Rat IL-6 ELISA kit
- Known as:
- Rat Interleukin-6 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- BEK1110
- Product Quantity:
- 96 T
- Category:
- Elisa Kits
- Supplier:
- Biospect
- Gene target:
- Rat IL-6 ELISA kit
Related genes to: Rat 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
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- This research sought to investigate the therapeutic efficacy and underlying mechanisms of Shengjiang Powder (SJP) in the context of chronic gastritis. - Source: PubMed
Publication date: 2026/08/14
Liu YihuangLi XiaofengZhang XiaCao HuaZhang NailinSun JianhuiChen Pingping - Latent tuberculosis infection (LTBI) is associated with an increased risk of coronary artery disease (CAD), potentially mediated by systemic inflammation. Traditional lipid-based risk models may have limited predictive performance in tuberculosis-affected populations. - Source: PubMed
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Sun FengZhou YuqiangMa HaipingYe MeiYang Yining - Microglia are the main targets of HIV-1 infection in the central nervous system (CNS) and are considered important contributors to chronic neuroinflammation in people living with HIV (PLWH). In this study, we investigated the mechanisms leading to inflammatory responses during acute HIV-1 infection in an adult human microglia model. - Source: PubMed
Publication date: 2026/08/14
Gaete-Argel AracellyAnanías-Sáez CatarinaRojas-Fuentes CeciliaGiraldo-Ocampo SebastianJara DanielaHernández-Díaz TomásOrtega-Orellana CamilaLópez-Palma DeliaAkiyama HisashiGummuluru SuryaramGonzález Pablo AValiente-Echeverría FernandoSoto-Rifo Ricardo - Myeloid differentiation primary-response protein 88 (MyD88), an adapter protein used by many Toll-like receptors (TLRs), plays a critical role in initiating inflammatory responses. Our laboratory has previously shown that alcohol intoxication combined with burn injury causes intestinal tissue damage and leakiness. This is accompanied by increased intestinal neutrophil infiltration along with bacterial abundance and translocation. An overgrowth of bacteria can activate TLRs on intestinal epithelial cells (IECs), promoting inflammation and subsequent gut tissue damage. To examine the role of MyD88 in intestine inflammation/leakiness following ethanol and burn injury, we used MyD88-/- mice. MyD88 deficiency in mice prevented the increases in IL-6 and KC levels, MPO activity, as well as the expression of neutrophil mediators Lipocalin2, S100a8, and S100a9 in the intestine. It also attenuated neutrophil extracellular trap (NET) formation and release of superoxide anion (O2-). In addition, MyD88 deficiency improved tight junction; namely ZO-1, Occludin, Claudin 4 and Claudin 8 expression. Finally, using IEC specific MyD88-/-IEC mice, we further found that MyD88 deficiency mitigated intestinal permeability in ethanol and burn. Together, these findings suggest that MyD88 plays a critical role in intestinal inflammation and barrier leakiness following ethanol and burn injury, and therefore, targeting the MyD88 pathway may have therapeutic potential for intervention in burn injury. - Source: PubMed
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