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- Table of Contents
1 Citations 6 Q&As
Facts about C-C chemokine receptor type 7.
Receptor for the MIP-3-beta chemokine.
Probable mediator of EBV effects on B-lymphocytes or of normal lymphocyte functions..
Human | |
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Gene Name: | CCR7 |
Uniprot: | P32248 |
Entrez: | 1236 |
Belongs to: |
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G-protein coupled receptor 1 family |
BLR2; BLR2C-C chemokine receptor type 7; C-C CKR-7; CC-CKR-7; CCR7; CCR-7; CD197 antigen; CD197; CDw197; CDw197CC chemokine receptor 7; chemokine (C-C motif) receptor 7; CMKBR7; CMKBR7chemokine (C-C) receptor 7; EBI1; EBI1EBV-induced G protein-coupled receptor 1; EBV-induced G-protein coupled receptor 1; Epstein-Barr virus induced gene 1; Epstein-Barr virus induced G-protein coupled receptor; Epstein-Barr virus-induced G-protein coupled receptor 1; EVI1; lymphocyte-specific G protein-coupled peptide receptor; MIP-3 beta receptor
Mass (kDA):
42.874 kDA
Human | |
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Location: | 17q21.2 |
Sequence: | 17; NC_000017.11 (40553769..40565472, complement) |
Expressed in various lymphoid tissues and activated B- and T-lymphocytes, strongly up-regulated in B-cells infected with Epstein-Barr virus and T-cells infected with herpesvirus 6 or 7.
Cell membrane; Multi-pass membrane protein.
If you're looking for a specific antibody against the CCR7 protein, you may be surprised to find that Boster offers high-affinity primary antibodies. Boster antibodies are highly cited and have been validated using Western Blotting, Immunohistochemistry, and ELISA. Boster antibodies will give your results more confidence. You can read on to find out more about the quality of these antibodies, and why they are the best.
CCR7 is a useful marker to determine the course of TPLL treatment. A CCR7-positive patient was matched with a CCR7+ patient. This means that they had a similar disease but a different outcome. CCR7 had no significant difference in prognosis compared to the controls.
In order to test this hypothesis, we used a CCR7-targeting mAb in T-PLL cells. The cells were cultured with 1% FBS-RPMI-1640 medium and incubated using ligands as well as anti-CCR7 antibodies. BD Biosciences provided an apoptosis kit that could be used to determine cell viability after 24 hours.
The study found that one dose anti-CCR7 mAb significantly delayed disease onset and reduced tumor burden. However, there were no significant differences in the risk of death among the groups. Further, there were no significant differences between groups when CCR7 was analyzed. It is important to note that this study was conducted with human T-PLL cells and is not applicable to all cases.
T-PLL can be a rare, aggressive form of hematological malignancy. Unfortunately, the mechanisms behind its pathogenesis are not yet fully understood. GSE5788 Affymetrix Microarray data was used by the authors to identify the differentially expressed gene (DEGs), as well as pathways associated with tumor development. The PPI network analysis (PPI) was used to investigate functional changes.
These findings are just a few of the many gene pathways implicated in MCL pathogenesis. These pathways are described in Figure 1.
CCR7, although not a prognostic biomarker is used in initial radiation therapy. CCR7-expressing cell lines have significantly lower mortality rates than those that don't. Initial radiation therapy is associated with improved survival in T-PLL patients. This study will help clinicians determine the best treatment regimen for their patients.
An immunoglobulin- heavy chain (IGVH), gene, is a key marker in MCL. It helps distinguish between two subtypes. The blastoid type has a more severe course and is often associated to a worse prognosis. MCL is an example mature B cell malignancy. It is also known to be marginal zone lymphoma.
To determine if this antibody inhibits invasion cells, we used the boster Bio CCR7 mAb. We first extracted total RNA form intestinal tissues. Then, we used primers for MMP-2, MMP-9, and VEGF. The A590 colorimetric detect kit was used for Western blot analysis. The membrane was precoated with a matrix made of basement membrane and was surrounded by invasive cells. The membrane's lower layer was stained with the staining solution for the invasive bacteria. The assays had to be repeated in three copies.
The result of this study shows that AMD3100 inhibits the migration of SW480 cells by blocking CXCL12-mediated interactions. Blue-stained cells migrate through the polycarbonate membrane and migrate to the lower surface. Bars indicate means + SDs of triplicate studies. After 24 h, the cells migrate toward the lower surface. AMD3100 inhibits CXCL12–mediated migration, while CCR7mAb blocks ECM-dependent indirect invasion.
