eBioscience BMS178 抗体,IL-6 Monoclonal Antibody (6B4 IGH 54), eBioscience/IL-6单克隆抗体(6B4 IGH 54)

2024-10-23

IL-6 Monoclonal Antibody (6B4 IGH 54), eBioscience/IL-6单克隆抗体(6B4 IGH 54)

货号:BMS178

规格:100 µg

价格:2806

产品类型:抗体和ELISA

品牌:eBioscience

类型:

单抗

同型对照:

浓度:

1 mg/mL

用法:

Assay-Dependent(ELISA);Assay-Dependent(FN)
产品详细信息Description: Clone 6B4 IGH 54 can be used to neutralise the activity of 50pg/mL of recombinant mouse IL-6 by >95% in a functional assay.Applications Tested: ELISA, Functional Studies (Blocking).Purity: >95%.靶标信息Interleukin 6 (IL-6) is a multifunctional 26 kD protein originally discovered in the medium of RNA-stimulated fibroblastoid cells. IL-6 appears to be directly involved in the responses that occur after infection and cellular injury, and it may prove to be important as IL-1 and TNF-a in regulating the acute phase response. IL-6 is reported to be produced by fibroblasts, activated T cells, activated monocytes or macrophages and endothelial cells. IL-6 acts upon a variety of cells including myeloidprogenitor cells, T cells, B cells, and hepatocytes. In addition, IL-6 appears to interact with IL-2 in the proliferation of T lymphocytes. IL-6 potentiates the proliferative effect of IL-3 on multipotential hematopoietic progenitors. IL-6 plays a critical role in B-cell differentiation to plasma cells and is a potent growth factor for plasmacytoma and myeloma. IL-6 is a very useful culture supplement for the generation of a high number of antibody-producing hybridomas. Primarily produced at sites of acute and chronic inflammation, IL-6 is secreted into the serum and induces a transcriptional inflammatory response through interleukin 6 receptor, alpha. The functioning of IL-6 is implicated in a wide variety of inflammation-associated disease states including diabetes mellitus and systemic juvenile rheumatoid arthritis.

数据:

IL-6 Antibody (BMS178)Scientific reports 2016 -Figure 7 Suppressed production of IL-6 and TNF-alpha in Arg-II -/- macrophages accounts for reduced lipogenesis in hepatocyte AML12 cells. The serum-starved (overnight) WT- or Arg-II -/- -BMM were incubated in the absence or presence of 100 ng/ml LPS for 8 hours, the conditioned medium (CM) was then collected. (A) IL-6 and TNF-alpha production in CM collected from WT- or Arg-II -/- -BMMs in the absence or presence of LPS was evaluated by ELISA. ***p < 0.001 vs controls (-LPS), ### p < 0.001 vs WT+LPS. (B) AML12 hepatocytes were serum-starved for 6 hours in 0.2% bovine serum albumin (BSA)-ITS-DMEM-F-12 Ham medium and then incubated with CM of LPS-treated BMM from WT or Arg-II -/- mice as indicated in the presence of oleic acid (OA, 20 mmol/L) for 24 hours. The lipid was then extracted for measurement of the triglyceride content in the cells. *p < 0.05 vs WT-CM. (C) Experiment procedure is the same as in panel B, except that BMM-CM was pre-treated for 2 hours with control rat IgG (10 mug/ml) or neutralizing antibodies anti-IL-6 (18 mug/ml) or anti-TNF-alpha (0.4 mug/ml) or anti-IL-6 (18 mug/ml) plus anti-TNF-alpha prior to the addition to the cells. *p < 0.05, **p < 0.01, ***p < 0.001 vs (WT-BMM-CM + IgG); ## p < 0.01, ### p < 0.001 vs (Arg-II -/- - BMM-CM + IgG).

IL-6 Antibody (BMS178)Scientific reports 2016 -Figure 8 CM from Arg-II -/- -BMM elicits increased AMPK signaling and decreased SREPBP-1c and SCD-1 in hepatocytes. Experiment procedure is the same as in Fig. 7B , except that (A) AML12 hepatocyte cell lysates were prepared for immunoblotting analysis of AMPK activation. Quantification of the signals is presented below. (B,C ) RNA was extracted for qRT-PCR analysis of mRNA expression of SREBP-1c and SCD-1. For all the panels *p < 0.05, **p < 0.01, ***p < 0.001 between the indicated groups. Neutral. Abs means neutralizing antibodies. IgG was used as control (-) for neutralizing antibodies. (D) Schematic illustration of the major findings of this study.
参考文献:
1. Journal of immunology (Baltimore, Md. : 1950)Group 2 Innate Lymphoid Cells Promote an Early Antibody Response to a Respiratory Antigen in Mice.2. Scientific reportsTargeting arginase-II protects mice from high-fat-diet-induced hepatic steatosis through suppression of macrophage inflammation.
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