Chicken Interleukin 6,IL-6 ELISA Kit
- Known as:
- Chicken Interleukin 6,Interleukin-6 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- E0003Ch
- Product Quantity:
- 48T
- Category:
- Elisa Kits
- Supplier:
- JING
- Gene target:
- Chicken Interleukin 6 IL-6 ELISA Kit
Related genes to: Chicken Interleukin 6,IL-6 ELISA Kit
- Gene:
- CEBPB NIH gene
- Name:
- CCAAT enhancer binding protein beta
- Previous symbol:
- TCF5
- Synonyms:
- LAP, CRP2, NFIL6, IL6DBP, C/EBP-beta
- Chromosome:
- 20q13.13
- Locus Type:
- gene with protein product
- Date approved:
- 1991-02-27
- Date modifiied:
- 2018-02-23
- Gene:
- CEBPD NIH gene
- Name:
- CCAAT enhancer binding protein delta
- Previous symbol:
- -
- Synonyms:
- CRP3, CELF, C/EBP-delta, NF-IL6-beta
- Chromosome:
- 8q11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1992-06-24
- Date modifiied:
- 2018-02-23
- Gene:
- ENTPD6 NIH gene
- Name:
- ectonucleoside triphosphate diphosphohydrolase 6
- Previous symbol:
- CD39L2, IL6ST2
- Synonyms:
- NTPDase-6, dJ738P15.3
- Chromosome:
- 20p11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1998-03-20
- Date modifiied:
- 2019-02-28
- Gene:
- IL6 NIH gene
- Name:
- interleukin 6
- Previous symbol:
- IFNB2
- Synonyms:
- IL-6, BSF2, HGF, HSF
- Chromosome:
- 7p15.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2017-07-12
- Gene:
- IL6RP1 NIH gene
- Name:
- interleukin 6 receptor pseudogene 1
- Previous symbol:
- IL6RL1
- Synonyms:
- -
- Chromosome:
- 9q22.2
- Locus Type:
- pseudogene
- Date approved:
- 1991-08-18
- Date modifiied:
- 2014-11-19
Related products to: Chicken Interleukin 6,IL-6 ELISA Kit
Related articles to: Chicken Interleukin 6,IL-6 ELISA Kit
- Basal cell carcinoma (BCC) is the most common malignant skin tumor. Skin-resident lipophilic Malassezia yeasts are associated with various cutaneous disorders, while their correlative patterns and potential biological effects in BCC tissues remain insufficiently defined. We used RT-qPCR screening of archived FFPE BCC specimens and metagenomic sequencing of three paired fresh tumor and peritumoral tissues to characterize tissue-associated Malassezia colonization. M. globosa was the most abundant species in FFPE samples and was also detectable in fresh tissues. In vitro functional assays (CCK-8, EdU) in HaCaT keratinocytes and A-431 epidermoid carcinoma cells showed that 12 h stimulation with optimal concentrations of M. globosa (1.2 × 10 CFU/mL) and M. yamatoensis (1.6 × 10 CFU/mL) significantly promoted epithelial cell proliferation. Transcriptome sequencing and subsequent RT-qPCR validation further showed that both strains significantly upregulate pro-inflammatory genes (IL-1β, IL-6, TNF-α) and oxidative stress-related genes (SOD1, SOD2) in these cell lines. Collectively, our findings describe a correlative association between Malassezia colonization and BCC lesions and offer preliminary in vitro mechanistic clues. - Source: PubMed
Zhu XiaoleiZhang WenYe TinghongZhang HengTan JufangSun Yi - Sepsis is a complicated disorder caused by infection, which may trigger various symptoms. Lipopolysaccharides (LPS) are among the primary pathogens which can stimulate host's immunoreaction. In the late stage of sepsis, the patients' immune system is significantly suppressed, thus the mortality increases. Notably, autophagy is pivotal during sepsis, in which autophagosome-lysosome fusion mediated by syntaxin 17 (STX17) is a key step. Previous studies have shown that histone deacetylase 2 (HDAC2) deacetylated STX17 to promote autophagosome-lysosome fusion. Trichostatin A (TSA) as a HDAC inhibitor (HDACi) has the capability of inhibiting histone deacetylase activity, while such an effect can be reversed by ITSA-1. This time LPS was used to stimulate human monocyte-macrophages (THP-1 cells) to establish the