No Products on your Comparison List.
Your basket is empty.
Find out more
Show all synonyms
Select your origin of interest
Human CCL5 Protein expressed in Human Cells - ABIN2003576
Maghazachi, Al-Aoukaty, Schall: CC chemokines induce the generation of killer cells from CD56+ cells. in European journal of immunology 1996
Show all 5 Pubmed References
Human CCL5 Protein expressed in - ABIN1111925
Kato, Fujita, Nakane, Mizutani, Terazawa, Ehara, Kanimoto, Kojima, Nozawa, Deguchi, Ito: CCR1/CCL5 interaction promotes invasion of taxane-resistant PC3 prostate cancer cells by increasing secretion of MMPs 2/9 and by activating ERK and Rac signaling. in Cytokine 2014
CCL5 may contribute to promoting tumor growth, and CCL5 is a promising target that may help in understanding the pathogenesis of colorectal cancer
an acid sphingomyelinase ceramide kinase pathway in the regulation of the chemokine CCL5
CCL5 rs2280789 G alleles were associated with higher VEGF-A levels.
This study provided evidence that miR-146a targets CCL5 3' untranslated regions, downregulates its release from macrophages, and affects monocyte migration consequently. These findings drew a novel layer of posttranscriptional control of the chemokine CCL5 by miR-146a during HIV infection, which might contribute to HIV pathogenesis.
Long noncoding RNA SNHG16 regulated LPS-induced inflammation injury in WI-38 cells through competitively binding miR-146a-5p with CCL5 further mediating JNK and NF-kappaB pathways, which sheds novel light on diagnostics and therapeutics in pneumonia.
The CCL5 rs2107538 polymorphism was identified to be associated with a significantly lower risk of benign prostatic hyperplasia (BPH). This polymorphism was also associated with the development of larger prostate volumes in Chinese patients with BPH.
This study explored the interaction of CCL5 with GPR75, an orphan receptor of the Gqalpha family of GPCRs, which appears to be expressed more abundantly in neuron-like cells than astrocytes.
data show that a genetic variant of CCL5 confers protection against Chagas heart disease
CCL5 deficiency could reverse obliterative changes in pulmonary arteries via caveolin-1-dependent amplification of BMPR2 signaling.
loss of CCL5 could enhance CXCL1 expression in hepatocytes and activate CXCL1-CXCR2 axis in neutrophils to augment their hepatic infiltration
these findings show that IL-6 and CCL5 signaling, which promote crosstalk between triple-negative breast cancer (TNBC) and lymphatic vessels, are key enhancers of TNBC tumor growth and metastasis. Furthermore, these results demonstrate that a drug combination inhibiting these pathways may be a promising therapy for TNBC patients
CCL5/CCR5 axis may be involved in the perineural invasion of salivary adenoid cystic carcinoma cells
In burn wounds, RANTES/CCL5 levels were on average 14.86pg/ml in young vs 4.26pg/ml in aged (p=0.026).
Combination of IP-10 and RANTES could be potentially used as diagnostic and monitoring biomarker in pulmonary tuberculosis management.
Our findings reveal the structural determinants involved in the recognition of CCL5 by the CCR5 N terminus. These findings, together with existing structural data, provide a complete structural framework with which to understand the specificity of receptor:chemokine interactions.
Genetic variants in the CCL5/CCR5 pathway may serve as prognostic markers and may predict severe hand-foot skin reaction in metastatic colorectal cancer patients receiving regorafenib therapy.
The secretion of CCL5 and CCL2 was stimulated in undifferentiated and decidualized ESCs by the combination of TNF-alpha and IFN-gamma under non-apoptotic as well as apoptotic (with Fas-stimulation in parallel) conditions. TNF-alpha or IFN-gamma alone did not have this effect. The stimulatory influence of TNF-alpha plus IFN-gamma on CCL5 and CCL2 in ESCs was also seen on the transcriptional level.
this study shows that EMSY is increased and activates TSLP & CCL5 expression in eosinophilic esophagitis
These CCL5 derivatives may now be tested against several inflammation-related pathologies where the CCL5:CCR5 axis plays a relevant role.
The CCL5 In1.1T/C polymorphism may modulate pulmonary early-onset tuberculosis risk.
Our study provides the first evidence of an exercise-reducible myokine, CCL5, in the mouse skeletal muscle.
our results demonstrate a sequence of early events elicited by CCL5 chemoattracting macrophage that result in inflammatory aggravation of hepatic IRI.
the results show that Broadleaf Mahonia is a novel effective antiinflammatory herb in vitro and ex vivo, and that CCL5 may be closely associated with Granulomatous lobular mastitispathogenesis
miR-155 enhances venous neointima formation through the autocrine and paracrine effects of smooth muscle-like cell-derived RANTES in a nuclear factor kappaB-dependent manner in arteriovenous shunts.