The antigens were found to be highly effective in the treatment of metastatic colorectal cancer. Boster Bio CCR7 MAb inhibited invading cancer cells in both murine and human cells. The study revealed that AMD3100 prevented invading cells from mice and astrocytes. This study has important implications on the development of cancer therapies and holds great promise for future research.
In addition to inhibiting invading cell growth, the CCR7 MAb also inhibited cell invasion and proliferation. This study also showed the importance of the miR-142/HIF-1a-axis in hypoxia-induced cell growth and invasion. This study suggests that miR142 could be an avenue for pancreatic cancer therapy. CCR7, mAb also inhibited the expressions of many important genes.
One effective way to reduce inflammation in the synovium is to inhibit CCR7. First, by inhibiting CCR7 mAb, a mouse model of chronic inflammatory arthritis can be protected against lymphocytic aggregates. CCR7mAb also inhibits autoantibodies which are a hallmark sign of synovial inflammation. Third, inhibition of CCR7 inhibits the production of inflammatory cytokines, including CCL21 and CCL19.
While the protein expression levels of most of the genes studied were increased at 2 hours, the transcript levels were low at eight hours and then high at 24 hours. Many of these genes were found to be involved in secretory signals, cell cycle regulation, adhesion, and other functions. These transcripts that are upregulated are likely to be controlled by upstream genes or induced via cytokines.
Boster Bio’s CCR7 mAb was able to effectively suppress the signaling pathways of mouse lymphomas. This result supports the hypothesis of a patient-specific approach to improve immunotherapies. The patient-specific approach might make them more reliable and more broadly effective. This study could also guide future research into immunotherapy treatment. These outcomes could be improved if more research is done to determine if CCR7 mAb inhibits them.
The PDL1/PD-1 Signaling Axis plays an important role when HIV-1 is triggered. The inhibition of this pathway results in HIV-1-specific CTL immune responses. It also inhibits the formation a cell to-cell interface, which may hinder the proper induction HIV-specific responses. These are some of the reasons why CCR7 Ab may be of great value to the immune systems.
The CCR7 mAb inhibited the production of IL2 and several cytokines, including IFNg (inducible protein 16), IFNAR1 (IFNAR1), and CDK8. These proteins are abundant in resting cells and regulated via IL2, thereby inhibiting their activity. This suggests that CCR7 is important in the development of an inflammatory response.
CCR7, a chemokine receptor, serves many functions in our immune system. It also plays an important role in tumor cell movement. CCR7, as a functional receptor inhibits ligand-mediated signaling pathways and causes tumor cell death in primary specimens. This finding has important implications for novel mAbs-based cancer therapies, such as cancer chemotherapy. A recent drug screen was limited to small molecules and chemotherapy. But, a recently developed mAb that targets CCR7 induces the killing of tumor cells in primary samples.
The study found that CAP100 targeted human cancer cells with a cell line-based model. The antibody decreased the number and spread of tumor cells within the LN (BM), spleen, and spleen which were CCR7-mediated sites. CAP-100 therapy also decreased the viability of malignant cells in LN. The reduction in tumor cell viability and proliferation was observed as early as day 50 of treatment. This was consistent with the fact the LN tumor cells were smaller after treatment with CAP 100.
Pepscan created a library of linear and native mimics of the N-terminal ligand binding sites of the hCCR7 ligand. These mimics were synthesized using CLP on Scaffolds technology (CLIPS). The candidate peptides for use in the vaccine were chosen based purely on their apparent affinity. The mAb was then produced in hybridoma technology in mice by producing anti-hCCR7 MAbs.
BL-01, a mAb that targets the CCR7 receptor on cancer cells, has been developed using a bispecific backbone. It contains three peptide chains that have a fused and two unattached heavy chains. BL-01 binds with both heavy and lighter chains by introducing complementary mutations to the Ch2(2)/CL(2) sequences.
BL-01 binds simultaneously to CD20 & CD5. This interaction allows CIK cells to be reprogrammed to target the tumors. Targeting CCR7 by a mAb can inhibit tumor cell growth in vitro, and in mice with severe combined immunity. The BL-01 bsAb works in synergy with CIK-cells, which are a type if T cell.
PMID: 8383238 by Birkenbach M.P., et al. Epstein-Barr virus-induced genes: first lymphocyte-specific G protein-coupled peptide receptors.
PMID: 7851893 by Schweickart V.L., et al. Cloning of human and mouse EBI1, a lymphoid-specific G-protein- coupled receptor encoded on human chromosome 17q12-q21.2.
*More publications can be found for each product on its corresponding product page