IL-6, Human Protein
- Known as:
- Interleukin-6, Human Protein
- Catalog number:
- z03034-1
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- IL-6 Human Protein
Related 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
- Immune thrombocytopenic purpura (ITP) is the most common autoimmune bleeding disorder in children and poses a serious threat to pediatric health and survival. An imbalance in Th17 and Treg cell differentiation leads to uncontrolled inflammation. - Source: PubMed
Publication date: 2026/07/17
Ge JiaoLiu Yan - Arteriovenous fistula (AVF) non-maturation remains common. Although attention has historically focused on post-operative processes, evidence suggests that pre-anastomotic vessel wall signaling, at AVF creation, contributes to subsequent AVF outcomes. To integrate quantitative baseline biochemistry, and vein histology with single-nucleus RNA sequencing (snRNA-seq) from intraoperative tissue and relate structural, cellular, and molecular features to subsequent AVF maturation. - Source: PubMed
Publication date: 2026/07/17
Shah Nasir AThomas RenuThomas Shannon DAu Amy Y MDavidson TrentO'Keeffe Christopher JTong OrionEndre Zoltan HBarber Tracie JCochran Blake JErlich Jonathan H - Acute respiratory distress syndrome (ARDS) remains a critical condition associated with high morbidity and mortality, particularly when triggered by sepsis. Endothelial dysfunction is a central hallmark of ARDS pathology, but the precise mechanisms underlying pulmonary microvascular dysfunction remain poorly understood. Extracellular vesicles (EVs) have emerged as crucial mediators of cell-cell communication during inflammation; however, their role in endothelial dysfunction in ARDS is less clearly defined. We utilized a human pulmonary microvascular endothelial cell (HPMEC)-based model of sepsis-induced acute lung injury to investigate whether inflammatory EVs (iEVs), derived from endothelial cells treated with bacterial lipopolysaccharide (LPS), impair naïve HPMEC function. EVs were characterized by nanoparticle tracking analysis, transmission electron microscopy, and immunofluorescence, confirming purity and uptake. iEV exposure significantly reduced barrier integrity by electric cell-substrate impedance sensing (ECIS) and increased cell migration; effects partially reversed by the TLR4 inhibitor TAK-242. Adhesion and tube formation were unaffected. Pre-treatment of donor HPMECs with the neutral sphingomyelinase inhibitor GW4869 attenuated the barrier-disrupting capacity of the resulting iEVs, implicating ceramide-dependent EV biogenesis in generating pathogenic cargo. Trypan Blue staining confirmed that these effects reflect altered signaling rather than cell death. iEV exposure upregulated TLR4, MyD88, IL-6, ICAM-1, VCAM-1, E-selectin, and Jag1 mRNA, with TAK-242 attenuating IL-6 and ICAM-1 induction. Our results highlight endothelial-derived EVs and TLR4-dependent pathways as amplifiers of pulmonary vascular injury in sepsis-induced ARDS, identifying EV biogenesis and EV-mediated signaling as novel therapeutic targets. - Source: PubMed
Publication date: 2026/07/17
Cohen MayaHaigis LianaBlum RebeccaSherman-Roe AllysonPereira MandyChichger HavoviVentetuolo Corey ELiang OlinHarrington Elizabeth O - Despite the established epidemiological synergy between Porphyromonas gingivalis-induced periodontitis and oral squamous cell carcinoma (OSCC), a critical gap remains in developing single-agent therapeutics that simultaneously neutralize bacterial virulence and suppress host oncogenic signaling. This study aimed to comprehensively evaluate Curcumin 4'-O-β-D-gentiobioside (COG) as a novel, dual-pathway phytochemical intervention targeting the keystone virulence factor RgpB while concurrently disrupting OSCC progression networks. - Source: PubMed
Publication date: 2026/07/17
Aljarba Nada HChakraborty SayanChatterjee AniruddhaBishoyi Ashok KumarRoopashree RUti Daniel EjimAlum Esther Ugo - Atrazine (ATZ) and manganese (Mn) are individually known to influence reproductive health, but their combined impact on the male reproductive function remains unknown. Here, we investigate the combined reproductive effects of ATZ and Mn in male Wistar rats using biochemical analyses and an in silico approach. Rats (n = 6 per group), including control, ATZ (10 mg/kg), Mn (10 mg/kg), and combined low (2.5 + 2.5 mg/kg) and high dose (10 + 10 mg/kg), were treated for 28 days, respectively. Assessments include testicular function, reproductive hormones, sperm quality, oxidative and inflammatory response indices, and DNA fragmentation. An in silico approach to atrazine and manganese toxicities involved protein-protein interaction networks, KEGG pathway enrichment, and ADMET ATZ-profiling. Co-exposure significantly (p > 0.05) reduced biomarkers of testicular function and sperm quality, while increasing sperm abnormalities, oxidative stress, apoptosis, and pro-inflammatory cytokines. Computational analysis identified key hub proteins, including CASP3, TNF, TP53, IL6, NFE2L2, and HIF1A, as central mediators of the observed toxicity. Enrichment analyses highlighted activation of the TNF signalling and apoptosis pathways, which are associated with disruption of redox homeostasis and inflammatory responses. Docking analysis indicates that ATZ shows the strongest predicted interactions with NFE2L2, as supported by molecular dynamics simulations that establish its stability, suggesting that ATZ promotes oxidative stress and inflammation. In conclusion, combined exposure to ATZ and Mn induces reproductive toxicity via oxidative stress, inflammation, and apoptosis. A systems-level analysis identified critical molecular targets and signalling pathways, providing mechanistic insight into the synergistic effects of environmental toxicant-induced reproductive disturbances, particularly following co-exposure to ATZ and Mn in a rat model. - Source: PubMed
Publication date: 2026/07/17
Owumi SolomonChimezie JosephOtunla Moses TArunsi Uche OEso Victor OSanusi Abdullah AOwolabi Oluwaseun MBabalola Jesutosin OAkomolafe Ayomide PIrozuru Chioma EAmadi Chima M