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ccr5  (Miltenyi Biotec)


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    Structured Review

    Miltenyi Biotec ccr5
    Ccr5, supplied by Miltenyi Biotec, used in various techniques. Bioz Stars score: 95/100, based on 42 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ccr5/product/Miltenyi Biotec
    Average 95 stars, based on 42 article reviews
    ccr5 - by Bioz Stars, 2026-02
    95/100 stars

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    (A) Grafts of untreated recipients were harvested at POD+1. Grafts were analyzed by FACS for expression of <t>CCR5,</t> the receptor for CCL3, CCL4, and CCL5. Gating strategy is the same as shown in . (B) Schematic for treatment of recipient with maraviroc, a small molecule CCR5 inhibitor. Recipients were given 25 mg/kg/day maraviroc via i.p. injection on day-1 and 0 immediately following islet transplant. Grafts were harvested on POD+1 to enumerate graft infiltrating recipient cells using FACS. Graphs represent total number of each cell type in the graft. N=10 for each group. (C) Schematic for short-term peritransplant maraviroc treatment. Recipients were given daily injections as described above from day-1 through POD +7. Maraviroc-treated and vehicle-treated (control) recipients were both given POD+1 and +7 donor ECDI-SPs infusions. Graft survival for each group is plotted as days post-transplant. *p < 0.05
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    (A) Grafts of untreated recipients were harvested at POD+1. Grafts were analyzed by FACS for expression of <t>CCR5,</t> the receptor for CCL3, CCL4, and CCL5. Gating strategy is the same as shown in . (B) Schematic for treatment of recipient with maraviroc, a small molecule CCR5 inhibitor. Recipients were given 25 mg/kg/day maraviroc via i.p. injection on day-1 and 0 immediately following islet transplant. Grafts were harvested on POD+1 to enumerate graft infiltrating recipient cells using FACS. Graphs represent total number of each cell type in the graft. N=10 for each group. (C) Schematic for short-term peritransplant maraviroc treatment. Recipients were given daily injections as described above from day-1 through POD +7. Maraviroc-treated and vehicle-treated (control) recipients were both given POD+1 and +7 donor ECDI-SPs infusions. Graft survival for each group is plotted as days post-transplant. *p < 0.05
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    (A) Grafts of untreated recipients were harvested at POD+1. Grafts were analyzed by FACS for expression of <t>CCR5,</t> the receptor for CCL3, CCL4, and CCL5. Gating strategy is the same as shown in . (B) Schematic for treatment of recipient with maraviroc, a small molecule CCR5 inhibitor. Recipients were given 25 mg/kg/day maraviroc via i.p. injection on day-1 and 0 immediately following islet transplant. Grafts were harvested on POD+1 to enumerate graft infiltrating recipient cells using FACS. Graphs represent total number of each cell type in the graft. N=10 for each group. (C) Schematic for short-term peritransplant maraviroc treatment. Recipients were given daily injections as described above from day-1 through POD +7. Maraviroc-treated and vehicle-treated (control) recipients were both given POD+1 and +7 donor ECDI-SPs infusions. Graft survival for each group is plotted as days post-transplant. *p < 0.05
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    Comprehensive characterization of <t>CCR5</t> expression, predictive significance, functional pathways, and immune contexture in breast cancer. A Expression distribution of CCR5 across normal human tissues. B Multivariate logistic regression analysis showing that high CCR5 expression is independently associated with reduced likelihood of achieving pathological complete response (pCR) after neoadjuvant chemotherapy (NAC). C Sensitivity analysis using a data-augmented cohort confirms the negative association between CCR5 and pCR, with a narrower confidence interval. D Gene Ontology (GO) gene set enrichment analysis (GSEA) reveals that CCR5-high tumors are enriched in immune-related processes including T cell activation and leukocyte adhesion, as well as cellular transport and metabolic pathways. E Hallmark GSEA indicates concurrent activation of pro-inflammatory pathways (e.g., IFN-γ response, TNFα–NF-κB, IL6–JAK–STAT3) and tumor-promoting programs such as epithelial-mesenchymal transition (EMT) and mTORC1 signaling. F KEGG pathway enrichment highlights both immunostimulatory (e.g., NK cell cytotoxicity) and protumorigenic (e.g., PI3K–Akt signaling) pathways in CCR5-high tumors. G Immune cell infiltration analysis based on multiple algorithms shows that CCR5-high tumors are associated with elevated CD8⁺ T cells, M1 macrophages, and activated dendritic cells, but also with immunosuppressive Tregs, M2 macrophages, and high stromal/immune scores, suggesting a biphasic immune microenvironment
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    Image Search Results


