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fpr3  (Cusabio)


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    Structured Review

    Cusabio fpr3
    Fpr3, supplied by Cusabio, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/fpr3/product/Cusabio
    Average 94 stars, based on 1 article reviews
    fpr3 - by Bioz Stars, 2026-04
    94/100 stars

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    A UMAP plot displaying identified clusters in glioma. B WGCNA identifies M0, M1, and M2-like macrophage correlated modules. C The volcano plot showing differentially expressed genes between gliomas with high- and low-M2 macrophage ssGSEA score. D Venn diagram demonstrating the overlapping of genes in brown modules and differentially expressed genes. E Expression of CD163 and <t>FPR3</t> overlaid on the UMAP space. F Correlation analysis of FPR3 and M2 macrophage ssGSEA score in glioma. G Correlation analysis of FPR3 and CD163 expression in TCGA cohort. H IF staining of FPR3 and CD163 in human glioma were shown. I Representative IHC staining of FPR3 and CD163 in glioma microarray; scale bar represents 100 µm.
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    Image Search Results


    Journal: Cell Reports Medicine

    Article Title: Myeloid cells coordinately induce glioma cell-intrinsic and cell-extrinsic pathways for chemoresistance via GP130 signaling

    doi: 10.1016/j.xcrm.2024.101658

    Figure Lengend Snippet:

    Article Snippet: FPR3 TaqMan Genexpression Assay , ThermoFisher Scientific , Cat#: Hs01574392_m1.

    Techniques: Plasmid Preparation, Recombinant, Transfection, Fluorescence, Staining, Reverse Transcription, Gene Expression, Liposomes, Mutagenesis, shRNA, Control, Construct, Software, Imaging, Functional Assay, Dissection, Sequencing, Real-time Polymerase Chain Reaction

    A UMAP plot displaying identified clusters in glioma. B WGCNA identifies M0, M1, and M2-like macrophage correlated modules. C The volcano plot showing differentially expressed genes between gliomas with high- and low-M2 macrophage ssGSEA score. D Venn diagram demonstrating the overlapping of genes in brown modules and differentially expressed genes. E Expression of CD163 and FPR3 overlaid on the UMAP space. F Correlation analysis of FPR3 and M2 macrophage ssGSEA score in glioma. G Correlation analysis of FPR3 and CD163 expression in TCGA cohort. H IF staining of FPR3 and CD163 in human glioma were shown. I Representative IHC staining of FPR3 and CD163 in glioma microarray; scale bar represents 100 µm.

    Journal: NPJ Precision Oncology

    Article Title: Machine learning algorithms for predicting glioma patient prognosis based on CD163+FPR3+ macrophage signature

    doi: 10.1038/s41698-024-00692-w

    Figure Lengend Snippet: A UMAP plot displaying identified clusters in glioma. B WGCNA identifies M0, M1, and M2-like macrophage correlated modules. C The volcano plot showing differentially expressed genes between gliomas with high- and low-M2 macrophage ssGSEA score. D Venn diagram demonstrating the overlapping of genes in brown modules and differentially expressed genes. E Expression of CD163 and FPR3 overlaid on the UMAP space. F Correlation analysis of FPR3 and M2 macrophage ssGSEA score in glioma. G Correlation analysis of FPR3 and CD163 expression in TCGA cohort. H IF staining of FPR3 and CD163 in human glioma were shown. I Representative IHC staining of FPR3 and CD163 in glioma microarray; scale bar represents 100 µm.

    Article Snippet: IHC was performed using a primary antibody targeting FPR3 (Proteintech, China).

    Techniques: Expressing, Staining, Immunohistochemistry, Microarray

    The expression level of FPR3 in the normal tissues and glioma tissues in TCGA cohort ( A ), GSE16011 ( B ), Rembrandt cohort ( C ) and in-house cohort ( D ). E The expression of FPR3 in peritumor and glioma tissues was analyzed by RT-qPCR. F The expression level of FPR3 in the normal tissues and glioma tissues was analyzed by immunohistochemical staining. G The expression of FPR3 in glioma and peritumor tissues was analyzed by IHC. H Kaplan–Meier survival plot of FPR3 expression of glioma patients in the six cohorts. I Kaplan–Meier survival plot of FPR3 expression of glioma patients by RT-qPCR. J Kaplan–Meier survival plot of FPR3 expression of glioma patients by IHC. P < 0.05, log-rank test. (“**, ***” respectively means P < 0.01, P < 0.001).

