Recombinant Rat IL-6, 10 ug.
- Known as:
- Recombinant Rat Interleukin-6, 10 ug.
- Catalog number:
- PR15060-10
- Product Quantity:
- 1
- Category:
- -
- Supplier:
- Neuromi
- Gene target:
- Recombinant Rat IL-6 10 .
Related genes to: Recombinant Rat IL-6, 10 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 Rat IL-6, 10 ug.
Related articles to: Recombinant Rat IL-6, 10 ug.
- Oral lichen planus (OLP) is a chronic inflammatory disease characterized by T-cell infiltration and basal keratinocyte apoptosis. The molecular mechanisms linking immune activation to epithelial damage remain elusive. RAC2, a hematopoietically-enriched Rho GTPase, is a key regulator of immune cell functions. However, the relationship between RAC2 and OLP remains unclear. This study aimed to elucidate the precise localization and functional role of RAC2 in OLP pathogenesis. - Source: PubMed
Publication date: 2026/06/03
Sen MuHuishu LiYunfei XiaYaping HuangJiaqi KongZhuoran ZhangQianyang ZhangMingxing WangJingru WangXinru GuoNan MiaoYing YanYuanbo Zhan - Mastitis is the most common dairy disease, impairing milk quality and yield. Quercetin (QUE), a natural compound with anti-inflammatory, antioxidant, and antimicrobial activities, lacks a clear mechanism against mastitis. This study evaluated QUE in a mouse model of Streptococcus agalactiae (commonly known as Group B Streptococcus (GBS))-induced mastitis. Mice (n = 25) were randomized into five groups (n = 5/group): control, GBS model, and QUE (25, 50, 100 mg/kg). QUE or vehicle was administered intraperitoneally 24 h before mammary duct injection of GBS. Pathohistological analysis demonstrated that QUE inhibited GBS-induced histopathological damage and myeloperoxidase activity in mouse mammary tissue (p < 0.01). Immunofluorescence experiments revealed that QUE upregulated the tight junction proteins Occludin and tight junction protein 1, thereby maintaining the integrity of the mammary blood-milk barrier. The results of qPCR and ELISA demonstrated that QUE was effective in reducing the gene expression and content of pro-inflammatory factors IL-6, IL-1β, and TNF-α (p < 0.01). Western blotting and qPCR demonstrated that QUE impeded the NF-κB pathway and diminished the activity of the NLRP3 inflammasome. Concurrently, QUE diminished the iron content of mouse mammary tissues induced by GBS, repressed TfR and ACSL4 protein expression, and FTH1, PTGS2, NCOA4 gene transcript levels, while elevating SLC7A11 and GPX4 protein expression (p < 0.01). These findings indicated that QUE mitigated GBS-induced mammary gland injury in mice by inhibiting the NF-κB/NLRP3 signaling pathway and ferroptosis. This study elucidated the potential mechanism of QUE on GBS-induced mastitis and enhanced the theoretical foundation for future prevention and treatment of mastitis. - Source: PubMed
Publication date: 2026/06/02
Jia YayingSun QiWu TingXie YueqingYu HongsenJiang MingzhenLi XuhaiYang ZhengtaoZhou ErshunWang Jingjing - Despite restoration of systemic and pulmonary circulation and normalized oxygen saturation, patients with Fontan circulation experience frailty, exercise intolerance, and impaired exercise hemodynamics. Altered cytokine-chemokine profiles have been reported, but their relationship with Fontan pathophysiology remains poorly defined. - Source: PubMed
Publication date: 2026/06/06
Bagchi Ashim KLiu YixiuDhingra SanjivRavandi AmirSingal Pawan KShah Ashish H - Prehabilitation is an emerging preoperative strategy designed to optimise patients' functional capacity before surgery to improve postoperative outcomes. Previous studies have demonstrated its clinical benefit, including enhanced recovery and reduced postoperative complications. However, the mechanisms underlying these benefits remain poorly understood. This exploratory study investigates the potential effects of prehabilitation on pre- and postoperative immune function. - Source: PubMed
Publication date: 2026/06/06
Jacobs Lotte M CDrager Luuk Dvan Eijk Lucas THelder Leonie SJoosten Leo A BStrijker Dieuwkevan Laarhoven Cornelis J H Mvan den Heuvel BaukjeWarlé Michiel C - The purpose of this study is to clarify the role of LINC01094 in acute cerebral infarction (ACI) and to explore its potential molecular mechanisms. A total of 121 patients with ACI and 133 healthy controls were enrolled in this study. The expression levels of LINC01094, miR-499a-5p, and inflammatory markers (CRP, IL-6) were measured using RT-qPCR. The levels of MDA, SOD, and ROS were measured using commercial assay kits. The diagnostic value of LINC01094 for ACI was evaluated using ROC curve analysis. CCK-8 assay and flow cytometry were utilized to measure cell viability and apoptosis. The subcellular localization of LINC01094 in SH-SY5Y cells was determined. The predicted targeting relationship between LINC01094 and miR-499a-5p was validated using dual-luciferase reporter (DLR) and RNA immunoprecipitation (RIP) assays. Serum LINC01094 expression was significantly elevated in ACI patients and demonstrated diagnostic value for ACI. miR-499a-5p expression was markedly reduced in both ACI patients and in vitro/in vivo models, showing a significant negative correlation with LINC01094 expression in patients. Downregulation LINC01094 mitigated OGD/R-induced damage in SH-SY5Y cells and cerebral injury in MCAO rats, while inhibition miR-499a-5p reversed this protective effect. Furthermore, CACNB2 was confirmed as a direct target of miR-499a-5p. LINC01094 participates in the pathological process of ACI injury by competitively binding to and inhibiting the activity of miR-499a-5p. These findings suggest that LINC01094 may serve as a potential therapeutic target for ACI treatment. - Source: PubMed
Publication date: 2026/06/06
Dong JingFeng YilinGuo Mengnan