated with many chronic inflammatory conditions IL-1 beta neutralizing antibodies potential therapeutic value.

数据

IL-1 beta Antibody (14-7012-81)Nature communications 2015 -Figure 5 SENP1 deletion alters pancreatic adipocyte phenotype and augments NF-kappaB-dependent inflammation. ( a , b ) Pancreatic adipose was collected from 7 and 14 weeks old Ctrl and SENP1-aP2KO male (male, n =6). Morphology was visualized by haematoxylin and eosin stain staining. Scale bar, 20 mum ( a ). Cell sizes were quantified in ( b ). Three sections from each adipose tissue. Data are representative for three independent experiments. ( c ) Transcript levels of adipocyte differentiation markers (fatty acid synthase, adipose triglyceride lipase and lipoprotein lipase) in PATs were quantified by quantitative PCR with reverse transcription with GAPDH for normalization. n =6, male for each group. ( d ) Increased IKK-NF-kappaB activities in SENP1-aP2KO PATs. A representative western blot was from Ctrl and SENP1-aP2KO mice at the age of 7 weeks. Data are representative from three independent experiments is shown ( n =6, male). Relative protein levels were quantified from three blots by taking Ctrl as 1.0 ( n =6, male). ( e - h ) NF-kappaB activation is specifically detected in PATs of SENP1-aP2KO mice. ( e ) Phosphor-p65 staining (red) in PATs but not in pancreas. ( f ) Co-immunostaining of phosphor-p65 (green) and adipocyte marker FABP4 (red). ( g ) High-power images show co-staining of phosphor-p65 (red) in the nucleus of FABP4 + adipocytes (green). ( h ) Co-staining of phosphor-p65 (green) with APC-conjugated adipocyte marker FABP4 (green; yellow arrowheads), but not with IL-1 beta Antibody (14-7012-81)Nature communications 2015 -Figure 6 SENP1 deletion augments NEMO SUMOylation and cytokine expression in the adipocytes. ( a , b ). SUMOylation of NEMO, but not p65/RelA, was enhanced in the adipocytes of SENP1-aP2KO mice. Proteins extracted from the adipocytes of Ctrl and SENP1-aP2KO mice at the age of 5 weeks were subjected to immunoprecipitation with p65/RelA ( a ) or NEMO ( b ) antibodies followed by western blotting with anti-SUMO1, anti-p65/RelA or anti-NEMO. Proteins are indicated. Representative blots from one pair of Ctrl and SENP1-aP2KO mice are shown. Similar results were obtained from additional two pairs of mice. ( c ) Flag-tagged NEMO was transfected into adipocytes from Ctrl and SENP1-aP2KO mice at the age of 5 weeks. Proteins extracted were subjected to immunoprecipitation with SUMO1 antibody followed by western blotting with anti-flag. Input for flag-NEMO was detected with flag antibody. Representative blots from one pair of Ctrl and SENP1-aP2KO mice are shown. Similar results were obtained from additional two pairs of mice. ( d ) Effect of SENP1 deletion on stress-induced IKK activation, p65/RelA phosphorylation and NEMO SUMOylation. Adipocytes from Ctrl and SENP1-aP2KO mice were treated with VP16 (10 muM) for indicated times. IKK-NF-kappaB p65/RelA signalling molecules were determined by western blot. Ratios of p-IKK/IKK, p-p65/RelA/p65/RelA and pIkappaB-alpha were quantified by taking Ctrl as 1.0. Representative blots from one pair of Ctrl and SENP1-aP2KO mice are shown.

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参考文献：

1.Frontiers in immunologyDnase1L3 Regulates Inflammasome-Dependent Cytokine Secretion.2.Experimental and therapeutic medicineOrally administered sodium 4-phenylbutyrate suppresses the development of dextran sulfate sodium-induced colitis in mice.3.The Journal of clinical investigationIntestinal fungi contribute to development of alcoholic liver disease.4.PloS onePreclinical Development of Ipilimumab and Nivolumab Combination Immunotherapy: Mouse Tumor Models, In Vitro Functional Studies, and Cynomolgus Macaque Toxicology.5.PloS oneCholera Toxin Promotes Th17 Cell Differentiation by Modulating Expression of Polarizing Cytokines and the Antigen-Presenting Potential of Dendritic Cells.

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