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- Table of Contents
13 Citations 9 Q&As
14 Citations 11 Q&As
4 Citations 8 Q&As
2 Citations 1 Q&As
Facts about C-C motif chemokine 5.
May activate several chemokine receptors including CCR1, CCR3, CCR4 and CCR5. One of the major HIV-suppressive factors produced by CD8+ T-cells.
Human | |
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Gene Name: | CCL5 |
Uniprot: | P13501 |
Entrez: | 6352 |
Belongs to: |
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intercrine beta (chemokine CC) family |
CCL5; chemokine (C-C motif) ligand 5; D17S136Enormally T-expressed, and presumably secreted; EoCP; Eosinophil chemotactic cytokine; RANTES; SISd; SIS-delta; small inducible cytokine A5 (RANTES); small inducible cytokine subfamily A (Cys-Cys), member 5; Small-inducible cytokine A5; T cell-specific protein P228; T-cell specific protein p288; TCP228T-cell-specific protein RANTES
Mass (kDA):
9.99 kDA
Human | |
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Location: | 17q12 |
Sequence: | 17; NC_000017.11 (35871491..35880360, complement) |
Expressed in the follicular fluid (at protein level). T-cell and macrophage specific.
Secreted.
What are the Best Uses of The CCL5 Markers This article will examine the CCL5 marker and Arginine metabolic product. It will also explore neutralizing antibodies against CCL5 that are anti-CCL5, cisplatin(DDP), M2 macrophage metabolism metabolites. These results are accessible to all Boster scientists around the globe. You can submit your research and receive credit for your research if it is utilized in commercial applications.
Arginine is a nutrient that is essential to human existence, however its availability may limit its production. Fortunately, a metabolite , known as arginine is easily available in a variety of foods. Arginine synthesizing can be impeded by various diseases. Here are the steps involved in this process. This article will examine the importance and effects of arginine synthesizing on human health and disease.
After about 1-2 hours of in vitro interaction, Giardia intestinis experiences arginine depletion. In the arginine metabolism, there are numerous enzymes as well as transporters. Certain pathogenic microbes can alter the expression of these enzymes. In this article, we will discuss a few of these enzymes. For further information, see the article "Arginine Metabolism in Boster Bio
The increasing levels of recArg1 hinder osteoclast formation, but they don't completely abolish the process. This suggests that resupply with arginine may be able to compensate for the absence of arginine for osteoclast development. These intermediates are crucial to osteoclast development and are produced as a dynamic metabolic adaptation to ensure cellular fitness. It is utilized in many areas of biomedicine. This includes bone remodeling.
In ESRD the metabolism of arginine can be altered in some cases. The reduced kidney mass makes arginine synthesis possible. Furthermore, arginine metabolism can be affected in patients suffering from severe renal disease. The study of molecular pharmacology could provide better understanding of the mechanisms that underlie this and the role that this metabolic process plays in ESRD. Further research is needed to learn more about the pathophysiology and develop therapeutic strategies to control it.
CCL5 is a ligand for the receptor for chemokines inside macrophages. Its biochemical function can be used to determine a protein that is involved in the metabolism macrophages. This ligand is extremely specific for human macrophages and is useful for studying the metabolism of macrophages. In the last few years, scientists have been exploring the different applications of CCL5 in research.
The development of a tumor is contingent on the abnormality of energy metabolism. Metastasis and angiogenesis are stimulated by macrophages associated with tumors. The metabolic interactions between cancerous cells, macrophages and them remains largely unknown. We discovered that lactate activates human mammaphages and triggers their secretion CCL5 protein. CCL5 promotes cell migration and enhances aerobic glycolysis. Neutralizing CCL5 reduced the migration of cancer-cells.
Recently it was discovered that the CCL5 marker in macrophage metabolism has been identified as a biomarker of breast carcinoma. This marker is extremely specific for breast cancer cells, and is a powerful immunotherapeutic drug. Studies of breast cancer cells also have shown that CCL5 from macrophages can enhance the rate of metastasis. Anti-CCL5 antibodies have the potential to inhibit breast cancer cell migration.
CCL5 causes tumors to express MMP-9 in greater quantity. The increased activity of MMPs encourages the growth of prostate cancer cells. cancer. CCL5 activates Rac signaling and boosts MMP-2, MMP-9 release from prostate cancer cells. The CCL5/CCR5 interaction also activates the NF-kB and avb3 integrin.
