Cymax Mouse IL-6 ELISA Kit
- Known as:
- Cymax Mouse Interleukin-6 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- lf-ek0270
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Abfrontier
- Gene target:
- Cymax Mouse IL-6 ELISA Kit
Related genes to: Cymax Mouse 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: Cymax Mouse IL-6 ELISA Kit
Related articles to: Cymax Mouse IL-6 ELISA Kit
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Publication date: 2026/09/15
Lu XinjianWang ZhaoyangHu WeifengHu JiongZou Yang - This study aimed to investigate switching strategies of biologics in noninfectious uveitis (NIU) refractory to anti-tumor necrosis factor alpha (TNFα) agents. - Source: PubMed
Publication date: 2026/09/15
Chung Yoo-RiRodríguez-Fernández Carmen AntíaSong Ji HunKim Hae RangPark Ji HyunPark BumheeFernández-Ferreiro AnxoTouhami SaraSaadoun DavidBodaghi Bahram - Iodine-125 (I) seed therapy is recognized for treating abdominal solid tumors with minimal adjacent tissue damage but may induce radiation colitis when its implantation near colonic tissues, leading to a poor prognosis. Nevertheless, the underlying pathogenesis is not well understood. - Source: PubMed
Liu PingpingZeng XiongLiu WenjingXie HuichaoFang YongkunYang ErwanTang XiaoqiFan ChenglinChen Yihui - Bisphenol S (BPS) is a widespread BPA substitute with emerging immunotoxicity; this review synthesizes zebrafish and rodent experimental evidence to clarify BPS-induced inflammation. - Source: PubMed
Wan Azhan Wan Nur IzzatiZakaria Fatin NadzirahAl' Arifin Danial Akmal FuadAmlie Nur-ZulaikhaKamarudin EvanaPaiman FahezeRisandiansyah RioDasiman Razif - Enterovirus 71 (EV-A71) can cause inflammatory injury beyond the central nervous system, yet the host pathways driving EV-A71-associated skeletal muscle pathology remain poorly defined. Toll-like receptor 2 (TLR2) is a key innate immune sensor capable of amplifying inflammatory signaling during infection. Here, we established an EV-A71 infection model in 1-day-old BALB/c suckling mice by intraperitoneal inoculation for 3 consecutive days and administered the TLR2 inhibitor C29 intraperitoneally at 6 h post-inoculation. EV-A71 infection induced prominent skeletal muscle pathology characterized by inflammatory cell infiltration, muscle bundle disruption, and dissolution, and reduced myofiber cross-sectional area. Consistently, EV-A71 increased the levels of TLR2, nuclear factor-κB (NF-κB) signaling markers (p65 and phosphorylated p65), the pro-inflammatory cytokine IL-6, and the viral protein VP1 in skeletal muscle. EV-A71 infection was also associated with elevated α-SMA and collagen III, suggesting tissue remodeling in injured muscle. Notably, pharmacological inhibition of TLR2 with C29 markedly alleviated histopathological damage and reduced IL-6 expression in skeletal muscle. Collectively, these findings support a model in which EV-A71 activates a TLR2-NF-κB-linked inflammatory program that contributes to skeletal muscle immunopathology and highlights TLR2 as a tractable host-directed target for mitigating virus-associated skeletal muscle injury.IMPORTANCEVirus-associated skeletal muscle injury can cause functional impairment and may worsen outcomes, but actionable host determinants remain limited. Using a neonatal mouse model, we show that enterovirus 71 (EV-A71) infection is accompanied by activation of a Toll-like receptor 2 (TLR2)-linked inflammatory program in skeletal muscle and that pharmacological TLR2 inhibition reduces IL-6 expression and alleviates muscle pathology. These results support the concept that excessive innate immune signaling contributes to muscle immunopathology and identify TLR2 as a potential host-directed intervention point. This work provides a mechanistic framework for understanding and targeting skeletal muscle injury associated with EV-A71 and potentially other viral infections. - Source: PubMed
Publication date: 2026/09/15
Zou XinhongLi YaXinZhang XiaomengNiu HonglinZhou HairuiLiu LeiCui GuoliWang BaixinWu Rui