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These data demonstrated that CXCL5 expression was upregulated in prostate cancer tissues and that exogenous CXCL5 protein exposure or CXCL5 overexpression promoted malignant phenotypes of prostate cancer cells in vitro and in vivo.
activated CXCL5-CXCR2 (zeige CXCR2 Proteine) axis contributes to the metastatic phenotype of PTC (zeige F9 Proteine) cells by modulating Akt (zeige AKT1 Proteine)/GSK-3beta/beta-catenin (zeige CTNNB1 Proteine) pathway
study elucidates the important role of CXCL5 in the progression and prognosis of NSCLC. These findings suggested that CXCL5 might be a potential biomarker and novel therapeutic target for lung cancer
PERK (zeige EIF2AK3 Proteine)-p-eIF2alpha (zeige EIF2A Proteine) pathway could suppress metastasis in triple-negative breast cancer by inhibiting expression of PDL1 (zeige CD274 Proteine) and CXCL5 in tumor cells.
Mechanistically, AR modulated cytokine CXCL5 expression by altering AKT (zeige AKT1 Proteine) --> NF-kappaB (zeige NFKB1 Proteine) signaling, and interruption of AKT (zeige AKT1 Proteine) --> NF-kappaB (zeige NFKB1 Proteine) --> CXCL5 signaling using either specific inhibitors or siRNA suppressed AR-enhanced EC recruitment and AR-EC-promoted RCC (zeige XRCC1 Proteine) progression.
Curcumin suppressed CXCL5 expression by direct inhibition of IKKbeta (zeige IKBKB Proteine) phosphorylation, and inhibition of p38 MAPK (zeige MAPK14 Proteine) via induction of negative regulator MKP-1 (zeige DUSP1 Proteine).
The CXCL5 and the overexpression of miR (zeige MLXIP Proteine)-141 reduced levels of MMP-2 (zeige MMP2 Proteine) and MMP-9 (zeige MMP9 Proteine) in tumor necrosis factor-alpha (zeige TNF Proteine)-treated HT29 cells by means of repressing the inhibitory AKT (zeige AKT1 Proteine).
CXCL5 may promote mitomycin resistance by activating EMT (zeige ITK Proteine) and NF-kappaB (zeige NFKB1 Proteine) pathway. Thus, this study identifies CXCL5 as a novel chemoresistance-related marker in non-muscle invasive bladder cancer
findings for the first time provided evidence that ENA78 may play a key role of mediator in pathogenesis of Major Depressive Disorder(MDD) and in the mechanism of vinlafaxine effects on MDD.
Two haplotype blocks, one upstream to the coding region of UGT2A1 (rs146712414, P = 9.1 x 10(-5); odds ratio [OR], 1.34; 95% confidence interval [CI], 1.16-1.56) and one downstream of the genes PF4/PPBP/CXCL5 (rs1595009, P = 1.3 x 10(-4); OR, 1.32; 95% CI, 1.15-1.52), were associated with AgP.
Identify Cxcl5 as a novel target of AHR (zeige AHR Proteine)-mediated gene expression in primary mouse keratinocytes.
Parenchymal polymorphonuclear myeloid-derived suppressor cell (PMN (zeige TBCE Proteine)-MDSC), have a positive correlation with IL1a (zeige IL1A Proteine), IL8 (zeige IL8 Proteine), CXCL5, and Mip-1a (zeige CCL3 Proteine), suggesting they may attract PMN (zeige TBCE Proteine)-MDSC into the tumor
These data identify suppression of CXCL2 (zeige CXCL2 Proteine) and CXCL5 chemoattractant expression by 11beta-HSD1 (zeige HSD11B1 Proteine) as a novel mechanism with potential for regulation of neutrophil recruitment to the injured myocardium, and cardiac fibroblasts as a key site for intracellular glucocorticoid regeneration during acute inflammation following myocardial injury.
IL-17RA (zeige IL17RA Proteine) regulates CXL-1 and 5 production in the lungs during the adaptive response.
STAT3 (zeige STAT3 Proteine) is required for maximal OSM (zeige OSM Proteine)-induced CXCL5 expression.
CXCL5 has a role in neutrophil recruitment in TH17-mediated glomerulonephritis
Since adaptive villus growth occurs despite impaired CXCL5 expression and enhanced angiogenesis, this suggests that the growth of new blood vessels is not needed for resection-induced mucosal surface area expansion following massive SBR (zeige NXF1 Proteine).
CXCL5 regulates pulmonary responses to infection and plays a central role in conferring clock control of inflammation.
findings demonstrated that CXCL1 (zeige CXCL1 Proteine) and CXCL5 are increased in circulation with onset of T2D, are produced by islets under stress, and synergistically affect islet function, suggesting that these chemokines participate in pathogenesis of T2D.
TLR2-induced epithelial-derived CXCL5 is critical for polymorphonuclear leukocyte-driven destructive inflammation in pulmonary tuberculosis.
The protein encoded by this gene is an inflammatory chemokine that belongs to the CXC chemokine family. This chemokine is produced concomitantly with interleukin-8 (IL8) in response to stimulation with either interleukin-1 (IL1) or tumor necrosis factor-alpha (TNFA). This chemokine is a potent chemotaxin involved in neutrophil activation.
C-X-C motif chemokine 5
, epithelial-derived neutrophil-activating protein 78
, neutrophil-activating peptide ENA-78
, neutrophil-activating protein 78
, small inducible cytokine subfamily B (Cys-X-Cys), member 5 (epithelial-derived neutrophil-activating peptide 78)
, CXC chemokine LIX
, chemokine (C-X-C motif) ligand 6 (granulocyte chemotactic protein 2)
, cytokine LIX
, small-inducible cytokine B5
, C-X-C motif chemokine 6
, chemokine (C-X-C motif) ligand 5
, granulocyte chemotactic protein 2
, inducible cytokine subfamily B (Cys-X-Cys), member 6
, small-inducible cytokine B6
, granulocyte chemotactic protein-2
, small inducible cytokine B subfamily, member 5
, small inducible cytokine subfamily B, member 15