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抗Human CXCL5 抗体:
抗Rat (Rattus) CXCL5 抗体:
抗Mouse (Murine) CXCL5 抗体:
Mouse (Murine) Polyclonal CXCL5 Primary Antibody for IF (p), IHC (p) - ABIN741900
Heilmann, Schinke, Bindl, Wehner, Rapp, Haffner-Luntzer, Nemitz, Liedert, Amling, Ignatius: The Wnt serpentine receptor Frizzled-9 regulates new bone formation in fracture healing. in PLoS ONE 2014
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Human Monoclonal CXCL5 Primary Antibody for IHC (p), ELISA - ABIN562826
Zhou, Dai, Zhou, Wang, Yang, Wang, Huang, Fan, Zhou: Overexpression of CXCL5 mediates neutrophil infiltration and indicates poor prognosis for hepatocellular carcinoma. in Hepatology (Baltimore, Md.) 2012
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Human Polyclonal CXCL5 Primary Antibody for ELISA, WB - ABIN2473135
Strieter, Belperio, Phillips, Keane: CXC chemokines in angiogenesis of cancer. in Seminars in cancer biology 2004
Human Monoclonal CXCL5 Primary Antibody for CyTOF, ELISA (Capture) - ABIN4900299
Edwards, Johnson, Johnston: Combination therapy: Synergistic suppression of virus-induced chemokines in airway epithelial cells. in American journal of respiratory cell and molecular biology 2006
Curcumin suppressed CXCL5 expression by direct inhibition of IKKbeta (显示 IKBKB 抗体) phosphorylation, and inhibition of p38 MAPK (显示 MAPK14 抗体) via induction of negative regulator MKP-1 (显示 DUSP1 抗体).
The CXCL5 and the overexpression of miR (显示 MLXIP 抗体)-141 reduced levels of MMP-2 (显示 MMP2 抗体) and MMP-9 (显示 MMP9 抗体) in tumor necrosis factor-alpha (显示 TNF 抗体)-treated HT29 cells by means of repressing the inhibitory AKT (显示 AKT1 抗体).
CXCL5 may promote mitomycin resistance by activating EMT (显示 ITK 抗体) and NF-kappaB (显示 NFKB1 抗体) 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.
Parenchymal polymorphonuclear myeloid-derived suppressor cell (PMN (显示 TBCE 抗体)-MDSC), have a positive correlation with IL1a (显示 IL1A 抗体), IL8 (显示 IL8 抗体), CXCL5, and Mip-1a (显示 CCL3 抗体), suggesting they may attract PMN (显示 TBCE 抗体)-MDSC into the tumor
These data identify suppression of CXCL2 (显示 CXCL2 抗体) and CXCL5 chemoattractant expression by 11beta-HSD1 (显示 HSD11B1 抗体) 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 (显示 IL17RA 抗体) regulates CXL-1 and 5 production in the lungs during the adaptive response.
STAT3 (显示 STAT3 抗体) is required for maximal OSM (显示 OSM 抗体)-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 (显示 NXF1 抗体).
CXCL5 regulates pulmonary responses to infection and plays a central role in conferring clock control of inflammation.
findings demonstrated that CXCL1 (显示 CXCL1 抗体) 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.
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.
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