    Journal: NPJ Precision Oncology

    Article Title: Machine learning algorithms for predicting glioma patient prognosis based on CD163+FPR3+ macrophage signature

    doi: 10.1038/s41698-024-00692-w

    Figure Lengend Snippet: The expression level of FPR3 in the normal tissues and glioma tissues in TCGA cohort ( A ), GSE16011 ( B ), Rembrandt cohort ( C ) and in-house cohort ( D ). E The expression of FPR3 in peritumor and glioma tissues was analyzed by RT-qPCR. F The expression level of FPR3 in the normal tissues and glioma tissues was analyzed by immunohistochemical staining. G The expression of FPR3 in glioma and peritumor tissues was analyzed by IHC. H Kaplan–Meier survival plot of FPR3 expression of glioma patients in the six cohorts. I Kaplan–Meier survival plot of FPR3 expression of glioma patients by RT-qPCR. J Kaplan–Meier survival plot of FPR3 expression of glioma patients by IHC. P < 0.05, log-rank test. (“**, ***” respectively means P < 0.01, P < 0.001).

    Article Snippet: IHC was performed using a primary antibody targeting FPR3 (Proteintech, China).

    Techniques: Expressing, Quantitative RT-PCR, Immunohistochemical staining, Staining, Paraffin-embedded Immunohistochemistry

    A A UMAP projection of de novo clustered myeloid cells. B Expression of CD163 and FPR3 overlaid on the UMAP space. C GSEA analysis of specific gene of the CD163+FPR3+ macrophage subset. D Two immune phenotypes in the glioma microarray cohort were detected using IF. E The expression level of FPR3 between glioma with two immune phenotypes. F The expression of PD-L1, CD40, PD-1, P65, and STAT3 expression in glioma with the CD163+FPR3+ and CD163+FPR3− macrophage subset. (“*”means P < 0.05).

    Journal: NPJ Precision Oncology

    Article Title: Machine learning algorithms for predicting glioma patient prognosis based on CD163+FPR3+ macrophage signature

    doi: 10.1038/s41698-024-00692-w

    Figure Lengend Snippet: A A UMAP projection of de novo clustered myeloid cells. B Expression of CD163 and FPR3 overlaid on the UMAP space. C GSEA analysis of specific gene of the CD163+FPR3+ macrophage subset. D Two immune phenotypes in the glioma microarray cohort were detected using IF. E The expression level of FPR3 between glioma with two immune phenotypes. F The expression of PD-L1, CD40, PD-1, P65, and STAT3 expression in glioma with the CD163+FPR3+ and CD163+FPR3− macrophage subset. (“*”means P < 0.05).

    Article Snippet: IHC was performed using a primary antibody targeting FPR3 (Proteintech, China).

    Techniques: Expressing, Microarray

    A The C-index of 101 kinds of prediction models built by machine learning algorithms for the CD163+FPR3+ macrophage-associated signatures in the six glioma cohorts. B An ensemble of 17 cell death-associated genes with Cox coefficients. C The number of trees for determining the CD163+FPR3+ macrophage-associated signature with minimal error and the importance of CD163+FPR3+ macrophage-associated signatures based on the RSF algorithm. D The identification of optimal cutoffs for survival analyses in TCGA cohort. Kaplan–Meier survival curves of OS between high-score and low-score patients identified the scoring system in TCGA ( E ), CGGA-693 ( F ), CGGA-301 ( G ), CGGA-325 ( H ), GSE16011, ( I ) and Rembrandt ( J ) datasets. P values were calculated by the log-rank test, and P < 0.05 was considered significant.

    Journal: NPJ Precision Oncology

    Article Title: Machine learning algorithms for predicting glioma patient prognosis based on CD163+FPR3+ macrophage signature

    doi: 10.1038/s41698-024-00692-w

    Figure Lengend Snippet: A The C-index of 101 kinds of prediction models built by machine learning algorithms for the CD163+FPR3+ macrophage-associated signatures in the six glioma cohorts. B An ensemble of 17 cell death-associated genes with Cox coefficients. C The number of trees for determining the CD163+FPR3+ macrophage-associated signature with minimal error and the importance of CD163+FPR3+ macrophage-associated signatures based on the RSF algorithm. D The identification of optimal cutoffs for survival analyses in TCGA cohort. Kaplan–Meier survival curves of OS between high-score and low-score patients identified the scoring system in TCGA ( E ), CGGA-693 ( F ), CGGA-301 ( G ), CGGA-325 ( H ), GSE16011, ( I ) and Rembrandt ( J ) datasets. P values were calculated by the log-rank test, and P < 0.05 was considered significant.

    Article Snippet: IHC was performed using a primary antibody targeting FPR3 (Proteintech, China).