It has also been proven that the expression of CCL5 is essential for M2 macrophage polarization. It regulates several genes that are related to oxidative metabolism as well as the M2 phenotype. It is also vital for the production of IL-4 and IL-13, which are essential for inflammation. Therefore, it is crucial to investigate the role of CCL5 in the metabolism of macrophages in human disease.
CCL5 can be utilized for a variety of research purposes. Recombinant human CCL5 promotes glucose metabolism and boosts expression of glycolytic enzymes in MDA-MB-231 cells and MCF-7 cells. These results were obtained through co-cultures with human macrophages over 72 hours in 15 mM Lactate.
There are many suppliers that sell anti-CCL5 antibodies. The C-C motif encodes the protein CCL5. It is also called RANTES (D17S136E), SCYA5 (SCYA5) and (SCYA5), IL-10 (IL-10) and RANTES (D17S136E). It weighs about ten kilograms. It can be useful for studies of cytokine signals. Contact the supplier for more information.
A study of human cancer cells has shown that DDP treatment of CAFs increased the secretion of CCL5. The concentration of CCL5 was 72-fold higher in chemotherapy-resistant cells than in chemotherapy-sensitive tissues. CCL5 secretion also increased STAT3 and Akt the phosphorylation of ovarian cancer cell lines. These findings suggest that resistance to cisplatin could be associated with CCL5 secretion.
Recent research conducted by researchers from Boster Bio (UCSD), has shown that CCR5 neutralization can be controlled largely by the PLC. When activated, PLC and the IP3R activate chemical chemokines, increasing their activity. Boster Bio's neutralizing anti-CCL5 anti antibody blocks this process. In this way, it assists in identifying the protein that is responsible for the growth of ER calcium stores.
The study also looked at the effects of CCL5 upon ovarian cancer cell death. The study used an Annexin V/PI dual stained to prove that CCL5 significantly decreased tumor cell apoptosis , and also reduced the number of viable cells. CCL5 treated cells had a 20% increase in colony formation and were less sensitive to Cisplatin.
Boser Bio's neutralizing antibody against CCL5 has a strong affinity for both the SARS-CoV-2 Delta strain as well as its human counterpart. The antibodies generated by the second dose of antibodies significantly decreased the severity of the delta infection when as compared to human serum samples. Although some mice were infected by the virus SARS-CoV-2, the antibodies produced at week three were 13x greater than those produced by the Pfizer vaccine.
The exosomes from DDP-resistant lung cancer cells showed low expression of miR-100-5p. This miR influences the expression of mTOR within recipient cells which, in turn, decreases DDP sensitiveness. These exosomes could also function as biomarkers that can be dynamically activated to observe the effects of DDP in lung cancer cells. This study highlights the possibility of exosomes acting as a biomarker for DDP resistance.
In this study, RNA total was isolated from CAFs and cell lines treated with various concentrations of DDP in culture medium. Fresh media was added after 48 hours. The cells were stained with crystal violet and the number of survivors was determined by a microplate reader. Each experiment was repeated three times. The results were statistically analysed using GraphPad Prism 5.
The studies demonstrated that miR-100-5p alters DDP sensitivities in A549 cells. They also identified that miR-100-5p targets mTOR and regulates the impact of DDP on the expression of mTOR protein. This study demonstrated that miR-100-5p is a crucial miRNA that regulates DDP resistance, was identified. In addition, this miR influences the expression of several gene-coding genes.
There are many mechanisms that can trigger resistance to DDP. In the A549 lung cancer model, this drug has shown high resistance to DDP. The findings suggest that DDP resistance may be related to the expression of GST-p, a gene involved in regulating cell apoptosis. This study could also help to identify a novel adjuvant strategy to chemotherapy for lung cancer. DDP could increase the effectiveness of chemotherapy for lung carcinoma by inhibiting the production ROS.
CCL5 promotes resistance to DDP in the ovarian cancer cells. CCL5 derived form CAFs hinders the expression of the apoptosis associated protein in ovarian cancer cell lines. In studies conducted in vitro and in vivo these cells were intolerant to DDP. DDP may increase the production of CCL5 or CCK8 according to the study. These cells also display increased levels of cell adhesion markers.
PMID: 2456327 by Schall T.J., et al. A human T cell-specific molecule is a member of a new gene family.
PMID: 10213461 by Nomiyama H., et al. Organization of the chemokine gene cluster on human chromosome 17q11.2 containing the genes for CC chemokine MPIF-1, HCC-2, LEC, and RANTES.
*Showing only the more recent 20. More publications can be found for each product on its corresponding product page