IL-6, human recombinant
- Known as:
- Interleukin-6, H. sapiens Rec.
- Catalog number:
- BC-279
- Product Quantity:
- 20 ug
- Category:
- -
- Supplier:
- kamyia
- Gene target:
- IL-6 human recombinant
Related genes to: IL-6, human recombinant
- 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: IL-6, human recombinant
Related articles to: IL-6, human recombinant
- Hyperglycemia drives peripheral nerve damage through oxidative stress, inflammation, and apoptosis, yet the role of redox-sensitive ion channels in linking these processes remains poorly understood. - Source: PubMed
Publication date: 2026/06/27
Yildizhan KenanAltindağ FikretHafit Bayir MehmetKeleş Ömer Faruk - Inflammatory diseases arise from complex interactions between immune signaling and cellular stress. Although endoplasmic reticulum (ER) stress is a key modulator of immunity, the mechanisms by which it promotes inflammatory pathology remain incompletely understood. Notably, ER stress-induced NF-κB activation alone is insufficient to account for robust IL-6 production, thus suggesting the involvement of additional regulators. Using bone marrow-derived macrophages and sepsis model mice, we identified the inducible transcription factor IκBζ as a critical mediator of this response, with ER stress synergizing with TLR signaling to markedly upregulate IκBζ. Mechanistically, ER stress triggered calcium-dependent signaling that led to IκB kinase-mediated degradation of the RNase Regnase-1, likely stabilizing Nfkbiz mRNA and promoting the accumulation of IκBζ, which was found to cooperate with the ER stress factor XBP1s to drive transcription of selected secondary-response genes, particularly Il6 and Nos2. Importantly, this synergy was required for excessive IL-6 production in septic mice, highlighting a gene-specific amplification pathway. Together, these findings identify a dual mechanism in which transcriptional synergy between IκBζ and XBP1s is coupled to posttranscriptional mRNA stabilization via Regnase-1 degradation, thereby linking proteotoxic stress to hyperinflammatory responses. Our results establish ER stress-mediated IκBζ accumulation as a key driver of inflammatory pathogenesis and a potential therapeutic target in ER stress-associated inflammatory disorders. - Source: PubMed
Nakaminami YuriRuengsinpinya LerdluckSakihara RikoTakahata YoshifumiHata KenjiIwawaki TakaoNishimura RikoMurakami Tomohiko - Food-derived biopeptides have attracted increasing attention due to their potential health benefits and favorable safety profiles. In this study, rice protein hydrolysates (< 3 kDa) and their derived peptides were investigated for their protective effects against tumor necrosis factor (TNF)-α/interferon (IFN)-γ-induced injury in human keratinocyte cells (HaCaT). The hydrolysates significantly enhanced cell viability and migration, and five peptides were identified by LC-MS/MS and in-silico analysis. These peptides improved the viability of damaged cells, with PG9 (PSWVAFTGG) showing the greatest activity. PG9 significantly downregulated the mRNA expression of pro-inflammatory cytokines, including Regulated on Activation, Normal T-cell Expressed and Secreted (RANTES), Interleukin (IL)-1β, IL-6, and IL-23, while also markedly promoting keratinocyte migration. Molecular dynamics simulations revealed that PG9 formed stable hydrogen-bonds with key residues (Lys745 and Asp855) within the epidermal growth factor receptor (EGFR) binding site, suggesting its involvement in EGFR-mediated wound healing signaling. In addition, PG9 regulated the PI3K/AKT/mTOR pathway by reducing the expression of PI3K, AKT, mTOR, and inhibiting AKT phosphorylation. These results identify PG9 as a stable EGFR-binding peptide capable of modulating inflammatory signaling and supporting its potential as a natural agent for skin repair. - Source: PubMed
Publication date: 2026/06/27
Qu TingminWen ShiyuHu LiangjieWu YingHuang RuiboWu HaoMu DaichenHuang QingmingHu JianWen Li - Patients undergoing surgery for degenerative lumbar spinal diseases (DLSD) often experience impaired recovery due to acute pain, inflammation, muscular dysfunction, and residual numbness. Conventional pharmacotherapy relies heavily on nonsteroidal anti-inflammatory drugs (NSAIDs) and opioids, but their significant side effects limit widespread use. Consequently, non-pharmacological adjunctive therapies such as acupuncture are gaining increased attention. - Source: PubMed
Publication date: 2026/06/27
Changsheng HuangLei YueCong LeiXingsheng ZhangSijia WangMo ZhangGuang YangHaolin Sun - Atherosclerosis (AS) is a leading cause of cardiovascular morbidity and mortality worldwide. This study investigated the protective effects and underlying mechanisms of asiatic acid (AA), a bioactive triterpenoid from Centella asiatica, in high-fat diet (HFD)-fed ApoE mice and in ox-LDL-stimulated RAW264.7 macrophages. In vivo, AA, particularly at the high dose, was associated with reduced aortic atherosclerotic lesions and attenuated hepatic steatosis, accompanied by an improved serum lipid profile (lower TC, TG, and LDL-C; higher HDL-C) and by attenuated systemic inflammation (IL-6, IL-1β, and TNF-α) and oxidative stress. Mechanistically, AA was associated with upregulation of the PPARγ/LXRα/ABCG1 axis in the liver; consistently, in ox-LDL-induced macrophage-derived foam cells, AA dose-dependently reduced intracellular total and free cholesterol in parallel with restoration of the same PPARγ/LXRα/ABCG1 axis, findings that may reflect improved macrophage cholesterol efflux. Untargeted serum metabolomics further showed that AA reversed a focused set of disease-associated metabolites enriched in pro-inflammatory arachidonic acid-derived oxylipins (e.g., 12R-HETE, 15(S)-HPETE, leukotriene B4, and PGE2-related metabolites). Collectively, these findings suggest that AA exerts multi-target anti-atherosclerotic activity, integrating lipid-regulating, antioxidant, and anti-inflammatory actions, and support its potential as a candidate agent for the prevention and management of atherosclerotic cardiovascular disease. - Source: PubMed
Publication date: 2026/06/27
Wu ZhihaoYang LuyinYang JieGou ZhongjiYu HongRen Wei