IL-6, Human Protein
- Known as:
- Interleukin-6, Human Protein
- Catalog number:
- z03034-50
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- IL-6 Human Protein
Ask about this productRelated genes to: IL-6, Human Protein
- 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 Protein
Related articles to: IL-6, Human Protein
- To elucidate the molecular targets and physiological mechanisms underlying the therapeutic efficacy of Jianpi Qingre Lishi prescription (, JQLP) in the treatment of non-alcoholic steatohepatitis (NASH). - Source: PubMed
Mengjun X UZixing YanXi ChenJuanjuan CaiHaiou ZhangZhenwen Lin - Antiretroviral therapy (ART) suppresses HIV replication and partially restores immune function, but immune recovery is often incomplete. Interleukin-6 (IL-6) and Interleukin-10 (IL-10) reflect opposing sides of the immune response, pro-inflammatory and regulatory, respectively. They may provide insight into the degree of residual immune dysregulation in people living with HIV (PLHIV) on treatment. This study aims to determine serum IL-6 and IL-10 levels in PLHIV on ART compared to HIV-negative controls. - Source: PubMed
Publication date: 2026/06/27
Adegoke Adekunle AyomideOnyeaghala ChizaramOlojede Abel OluwaseunOmitola Olufemi GNwauche Chijioke A - Lavandula species are rich in bioactive compounds, among which rosmarinic acid (RA) is a major phenolic known for potent antioxidant and anti-inflammatory activities. In this study, Lavandin (Lavandula × intermedia), a sterile hybrid widely cultivated for essential oil production, was used to develop RA-enriched cell extracts through plant cell culture technology combined with methyl jasmonate (MJ) elicitation. Lavandin cell suspension cultures accumulated higher levels of RA compared to those of L. angustifolia, and MJ treatment further enhanced RA biosynthesis, as confirmed by the upregulation of RA biosynthetic genes. Extracts derived from untreated and MJ-treated lavandin cell suspension cultures were assessed in LPS-stimulated RAW 264.7 macrophages. Both extracts were non-cytotoxic and significantly suppressed nitric oxide production, pro-inflammatory cytokines (TNF-α, IL-1β, IL-6), and the expression of iNOS and COX-2. Notably, the MJ-treated lavandin cell extract exhibited superior anti-inflammatory efficacy. Mechanistic analyses revealed that lavandin cell extract selectively inhibited the IKK/IκB/NF-κB pathway with minimal influence on MAPK pathways, while concurrently activating the AMPK/Nrf2/HO-1 axis. These findings demonstrate that MJ-elicited lavandin cell extract enriched in RA possesses strong anti-inflammatory activity and highlight its potential as a functional biomaterial for mitigating oxidative stress-related and inflammatory conditions. - Source: PubMed
Publication date: 2026/06/27
Jeon GyeongchanKim Bo RyeongJeong Yu JeongKim SoyoungLee JiyoungLee Ok RanJeong Hyung JaeJeong Jae CheolKim Cha Young - The CD74-ROS1 fusion protein is an aggressive oncogenic driver detected in non-small cell lung cancer (NSCLC) patients from stages I-IV. Despite its rare occurrence, CD74-ROS1 has a notable clinical value, with ROS1 inhibitors used as first-line therapeutics in precision medicine. Upon targeting the cancer with ROS1 tyrosine kinase inhibitors (TKIs), resistance occasionally emerges for reasons that are not well-understood. Therefore, analyzing the individual roles of CD74 and ROS1 in the context of the CD74-ROS1 fusion may reveal mechanistic insights that would guide the scientific community to more effective therapies. Here, we describe the development and characterization of A549-transfected CD74-ROS1 and CD74-ROS1 variants, which together with wild-type CD74-ROS1 and control cells, enable interrogation of each protein partner. Expression analysis of 23,342 genes demonstrates distinct profiles among the variants, with 62 genes identified as differentially expressed between the control and CD74-ROS1 transfected cells. Further