inflammatory cell model. TSA and ITSA-1 were administrated. The cell proliferation was examined by WST-1. Cytokines such as TNF-? and IL-6, as well as HDAC2 activity and deacetylated STX17 (DA-STX17) expression were detected by ELISA. Also, autophagy-related proteins such as P62 and microtubule-associated protein light chain 3 (LC3) were detected by Western Blotting (WB), and autophagosome-lysosome fusion was observed by fluorescence assay. Cell apoptosis was measured by flow cytometry. Besides, network pharmacology analysis was conducted. The data showed that TSA inhibited HDAC2 activity, and remarkably downregulated DA-STX17 expression, accompanied by the lower expression of P62 and LC3 ?/I. Decreased DA-STX17 promoted autophagosome-lysosome fusion, and inhibited TNF-? secretion. Furthermore, network pharmacology analysis revealed an inner relationship concerning HDAC2 between TSA and sepsis. Therefore, TSA can be considered a potential drug to cure sepsis-related diseases. - Source: PubMed
Sang LeZang RanYu ZeweiGong XiaHuang YunleiJin XingyuSun Jian - Atrial inflammation and fibrosis are the pathogenesis of postoperative atrial fibrillation (POAF). It has been reported that invariant natural killer T (iNKT) cells can coordinate tissue inflammation, but whether it can regulate POAF is still unknown. A sterile pericarditis (SP) model was constructed on C57BL/6J mice and Jalpha18-/- mice to simulate POAF. Intraperitoneal injection of anti-interleukin (IL) -6 neutralizing antibody (anti-IL-6) was used for intervention, and atrial fibrillation (AF) was induced by transesophageal sinus atrial node pulse pacing. The levels of iNKT cells and IL-6/signal transducer and activator of transcription 3 (STAT3) signaling pathway were detected by flow cytometry and western blot. HE stain, Masson stain, and immunohistochemistry were used to evaluate the process of inflammation and fibrosis in atrial tissue. The calcium homeostasis and function of atrial mitochondria were evaluated by biochemical detection and fluorescent staining. The expression of iNKT cells was up-regulated in SP mice. The defect of iNKT cells increased the AF induction rate and duration of SP mice, enhanced AF susceptibility, aggravated atrial electrical remodeling, promoted inflammatory cell infiltration and fibrosis, and increased inflammatory factors and fibrotic proteins. Compared with SP mice, iNKT cell defects also aggravated endoplasmic reticulum-mitochondrial calcium coupling disorder, mitochondrial calcium homeostasis imbalance, reduced mitochondrial DNA (mtDNA), adenosine triphosphate (ATP) content, and mitochondrial complex enzyme activity, and increased IL-6 and STAT3 phosphorylation levels. Anti-IL-6 significantly inhibited IL-6/STAT3 signaling pathway, reduced AF induction rate and duration, and improved atrial mitochondrial calcium homeostasis, mitochondrial dysfunction, inflammation, and fibrosis. The deficiency of iNKT cells aggravated atrial tissue mitochondrial dysfunction, inflammation, and fibrosis in POAF mice via activating IL-6/STAT3 axis, and aggravated AF susceptibility. - Source: PubMed
Tian XiaoTian GuangshuLiu ZhishuoLv LihuaXia LinYang Lihua - Postoperative inflammation after arthroplasty contributes to pain, delayed mobilization and prolonged hospitalization. Recent randomized trials have evaluated pharmacological anti-inflammatory strategies within contemporary enhanced recovery pathways, but evidence after hip and shoulder arthroplasty remains scattered across different drug classes and perioperative regimens. - Source: PubMed
Ling HuangYu ZhangShu Deng - Gastric cancer (GC) remains a leading cause of cancer-related mortality worldwide and effective therapeutic targets remain limited. - Source: PubMed
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