Recombinant Mouse IL-6, 5 ug.
- Known as:
- Recombinant Mouse Interleukin-6, 5 ug.
- Catalog number:
- PR15059-05
- Product Quantity:
- 1
- Category:
- -
- Supplier:
- Neuromi
- Gene target:
- Recombinant Mouse IL-6 5 .
Related genes to: Recombinant Mouse IL-6, 5 ug.
- 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: Recombinant Mouse IL-6, 5 ug.
Related articles to: Recombinant Mouse IL-6, 5 ug.
- Autoimmune encephalitis (AE) is a major cause of acute and subacute neuropsychiatric syndromes. - Source: PubMed
Publication date: 2026/06/09
Srivastava ArpnaSingh Rajesh KumarBanerjee JyotirmoyA ElavarasiDas AnimeshRamanujam BhargaviParihar JasminePandit Awadh KishorV Y VishnuVibha DeeptiChandra SaratSrivastava M V PadmaTripathi Manjari - BufeiJianpi Mixture (BFJPM) is a modified herbal formula developed from long-term clinical practice for the management of allergic constitution in children. To evaluate the therapeutic efficacy of BFJPM in an OVA-induced murine model of food allergy and to investigate its effects on the gut microbiota through integrated animal experiments, 16S rRNA gene sequencing, and network pharmacology. - Source: PubMed
Publication date: 2026/05/28
Yang XuePeng HuiyiHu RaoLi YifanJiang Ping - Dysregulated cytokine signaling is implicated in persistent inflammation and fibrosis in oral submucous fibrosis (OSMF) and has been reported in association with pathways observed in oral squamous cell carcinoma (OSCC). This study investigated cytokine associated inflammatory and fibrotic responses following treatment with a mucoadhesive buccal patch containing isotretinoin, bromelain, and limonene. - Source: PubMed
Publication date: 2026/05/28
Kokkanti Rekha RaniViswanathan SandhiyaParida NanditaBiswas SoumyajitKushwaha Gajraj SinghDeheri Pratap KumarPanda Alok KumarPanda AbikshyeetBajoria Atul AnandPatnaik Srinivas - Later life is accompanied by testosterone declines alongside the development of chronic inflammation, termed inflammaging. A new theoretical model posits these processes are related through an energetic trade-off. As somatic damage accumulates, this should chronically activate the energetically costly inflammatory response. As an energy conserving response to promote cellular repair, testosterone production is expected to be suppressed. Consistent with this model, we find that markers of inflammaging, including IL-6 and GDF-15, mediate age-related testosterone declines in a large sample of male participants from the UK Biobank (n = 18,347, mean age 57 years, range 40-70). GDF-15, a marker of chronic inflammation and a key metabolic stress signaling protein, was the strongest predictor and mediator of testosterone declines. Further, individuals with high testosterone given their health and level of inflammation showed elevated mortality risk over follow up, consistent with a trade-off between maintenance and reproduction. Our results highlight the importance of considering energetic trade-offs to understand later life testosterone declines. They also highlight the importance of alleviating cellular damage that augments inflammaging and its down-stream hormonal effects. Finally, our study raises concern for exogenous testosterone therapies in the context of chronic inflammation, which could increase mortality risk. - Source: PubMed
Publication date: 2026/06/05
Aronoff Jacob ETrumble Benjamin C - Periodontitis (PD) is a common chronic inflammatory condition and a risk factor for cardiovascular diseases (CVD), yet underlying linking mechanisms remain unclear. The cytokine Oncostain M (OSM) is elevated in both PD and CVD and has emerged as a potential mediator linking oral inflammation to vascular dysfunction. Neutrophils represent a prominent source of OSM during PD and OSM production is elevated by the periodontal pathobiont (Td). This study investigated the role of exogenous and neutrophil-derived OSM in endothelial cell (EC) dysfunction and the contribution of heterogenous oral species in OSM production. Human aortic endothelial cells (HAoEC) were used to evaluate the effects of exogenous purified OSM and neutrophil-derived OSM on endothelial cell function. Endothelial permeability, neutrophil transmigration, cytokine production, cell activation and junctional integrity were assessed using transwell assays, ELISAs, real-time PCR, immunoblotting and immunofluorescence microscopy. Exogenous OSM significantly increased HAoEC permeability, neutrophil transmigration and promoted endothelial activation; characterized by increased E-selectin, ICAM-1 and IL-6 expression. Mechanistically, OSM activated OSMR-STAT3 signaling and altered organization of VE-cadherin in adherens junctions and decreased expression of occludin in tight-junctions. Heterogenous oral species promote OSM production from mouse and human neutrophils in vitro and in vivo using a mouse air pouch model of infection. most robustly induced OSM release, likely independent of prominent virulence factors dentilisin and Msp. Co-culture model experiments revealed conditioned media from -stimulated neutrophils promoted endothelial cell permeability and IL-6 while reducing endothelial nitric oxide synthase (eNOS) production. These effects were abolished by antibody neutralization of OSM, supporting a casual role of neutrophil-derived OSM. Overall, these findings provide mechanistic insight into putative links between PD and adverse cardiovascular events and identify OSM signaling as critical mediator in inflammation-driven endothelial dysfunction. - Source: PubMed
Publication date: 2026/06/02
Leyva-Rodriguez Dayron MVisser Michelle B