Canine Interleukin 8,IL-8 ELISA Kit
- Known as:
- Canine Interleukin 8,Interleukin-8 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- E0004Ca
- Product Quantity:
- 48T
- Category:
- Elisa Kits
- Supplier:
- JING
- Gene target:
- Canine Interleukin 8 IL-8 ELISA Kit
Related genes to: Canine Interleukin 8,IL-8 ELISA Kit
- Gene:
- CXCL8 NIH gene
- Name:
- C-X-C motif chemokine ligand 8
- Previous symbol:
- IL8
- Synonyms:
- SCYB8, LUCT, LECT, MDNCF, TSG-1, IL-8, NAP-1, 3-10C, MONAP, AMCF-I, LYNAP, NAF, b-ENAP, GCP-1, K60, GCP1, NAP1
- Chromosome:
- 4q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1989-06-30
- Date modifiied:
- 2016-10-05
- Gene:
- CXCR1 NIH gene
- Name:
- C-X-C motif chemokine receptor 1
- Previous symbol:
- CMKAR1, IL8RA
- Synonyms:
- CKR-1, CDw128a, CD181
- Chromosome:
- 2q35
- Locus Type:
- gene with protein product
- Date approved:
- 1992-11-09
- Date modifiied:
- 2016-03-14
- Gene:
- CXCR2 NIH gene
- Name:
- C-X-C motif chemokine receptor 2
- Previous symbol:
- IL8RB
- Synonyms:
- CMKAR2, CD182
- Chromosome:
- 2q35
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-19
- Date modifiied:
- 2016-03-14
- Gene:
- CXCR2P1 NIH gene
- Name:
- C-X-C motif chemokine receptor 2 pseudogene 1
- Previous symbol:
- IL8RBP, CXCR2P
- Synonyms:
- -
- Chromosome:
- 2q35
- Locus Type:
- pseudogene
- Date approved:
- 1992-11-27
- Date modifiied:
- 2016-03-14
Related products to: Canine Interleukin 8,IL-8 ELISA Kit
Related articles to: Canine Interleukin 8,IL-8 ELISA Kit
- Immune checkpoint inhibitor (ICI) resistance remains a major challenge in esophageal squamous cell carcinoma (ESCC). This study investigates the role of glutaminase (GLS) in modulating the tumor immune microenvironment and its impact on immunotherapy response. Bioinformatic analysis of TCGA data revealed an inverse correlation between GLS expression and CD8 T cell infiltration. In ESCC clinical specimens, high GLS expression correlated with elevated CXCL8 levels and reduced CD8 T cell infiltration. Mechanistically, our data support an association between GLS expression and increased CXCL8 transcription, accompanied, at least in part, by HAT-dependent enhancement of H3K27 acetylation at the CXCL8 promoter region. In advanced ESCC patients receiving immunochemotherapy, high tumoral GLS expression was associated with significantly shorter progression-free survival. and functional studies showed that GLS knockdown in ESCC cells was associated with enhanced T-cell effector cytokine secretion, increased tumor infiltration of CD8 T cells, and greater tumor suppression when combined with anti-PD-1 therapy in a humanized mouse model. Importantly, exogenous CXCL8 supplementation partially reversed the increased Granzyme B and IFNγ secretion induced by GLS knockdown in the co-culture system, supporting a functional role for CXCL8 in GLS-associated immune suppression. These results support a model in which GLS contributes to an immunosuppressive microenvironment in ESCC, at least in part through epigenetic upregulation of CXCL8. These findings support further investigation of GLS targeting as a potential strategy to improve immunotherapy response in ESCC. - Source: PubMed
Publication date: 2026/09/01
Zhang XiuChao JiangJi ZhuqingChen Kai - Nasopharyngeal cancer is the most common head-and-neck cancer in Indonesia. It occurs in the mucosal epithelium of the nasopharyngeal region. This study aimed to evaluate the role of gene expression in the occurrence of synchronous bone metastasis in nasopharyngeal cancer. - Source: PubMed