analysis designates 13 and 5 of these genes with expression patterns that were influenced by either truncation of the CD74 intracellular domain or the kinase inactivation mutant, respectively. From the genes specified, IL-6 stands out because of its well-established role in NSCLC and its association with CD74. In alignment with the mRNA findings, the phospho-kinase array results expose variant-mediated signaling events that were not previously linked with the functionality of CD74-ROS1. Taken altogether, this study provides an innovative view of CD74 as a fusion partner in CD74-ROS1 and contributes a list of novel molecular targets for mechanistic analysis and drug development. - Source: PubMed
Publication date: 2026/06/27
Vargas JasmineOlivieri JuliaPantouris Georgios - Exposure to D-galactose (D-gal) induces psychiatric problems and cognitive decline characterized by oxidative stress and neuronal dysfunction. In this study, linezolid (Lnz) was used to evaluate its mitigating effects on D-gal-induced neurological deficits. Lnz has been reported as an antidepressant and anxiolytic agent that can alleviate neurological and behavioral alterations. Thirty-six animals were separated into 6 sets (n = 6): [Veh + Veh], [Veh + Lnz] (10 mg/kg), [Veh + Lnz] (20 mg/kg), [Veh + D-gal] (100 mg/kg), [D-gal + Lnz] (10 mg/kg), and [D-gal + Lnz] (20 mg/kg). Both D-gal and Lnz were administered intraperitoneally (i.p) for 2 weeks. After treatment, behavioral tests, i.e., light-dark activity (LDA), tail suspension test (TST), and Morris Water Maze (MWM) were performed on days 14, 15, and 16-18, respectively, to assess anxiety, depression, and memory function. The rodents were decapitated on day 19, and their brains (particularly hippocampus and other brain regions) were isolated, stored at - 40 °C, and then assessed through biochemical and neurochemical estimation. The findings demonstrated that Lnz treatment increased [p < 0.05] the time spent in the light box of LDA and lowered [p < 0.05] immobility time in TST, suggesting anxiolytic- and antidepressant-like effects both alone and in D-gal-treated animals. In the MWM, there was no significant main effect of D-gal on escape latency, but a significant effect of Lnz [p < 0.05] and a significant D-gal × Lnz interaction [p < 0.05] across acquisition, STM and LTM phases. Post hoc comparisons further revealed that Lnz reduced escape latency in both vehicle- and D-gal-treated animals. The reductions were more pronounced in D-gal-exposed groups suggesting a possible modulatory role of Lnz on the performance associated with memory under the conditions of D-gal exposure. Lnz also elevated [p < 0.05] antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and decreased [p < 0.05] the contents of oxidative stress marker (MDA), and inflammatory mediators [interleukin-6 (IL-6), and tumor necrosis factor (TNF-α)] in the hippocampus and rest of the brain following D-gal administration. Moreover, Lnz lowered [p < 0.05] acetylcholinesterase (AChE) activity and raised [p < 0.05] 5-hydroxytryptamine (5-HT) and 5-hydroxyindolacetic acid (5-HIAA) contents in the hippocampus and the rest of the brain after D-gal administration. In molecular docking, Lnz exhibits potential binding affinities of - 8 kcal/mol and - 10 kcal/mol with monoamine oxidase enzymes (MAO-A and MAO-B), docking results provided preliminary evidence of potential binding interactions between Lnz and MAO enzymes, but did not show functional MAO inhibition. Taken together, these findings suggest that Lnz might possess antioxidant and neuroprotective-like effects besides its antibiotic properties, which could modulate D-gal-induced behavioral changes, including anxiety- and depression-like responses and a potential tendency to improve memory-like performance. These observations are exploratory and deserve further investigation. - Source: PubMed
Publication date: 2026/06/27
Bukhari Syeda Masooma ZahraManzoor NatashaSamad Noreen