    Techniques:

    A Time-dependent ROC curves displaying the prognostic accuracy of the risk score at 1, 3, and 5 years in TCGA, CGGA-693, CGGA-301, CGGA-325, GSE16011, and Rembrandt cohorts. B C-index of the risk score in the six cohorts. The performance of risk score was compared with other clinical and molecular variables in predicting prognosis in TCGA ( C ), CGGA-693 ( D ), GSE16011 ( E ), and Rembrandt ( F ) datasets. The performance of risk score + grade was compared with risk score and grade alone in predicting prognosis in TCGA ( G ), CGGA-693 ( H ), GSE16011 ( I ), and Rembrandt ( J ) datasets. K The 1-year, 2-year, and 3-year calibration curves of the CD163 + FPR3+ macrophage-associated signature in the four datasets. The P values are labeled above each boxplot with asterisks (-, no significant, “*, **, ***” respectively means P < 0.05, P < 0.01, P < 0.001).

    Journal: NPJ Precision Oncology

    Article Title: Machine learning algorithms for predicting glioma patient prognosis based on CD163+FPR3+ macrophage signature

    doi: 10.1038/s41698-024-00692-w

    Figure Lengend Snippet: A Time-dependent ROC curves displaying the prognostic accuracy of the risk score at 1, 3, and 5 years in TCGA, CGGA-693, CGGA-301, CGGA-325, GSE16011, and Rembrandt cohorts. B C-index of the risk score in the six cohorts. The performance of risk score was compared with other clinical and molecular variables in predicting prognosis in TCGA ( C ), CGGA-693 ( D ), GSE16011 ( E ), and Rembrandt ( F ) datasets. The performance of risk score + grade was compared with risk score and grade alone in predicting prognosis in TCGA ( G ), CGGA-693 ( H ), GSE16011 ( I ), and Rembrandt ( J ) datasets. K The 1-year, 2-year, and 3-year calibration curves of the CD163 + FPR3+ macrophage-associated signature in the four datasets. The P values are labeled above each boxplot with asterisks (-, no significant, “*, **, ***” respectively means P < 0.05, P < 0.01, P < 0.001).

    Article Snippet: IHC was performed using a primary antibody targeting FPR3 (Proteintech, China).

    Techniques: Labeling

    GP130 is essential for humanin-induced chemoresistance (A) Quantitative reverse-transcription PCR (RT-PCR) for the humanin receptor subunit IL6ST (encoding GP130) was performed; note that IL6ST levels are much higher in humanin-sensitive than humanin-insensitive hGBMs. (B) hGBMs were stimulated with HN or HNG, partly sc144 was coapplied, which consistently abrogated the protumorigenic effect of HN and HNG (dashed line: controls without HN or sc144). (C) Expansion of hGBM1-HN-WT, HN-C8A, or HN-L9R cells, with or without sc144. (D) Humanin expression levels in brain slices with hiPSC-derived microglia and hGBM1 cells were attenuated after addition of sc144 (graphically summarized in E). The number of biological replicates is indicated (dots in graphs indicate data from individual experiments); all error bars are presented as mean ± SDM. Statistical significance is shown by one-way ANOVA in (A) and t test in (B–D): ∗∗ p < 0.01; ∗∗∗∗ p < 0.0001; NS, not significant.

    Journal: Cell Reports Medicine

    Article Title: Myeloid cells coordinately induce glioma cell-intrinsic and cell-extrinsic pathways for chemoresistance via GP130 signaling

    doi: 10.1016/j.xcrm.2024.101658

    Figure Lengend Snippet: GP130 is essential for humanin-induced chemoresistance (A) Quantitative reverse-transcription PCR (RT-PCR) for the humanin receptor subunit IL6ST (encoding GP130) was performed; note that IL6ST levels are much higher in humanin-sensitive than humanin-insensitive hGBMs. (B) hGBMs were stimulated with HN or HNG, partly sc144 was coapplied, which consistently abrogated the protumorigenic effect of HN and HNG (dashed line: controls without HN or sc144). (C) Expansion of hGBM1-HN-WT, HN-C8A, or HN-L9R cells, with or without sc144. (D) Humanin expression levels in brain slices with hiPSC-derived microglia and hGBM1 cells were attenuated after addition of sc144 (graphically summarized in E). The number of biological replicates is indicated (dots in graphs indicate data from individual experiments); all error bars are presented as mean ± SDM. Statistical significance is shown by one-way ANOVA in (A) and t test in (B–D): ∗∗ p < 0.01; ∗∗∗∗ p < 0.0001; NS, not significant.

    Article Snippet: IL6ST TaqMan Genexpression Assay , ThermoFisher Scientific , Cat#: Hs00174360_m1.