Cahyanur RahmatIrawan CosphiadiRachmadi LisnawatiAdham MarlindaKamal Achmad FauziHandoyo Utomo Ahmad RusdanHardianti Mardiah SuciSalamah ThariqahMansyur Muchtaruddin - Gout and calcium pyrophosphate crystal deposition disease (CPPD) are frequently associated with comorbid disorders, including coronary artery disease and osteoarthritis, in which ectopic calcification with basic calcium phosphate crystals commonly affects arteries and articular cartilage, respectively. Accepting the 2024 G-CAN Gold Medal, I review my research philosophy for translational etiopathogenesis investigation in gout and CPPD, atherosclerosis, responses to arterial injury, and osteoarthritis. Since molecular homeostasis points to pathophysiology and vice versa, I have followed selected molecular players and pathways to phenotypes. Typically, behind each disease target is another target. Illuminating passageways between etiopathogenic pathways is especially productive when using approaches beyond conventional "omics" to reveal the impact of specific post-translational protein modifications, and changes in protein conformation, complex assembly, and interactomes. Highlighting these concepts, I review my past studies on specific molecular pathways, and current perspectives for the following: (i) PP, NPP1, ANKH, and transglutaminase 2 (TG2); (ii) relationships between NPP1, ANKH, Vanin-1 Pantetheinase, and ectopic chondrogenesis; (iii) intersections between adenosine, AMPK, CXCL8 and its receptor CXCR2, the receptor for advanced glycation endproducts (RAGE) and chondrocyte hypertrophy; (iv) lubricin homeostasis and proteolysis; (v) receptor for advanced glycation endproducts (RAGE) and TG2-catalyzed post-translational calgranulin modification; (vi) complement activation and C5b-9 assembly, and the nucleotide-bound conformation of TG2. The inescapable conclusion is that these molecular pathways tightly knit crystal arthropathy with both arterial and osteoarthritis comorbidity. - Source: PubMed
Publication date: 2025/09/02
Terkeltaub Robert - Toll-like receptors (TLRs) and P2 receptors are key regulators of innate immunity. During infection, pathogen-associated molecular patterns (PAMPs) activate TLRs, whereas extracellular nucleotides engage P2 receptors and influence inflammatory responses. Here, we show that polyinosinic:polycytidylic acid (poly[I:C])-activated TLR3 and P2Y signalling functionally interact in intestinal epithelial cells (IECs) to regulate chemokine production. HT-29 cells were stimulated with PAMPs, including the TLR3 agonist poly(I:C), in the presence or absence of P2 receptor signalling inhibitors. CXCL8/IL-8 or CXCL10/IP-10 secretion was assessed by ELISA and mRNA expression by quantitative real-time PCR (RT-qPCR). Primary IECs from P2Y knock-out (KO) and wild-type (WT) mice were also treated with poly(I:C), and CXCL1/KC secretion was measured. Poly(I:C) stimulation induced robust CXCL8/IL-8 and CXCL10/IP-10 release in HT-29 cells. This response was inhibited by nucleotide scavenging, P2 receptor blockade, and P2Y targeting using either specific antagonists or siRNAs. P2Y was the dominant receptor expressed, and its ligands ATP/UTP constitutively released by these cells amplified CXCL8/IL-8 production induced by a suboptimal concentration of poly(I:C), while alone they had no effect. In support of these findings, primary IECs from P2Y KO mice secreted significantly less CXCL1/KC than WT controls. Altogether, extracellular nucleotide signalling regulates TLR3-induced chemokine release in IECs through P2Y receptors. - Source: PubMed
Ouattara Abdoul KarimBahrami FariborzTurcitu Radu AdrianKukulski FilipLecka JoannaPelletier JulieEspindola Gelsleichter NicollyVidal TaisSévigny Jean - Bisphenol A (BPA) is a common environmental endocrine disruptor linked to type 2 diabetes mellitus (T2DM) and colorectal cancer (CRC), but the exact mechanism connecting BPA exposure to their comorbidity is unclear. - Source: PubMed
Publication date: 2026/08/27
Ao WeiLi HaoranZhang YuhangWu ZhenhengYang HaoChen Zhigang