Chemokine (C-X-C Motif) Ligand 16 (CXCL16) ELISA Kits

Mouse (Murine) Chemokine (C-X-C Motif) Ligand 16 (CXCL16) Interaktionspartner

1. the results of the present study suggested that CXCL16 may regulate the TRL4/NFkappaB/CXCL16 signaling pathway, and that miR146a and miR146b may negatively regulate CXCL16 via this pathway in atherosclerosis in vivo.

2. Inflammation accelerates renal tubulointerstitial lesions in mouse model of diabetic nephropathy by increasing the activity of CXCL16 pathway.

3. CXCL16 increases the frequency of the miniature excitatory synaptic currents (mEPSCs) and reduces the PPR of evoked excitatory transmission, indicating that the chemokine also modulates and enhances the release of glutamate.

4. results indicate that CXCL16 plays a key role in the pathogenesis of renal injury and fibrosis in salt-sensitive hypertension through regulation of bone marrow-derived fibroblast accumulation and macrophage and T cell infiltration.

5. Data indicate that chemokine C-X-C ligand 16 (CXCL16) is a critical regulator of liver immune response to acetaminophen (APAP)-induced hepatotoxicity, suggesting a potential strategy for the treatment of drug-induced acute liver failure by targeting CXCL16.

6. CXCL16 plays a crucial role in the pathogenesis of cisplatin-induced acute kidney injury through regulation of apoptosis and inflammation.

7. These findings suggest that the CXCL16 gene product promotes inflammatory factors and cell infiltration factors, and inhibits the expression of antioxidant factors to accelerate the development of DN, and CXCL16 deficiency attenuates DN may be involved in the AKT signaling pathway.

8. Results indicate that CXCL16 plays a pivotal role in the pathogenesis of renal artery stenosis-induced renal injury and fibrosis through regulation of bone marrow-derived fibroblast accumulation and macrophage and T-cell infiltration.

9. Simvastatin exerts a protective effect on renal function and structure in mice with ADR nephropathy which related to the decreasing expression of CXCL16 in glomerular podocytes followed by the decreasing endocytosis of ox-LDL in podocytes and inhibition of NF-kappaB pathway activation.

10. These results indicate that MEK inhibitor diminishes Nasopharyngeal carcinoma cell proliferation and NPC-induced osteoclastogenesis via modulating CCL2 and CXCL16 expressions.

11. Serum CXCL16 is increased in severe pancreatitis with infected pancreatic necrosis and identifies patients who benefit from surgical necrosectomy

12. injured hepatocytes up-regulated CXCL16 expression, indicating that scavenging functions of CXCL16 might be additionally involved in the pathogenesis of NAFLD.

13. role of IFN-gamma, CXCL16, and ADAM10 in oxLDL-induced lipid accumulation in glomerular podocytes

14. CXCL16 suppresses liver metastasis of colorectal cancer by promoting TNF-alpha-induced apoptosis by tumor-associated macrophages.

15. Loss of sst2 from pancreatic tissues activates PI3K signaling via AKT, leading to activation of NF-kappaB, amplification of oncogenic KRAS signaling, increased expression of CXCL16, and pancreatic tumor formation.

16. CXCL16 was constitutively expressed by CX3CR1(+) intestinal dendritic cells (DCs) and coexpressed with IL-23 after Citrobacter rodentium infection.

17. CCL2 and CXCL16 chemokines produced by tumor-conditioned Gr-1(+)CD11b(+) myeloid cells synergistically induce angiogenesis in vitro by stimulating the ERK1/2 signaling pathway.

18. CXCL16 expression inhibits liver metastasis in a murine model of colorectal cancer.

19. our results indicate that CXCL16 plays a pivotal role in the pathogenesis of angiotensin II-induced renal injury and fibrosis through regulation of macrophage and T cell infiltration and bone marrow-derived fibroblast accumulation.