    (A) Grafts of untreated recipients were harvested at POD+1. Grafts were analyzed by FACS for expression of CCR5, the receptor for CCL3, CCL4, and CCL5. Gating strategy is the same as shown in . (B) Schematic for treatment of recipient with maraviroc, a small molecule CCR5 inhibitor. Recipients were given 25 mg/kg/day maraviroc via i.p. injection on day-1 and 0 immediately following islet transplant. Grafts were harvested on POD+1 to enumerate graft infiltrating recipient cells using FACS. Graphs represent total number of each cell type in the graft. N=10 for each group. (C) Schematic for short-term peritransplant maraviroc treatment. Recipients were given daily injections as described above from day-1 through POD +7. Maraviroc-treated and vehicle-treated (control) recipients were both given POD+1 and +7 donor ECDI-SPs infusions. Graft survival for each group is plotted as days post-transplant. *p < 0.05

    Journal: bioRxiv

    Article Title: Donor Macrophage Depletion Permits Post-Transplant Tolerance Induction in a Murine Islet Transplant Model

    doi: 10.64898/2026.01.08.698403

    Figure Lengend Snippet: (A) Grafts of untreated recipients were harvested at POD+1. Grafts were analyzed by FACS for expression of CCR5, the receptor for CCL3, CCL4, and CCL5. Gating strategy is the same as shown in . (B) Schematic for treatment of recipient with maraviroc, a small molecule CCR5 inhibitor. Recipients were given 25 mg/kg/day maraviroc via i.p. injection on day-1 and 0 immediately following islet transplant. Grafts were harvested on POD+1 to enumerate graft infiltrating recipient cells using FACS. Graphs represent total number of each cell type in the graft. N=10 for each group. (C) Schematic for short-term peritransplant maraviroc treatment. Recipients were given daily injections as described above from day-1 through POD +7. Maraviroc-treated and vehicle-treated (control) recipients were both given POD+1 and +7 donor ECDI-SPs infusions. Graft survival for each group is plotted as days post-transplant. *p < 0.05

    Article Snippet: To inhibit CCR5 activity in vivo , maraviroc (MedChem Express) was administered to recipients at 25 mg/kg/day.

    Techniques: Expressing, Injection, Control

    Comprehensive characterization of CCR5 expression, predictive significance, functional pathways, and immune contexture in breast cancer. A Expression distribution of CCR5 across normal human tissues. B Multivariate logistic regression analysis showing that high CCR5 expression is independently associated with reduced likelihood of achieving pathological complete response (pCR) after neoadjuvant chemotherapy (NAC). C Sensitivity analysis using a data-augmented cohort confirms the negative association between CCR5 and pCR, with a narrower confidence interval. D Gene Ontology (GO) gene set enrichment analysis (GSEA) reveals that CCR5-high tumors are enriched in immune-related processes including T cell activation and leukocyte adhesion, as well as cellular transport and metabolic pathways. E Hallmark GSEA indicates concurrent activation of pro-inflammatory pathways (e.g., IFN-γ response, TNFα–NF-κB, IL6–JAK–STAT3) and tumor-promoting programs such as epithelial-mesenchymal transition (EMT) and mTORC1 signaling. F KEGG pathway enrichment highlights both immunostimulatory (e.g., NK cell cytotoxicity) and protumorigenic (e.g., PI3K–Akt signaling) pathways in CCR5-high tumors. G Immune cell infiltration analysis based on multiple algorithms shows that CCR5-high tumors are associated with elevated CD8⁺ T cells, M1 macrophages, and activated dendritic cells, but also with immunosuppressive Tregs, M2 macrophages, and high stromal/immune scores, suggesting a biphasic immune microenvironment

    Journal: Discover Oncology

    Article Title: CCR5 expression and conformational stability as potential cooperative modulators of immune phenotypes and therapy response in breast cancer

    doi: 10.1007/s12672-025-04189-1

    Figure Lengend Snippet: Comprehensive characterization of CCR5 expression, predictive significance, functional pathways, and immune contexture in breast cancer. A Expression distribution of CCR5 across normal human tissues. B Multivariate logistic regression analysis showing that high CCR5 expression is independently associated with reduced likelihood of achieving pathological complete response (pCR) after neoadjuvant chemotherapy (NAC). C Sensitivity analysis using a data-augmented cohort confirms the negative association between CCR5 and pCR, with a narrower confidence interval. D Gene Ontology (GO) gene set enrichment analysis (GSEA) reveals that CCR5-high tumors are enriched in immune-related processes including T cell activation and leukocyte adhesion, as well as cellular transport and metabolic pathways. E Hallmark GSEA indicates concurrent activation of pro-inflammatory pathways (e.g., IFN-γ response, TNFα–NF-κB, IL6–JAK–STAT3) and tumor-promoting programs such as epithelial-mesenchymal transition (EMT) and mTORC1 signaling. F KEGG pathway enrichment highlights both immunostimulatory (e.g., NK cell cytotoxicity) and protumorigenic (e.g., PI3K–Akt signaling) pathways in CCR5-high tumors. G Immune cell infiltration analysis based on multiple algorithms shows that CCR5-high tumors are associated with elevated CD8⁺ T cells, M1 macrophages, and activated dendritic cells, but also with immunosuppressive Tregs, M2 macrophages, and high stromal/immune scores, suggesting a biphasic immune microenvironment

