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Decreased wound exudate ENA-78 was independently associated with wound healing of patients with diabetic foot. Exudate ENA-78 level is implicated as a novel predictor of wound healing in patients with diabetic foot ulcers.
CXCL5-overexpressing tumors recruited high amounts of neutrophils and exhibited significantly increased lymphangiogenesis in xenograft SCID mouse model. Clinically, CXCL5-overexpressing melanomas had significantly increased lymph node metastases. In human patient samples CXCL5 expression positively correlated with numbers of neutrophils in stage T4 primary melanoma, and the occurrence of locoregional metastasis.
CXCL5 may contribute to a dominant role in uterine cervix cancer progression; at the gene level, CXCL5 overexpression regulated the expression of tumor-related genes
Sensitivity and specificity of serum CXCL5 were found to be low as a result of the ROC analysis.
Serum CXCL5 levels from pemphigus vulgaris patients are significantly higher than those in bullous pemphigoid patients and healthy controls.
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 axis contributes to the metastatic phenotype of PTC cells by modulating Akt/GSK-3beta/beta-catenin 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-p-eIF2alpha pathway could suppress metastasis in triple-negative breast cancer by inhibiting expression of PDL1 and CXCL5 in tumor cells.
Mechanistically, AR modulated cytokine CXCL5 expression by altering AKT --> NF-kappaB signaling, and interruption of AKT --> NF-kappaB --> CXCL5 signaling using either specific inhibitors or siRNA suppressed AR-enhanced EC recruitment and AR-EC-promoted RCC progression.
Curcumin suppressed CXCL5 expression by direct inhibition of IKKbeta phosphorylation, and inhibition of p38 MAPK via induction of negative regulator MKP-1.
The CXCL5 and the overexpression of miR-141 reduced levels of MMP-2 and MMP-9 in tumor necrosis factor-alpha-treated HT29 cells by means of repressing the inhibitory AKT.
CXCL5 may promote mitomycin resistance by activating EMT and NF-kappaB 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.
our findings support CXCL5 as a promoter of colorectal cancer metastasis and a predictor of poor clinical outcomes in colorectal cancer patients.
CXCL5 levels were decreased in LSCC patient serum.
a finely tuned balance between the GAG-bound dimer and free soluble monomer regulates CXCL5-mediated receptor signaling and function.
CXCL5 plays a promoting role in glioma in autocrine- and paracrine-dependent manners.
The expression of CXCL5 is up-regulated in osteosarcoma cells.
The results suggest a notable angiogenic potential of cardiac progenitor cells and identify CXCL6 as an important paracrine factor for cardiac progenitor cells that signals mainly through CXCR2.
these findings suggest that the myeloid phagocytic clearance of apoptotic cancer cells accelerates CXCL5-mediated inflammation and tumor growth in bone, pointing to CXCL5 as a potential target for cancer therapeutics.
results indicate that CXCL5 and MMPs contribute to the resistance to pneumococcal infection in mice.
Identify Cxcl5 as a novel target of AHR-mediated gene expression in primary mouse keratinocytes.
Parenchymal polymorphonuclear myeloid-derived suppressor cell (PMN-MDSC), have a positive correlation with IL1a, IL8, CXCL5, and Mip-1a, suggesting they may attract PMN-MDSC into the tumor
These data identify suppression of CXCL2 and CXCL5 chemoattractant expression by 11beta-HSD1 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 regulates CXL-1 and 5 production in the lungs during the adaptive response.
STAT3 is required for maximal OSM-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.
CXCL5 regulates pulmonary responses to infection and plays a central role in conferring clock control of inflammation.
findings demonstrated that CXCL1 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.
data suggest that CXCL6 contributes to experimental pulmonary fibrosis, and CXCL6 inhibition might be used to reduce lung toxicity associated with bleomycin treatment.
Our data suggest that the differential regulation of the chemokine CXCL5 between osteoblasts and endothelial cells upon FGF2 treatment is involved in Hematopoietic stem cell mobilization from the osteoblast niche or bone marrow to peripheral blood.
CXCL5 modulated macrophage activation, increased expression of the cholesterol efflux regulatory protein ABCA1, and enhanced cholesterol efflux activity in macrophages.
The omentum is the main site of early neutrophil entry into the peritoneal cavity, where the action of CXCL5 synergizes with matrix metalloproteinases MMP-2 and -9 to promote neutrophil migration during the inflammatory process.
CXCL5-dependent signaling cascades are essential for the recruitment of macrophages to the lungs upon subacute second hand smoke exposure.
Cxcr2, Cxcl5, and commensal bacteria have critical roles in regulation of the IL-17/G-CSF axis and neutrophil homeostasis at mucosal sites
In a mouse model of lung ischemia-induced angiogenesis, LIX predominates in eliciting a pro-angiogenic phenotype among the three ELR+ CXC chemokines (KC, LIX, and MIP-2) studied.
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