20. Renal dendritic cell-derived CXCL16 might attract protective CXCR6(+) iNKT cells.

Human Chemokine (C-X-C Motif) Ligand 16 (CXCL16) Interaktionspartner

1. Plasma CXCL16 levels were elevated for 4 weeks after minimally invasive colorectal resection for cancer. Also, WF CXCL16 levels were 3-10 times greater than the corresponding plasma concentrations.

2. Activation of the CXCL16/CXCR6 Axis by TNF-alpha Contributes to Ectopic Endometrial Stromal Cells Migration and Invasion.. These findings indicate that the CXCL16/CXCR6 axis may contribute to the progression of endometriosis and could be served as a potential target for diagnosis and treatment.

3. Study data link innate immune stimulation to CXCL16 up-regulation and neutrophil infiltration into skin. CXCL16 could therefore represent a potent future target for treatment of psoriasis.

4. This study shows that the expression of CXCL16 and its receptor CXCR6 was highly elevated in rheumatoid arthritis fibroblast-like synoviocytes

5. demonstrate that macrophages can promote the migration and invasion of ovarian carcinoma cells by affecting the CXCL16/CXCR6 pathway

6. activation of cancer-associated fibroblasts and expression of CXCL16, shown to be a monocyte chemoattractant.

7. Enhanced CXCL16 expression in lung cancer tissue promoted the proliferation and invasion of lung cancer cells. CXCL16 might promote proliferation and invasion of lung cancer by regulating the NF-kappaB pathway.

8. increased plasma sCXCL16 might be implicated in the pathogenesis of immune thrombocytopenia and have a relationship with Th1/Th2 imbalance.

9. Serum CXCL16 levels are significantly increased in patients with gallstone, and are independently associated with liver injury in Chinese population, suggesting that CXCL16 may be a biomarker of liver injury in subjects with gallstone or NAFLD. Hepatic CXCL16 mRNA and protein levels were also significantly increased in gallstone patients

10. IFN-gamma, CXCL16 and uPAR are promising as effective biomarkers of disease activity, renal damage, and the activity of pathological lesions in systemic lupus erythematosus.

11. Data showed that reverse signaling via CXCL16 promotes migration in CXCL16-expressing melanoma and glioblastoma cells, but does not affect proliferation or protection from chemically-induced apoptosis.

12. Study showed, for the first time, highly significant relationships of circulating CXCL16 level with cardiac injury markers in dialysis patients.

13. Women with gestational diabetes mellitus and preeclampsia had a dysregulated CXC chemokine ligand 16 during pregnancy, and in gestational diabetes mellitus, the increase in CXC chemokine ligand 16 early in pregnancy and after 5 years was strongly associated with their lipid profile.

14. Data suggest that primary cells from papillary renal cell carcinoma secrete the chemokines IL8, CXCL16, and chemerin; these chemokines attract primary human monocytes and induce shift/transdifferentiation in monocytes toward M2 macrophage/foam cell phenotype. (IL8 = interleukin-8; CXCL16 = C-X-C motif chemokine ligand 16)

15. Our study demonstrated that CXCL16-CXCR6 mediates CD8(+) T-cell skin trafficking under oxidative stress in patients with vitiligo, and CXCL16 expression in human keratinocytes induced by ROS is, at least in part, caused by unfolded protein response activation

16. eGFR and serum albumin had an independent and significant negative correlation with plasma CXCL16 in diabetic kidney disease.

17. The expression of CXCL16 and and its receptor, CXCR6, their immunolocalization in disc tissue and their presence following exposure of cultured human annulus fibrosus cells to proinflammatory cytokines are reported.

18. Inflammation contributed to foam cell formation in the radial arteries of ESRD patients via activation of the CXCL16/CXCR6 pathway, which may be regulated by P2X7R.

19. CXCL16 single nucleotide polymorphisms significantly impacted myocardial infarction risk in a Chinese Han population.

20. Transmembrane-CXCL16 specifically acts as a receptor for soluble-CXCL16 in human meningioma cells.