    Article Snippet: For CCR5 protein detection, we performed IHC using a rabbit anti-CCR5 polyclonal antibody (Proteintech#17476-1-AP, 1:900 dilution).

    Techniques: Expressing, Functional Assay, Activation Assay, Protein-Protein interactions

    Correlation between CCR5 expression and gene signatures of tumor-associated macrophage (TAM) polarization in breast cancer. A Correlation heatmap showing weak-to-moderate associations between CCR5 and M1 macrophage markers (e.g., NOS2, ARG2, PTGS2). B CCR5 expression demonstrates strong positive correlations with canonical M2 macrophage markers, including MRC1 ( r = 0.65), CD163 ( r = 0.699), and MS4A4A ( r = 0.749). C CCR5 is also highly correlated with TAM-associated immunosuppressive genes such as CD86, CCL22, and IL10, indicating a preferential link to immunoregulatory macrophage phenotypes

    Journal: Discover Oncology

    Article Title: CCR5 expression and conformational stability as potential cooperative modulators of immune phenotypes and therapy response in breast cancer

    doi: 10.1007/s12672-025-04189-1

    Figure Lengend Snippet: Correlation between CCR5 expression and gene signatures of tumor-associated macrophage (TAM) polarization in breast cancer. A Correlation heatmap showing weak-to-moderate associations between CCR5 and M1 macrophage markers (e.g., NOS2, ARG2, PTGS2). B CCR5 expression demonstrates strong positive correlations with canonical M2 macrophage markers, including MRC1 ( r = 0.65), CD163 ( r = 0.699), and MS4A4A ( r = 0.749). C CCR5 is also highly correlated with TAM-associated immunosuppressive genes such as CD86, CCL22, and IL10, indicating a preferential link to immunoregulatory macrophage phenotypes

    Article Snippet: For CCR5 protein detection, we performed IHC using a rabbit anti-CCR5 polyclonal antibody (Proteintech#17476-1-AP, 1:900 dilution).

    Techniques: Expressing

    Structural confidence and stability changes of CCR5 protein with V131I mutation ( A ) AlphaFold-predicted 3D structure of CCR5 highlighting residue 131. Confidence levels are color-coded based on pLDDT scores: very low (< 50), low (50–70), high (70–90), and very high (> 90). B – C Root Mean Square Fluctuation (RMSF) and Root Mean Square Deviation (RMSD) plots comparing wild-type (WT) and V131I mutant (MT) CCR5 during 100 ns molecular dynamics simulations. D Radius of gyration (Rg) trajectory indicating global compactness differences between WT and MT. E Solvent-accessible surface area (SASA) profile across simulation time. F Predicted change in protein stability (ΔΔG) upon V131I substitution at position 131, visualized as a heatmap. Red shading denotes destabilizing mutations

    Journal: Discover Oncology

    Article Title: CCR5 expression and conformational stability as potential cooperative modulators of immune phenotypes and therapy response in breast cancer

    doi: 10.1007/s12672-025-04189-1

    Figure Lengend Snippet: Structural confidence and stability changes of CCR5 protein with V131I mutation ( A ) AlphaFold-predicted 3D structure of CCR5 highlighting residue 131. Confidence levels are color-coded based on pLDDT scores: very low (< 50), low (50–70), high (70–90), and very high (> 90). B – C Root Mean Square Fluctuation (RMSF) and Root Mean Square Deviation (RMSD) plots comparing wild-type (WT) and V131I mutant (MT) CCR5 during 100 ns molecular dynamics simulations. D Radius of gyration (Rg) trajectory indicating global compactness differences between WT and MT. E Solvent-accessible surface area (SASA) profile across simulation time. F Predicted change in protein stability (ΔΔG) upon V131I substitution at position 131, visualized as a heatmap. Red shading denotes destabilizing mutations

    Article Snippet: For CCR5 protein detection, we performed IHC using a rabbit anti-CCR5 polyclonal antibody (Proteintech#17476-1-AP, 1:900 dilution).

    Techniques: Mutagenesis, Residue, Solvent