Macrophage subtypes enhanced the osteogenesis in transwell setting and the transition from M1 to M2 was associated with an increase in bone anabolic factors CCL2/MCP-1, CCL5/RANTES and IGF-1 in vitro.
Taken together, our data suggest that CCR5 regulates insulin signaling in hypothalamus which contributes to systemic insulin sensitivity and glucose metabolism.
identifies the essential role of the chemoattractive cytokine CCL5 for liver disease progression and especially hepatocellular carcinoma development
Breast cancer cell CCL5 mediates bone marrow independent angiogenesis via paracrine signaling.
Studied the effects of CCL5-CCR5 interactions in breast cancer metabolism, and findings suggest that CCL5-CCR5 interactions in the tumor microenvironment modulate metabolic events during tumor onset to promote tumorigenesis.
RANTES levels were associated with TMS measures of cortical synaptic excitability, but not with long-term potentiation (LTP)-like plasticity.
study found that the inflammatory chemokine CCL5 is mostly retained (75%) during the resolution of zymosan A peritonitis in mice; CCL5 exerts a novel proresolving role on macrophages when acting in concert with apoptotic PMN-expressed D6.
A robust up-regulation of RANTES within the brain was seen in a mouse model of tick-borne encephalitis.
CCL5 paradoxically limits macrophage accumulation in the injured kidney during renin angiotensin system (RAS) activation by constraining the proinflammatory actions of CCL2.
This study showed that RANTES is important in the regulation of vascular dysfunction through modulation of perivascular inflammation.
IL-6 Mediates Macrophage Infiltration after Irradiation via Up-regulation of CCL2/CCL5 in Non-small Cell Lung Cancer
Blocking antibodies against RANTES and eotaxin reduced the infiltration of CD4(+) and CD8(+) T cells into the nigra, attenuated nigral expression of proinflammatory molecules, and suppressed nigral activation of glial cells. These findings paralleled dopaminergic neuronal protection, normalized striatal neurotransmitters, and improved motor functions in MPTP-intoxicated mice.
CCL5 deficiency resulted in reduced neointima formation after carotid artery injury and thrombosis.
RANTES produced by renal tubular cells act as a key chemokine in acute kidney injury and HIF-1alpha regulated LncRNA-PRINS might be involved in RANTES production.
Mycobacterium chelonae activates the gene expressions of chemokine (C-C motif) ligand 2 (CCL2) and CCL5 in murine bone marrow-derived macrophages and in vivo mouse model.
These results represent an important molecular mechanism whereby H. parasuis induced RANTES in the inflammatory response.
Foot-and-mouth disease virus leader proteinase inhibits dsRNA-induced RANTES transcription.
we cloned the nucleotide sequence of the 5'-flanking region of the porcine RANTES (poRANTES) gene and characterized the regulatory elements that activate transcription
The Toll-like receptor signaling pathway is involved in porcine reproductive and respiratory syndrome virus-induced RANTES activation.
These results suggest that porcine RANTES can play an important role in xenotransplant rejection, through participating in the interaction between porcine endothelial cells and human monocytes.
CCL5 but not CCL2 mainly attract bovine classical monocytes and promote their differentiation into LPS-hypo-responsive macrophages.
decrease in sensitivity of HIV variants to RANTES neutralization during the course of progressive infection, but not during follow-up of long term survivors; data suggest a role for RANTES neutralization sensitivity of HIV-1 in AIDS pathogenesis
In the pathogenesis of allergic rhinitis, substance P induces expression of RANTES in nasal mucosa.
CCL3, CCL4 and CCL5 gene expression was evaluated in response to simian-human immunodeficiency virus (SHIV) infection in a rhesus macaque model.
This gene is one of several CC cytokine genes clustered on the q-arm of chromosome 17. Cytokines are a family of secreted proteins involved in immunoregulatory and inflammatory processes. The CC cytokines are proteins characterized by two adjacent cysteines. The cytokine encoded by this gene functions as a chemoattractant for blood monocytes, memory T helper cells and eosinophils. It causes the release of histamine from basophils and activates eosinophils. This cytokine is one of the major HIV-suppressive factors produced by CD8+ cells. It functions as one of the natural ligands for the chemokine receptor CCR5 and it suppresses in vitro replication of the R5 strains of HIV-1, which use CCR5 as a coreceptor.
chemokine (C-C motif) ligand 5
, small inducible cytokine A5
, C-C motif chemokine 5
, T-cell-specific protein RANTES
, regulated upon activation normal T-cell expressed and secreted
, small-inducible cytokine A5
, T-cell specific protein p288
, beta-chemokine RANTES
, eosinophil chemotactic cytokine
, regulated upon activation, normally T-expressed, and presumably secreted
, small inducible cytokine subfamily A (Cys-Cys), member 5
, chemokine ah294
, small inducible cytokine A5 RANTES
, chemokine CCL5/RANTES
, chemokine ligand 5