    Techniques: Reverse Transcription, Reverse Transcription Polymerase Chain Reaction, Expressing, Derivative Assay

    Humanin-mediated BTB formation is blunted by GP130 blockage increasing chemotherapeutic efficacy and survival (A) Quantification of vascular mural coverage on tumor vessels in orthotopic HN-WT or HN-C8a GBMs with or without TMZ (indicated by blue bars). (B and C) Vascular mural coverage of tumor vessels in TMZ-treated orthotopic HN-WT GBMs with or without BZA. (D) Endothelial cells and pericytes were purified from a transgenic GBM mouse model (GL261, n = 11; infused with humanin, HN, or aCSF, control) and analyzed by transcriptomics; GSEA indicated enrichment for angiogenic traits in HN-stimulated endothelia (as compared to aCSF). (E) Signaling pathways between endothelia and pericytes were analyzed from HN-infused versus control GBMs; in HN-infused GBMs, pericytes promote IL6ST (GP130) signaling in endothelia; in HN-infused GBMs, endothelia promote BMP signaling in pericytes. (F) In HN-WT GBMs, receiving TMZ cotreatment with BZA reduced pericyte (PDGFRB+) coverage of tumor vessels (CD31 + ; as compared to cotreatment with vehicle). (G) Intravenous application of 70 kDA dextran as a tracer for vessel tightness showed that BZA-treated gliomas had significantly increased leakage (across CD31 + vessels) into the tumor parenchyma, as compared to vehicle-treated mice. (H) In mice with orthotopic HN-WT GBMs, intracerebral infusion of sc144 (10 μM) during TMZ chemotherapy prolonged survival as compared to intracerebral infusion of vehicle ( n = 12 per group). (I) Schematic summary: the BTB and DDR protect humanin-sensitive GBMs from TMZ. GP130 inhibitors reduce BTB tightness and blunt chemoresistance. Scale bars indicate 200 μm in (A) and 20 μm in (G). The number of biological replicates is indicated (dots in graphs indicate data from individual mice); all error bars are presented as mean ± SDM. Statistical significance is shown by one-way ANOVA (A), t test (F, G), or by Mantel-Cox test (F): ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

    Journal: Cell Reports Medicine

    Article Title: Myeloid cells coordinately induce glioma cell-intrinsic and cell-extrinsic pathways for chemoresistance via GP130 signaling

    doi: 10.1016/j.xcrm.2024.101658

    Figure Lengend Snippet: Humanin-mediated BTB formation is blunted by GP130 blockage increasing chemotherapeutic efficacy and survival (A) Quantification of vascular mural coverage on tumor vessels in orthotopic HN-WT or HN-C8a GBMs with or without TMZ (indicated by blue bars). (B and C) Vascular mural coverage of tumor vessels in TMZ-treated orthotopic HN-WT GBMs with or without BZA. (D) Endothelial cells and pericytes were purified from a transgenic GBM mouse model (GL261, n = 11; infused with humanin, HN, or aCSF, control) and analyzed by transcriptomics; GSEA indicated enrichment for angiogenic traits in HN-stimulated endothelia (as compared to aCSF). (E) Signaling pathways between endothelia and pericytes were analyzed from HN-infused versus control GBMs; in HN-infused GBMs, pericytes promote IL6ST (GP130) signaling in endothelia; in HN-infused GBMs, endothelia promote BMP signaling in pericytes. (F) In HN-WT GBMs, receiving TMZ cotreatment with BZA reduced pericyte (PDGFRB+) coverage of tumor vessels (CD31 + ; as compared to cotreatment with vehicle). (G) Intravenous application of 70 kDA dextran as a tracer for vessel tightness showed that BZA-treated gliomas had significantly increased leakage (across CD31 + vessels) into the tumor parenchyma, as compared to vehicle-treated mice. (H) In mice with orthotopic HN-WT GBMs, intracerebral infusion of sc144 (10 μM) during TMZ chemotherapy prolonged survival as compared to intracerebral infusion of vehicle ( n = 12 per group). (I) Schematic summary: the BTB and DDR protect humanin-sensitive GBMs from TMZ. GP130 inhibitors reduce BTB tightness and blunt chemoresistance. Scale bars indicate 200 μm in (A) and 20 μm in (G). The number of biological replicates is indicated (dots in graphs indicate data from individual mice); all error bars are presented as mean ± SDM. Statistical significance is shown by one-way ANOVA (A), t test (F, G), or by Mantel-Cox test (F): ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

    Article Snippet: IL6ST TaqMan Genexpression Assay , ThermoFisher Scientific , Cat#: Hs00174360_m1.

    Techniques: Purification, Transgenic Assay, Control, Protein-Protein interactions

    Journal: Cell Reports Medicine

    Article Title: Myeloid cells coordinately induce glioma cell-intrinsic and cell-extrinsic pathways for chemoresistance via GP130 signaling

    doi: 10.1016/j.xcrm.2024.101658

    Figure Lengend Snippet:

    Article Snippet: IL6ST TaqMan Genexpression Assay , ThermoFisher Scientific , Cat#: Hs00174360_m1.

    Techniques: Plasmid Preparation, Recombinant, Transfection, Fluorescence, Staining, Reverse Transcription, Gene Expression, Liposomes, Mutagenesis, shRNA, Control, Construct, Software, Imaging, Functional Assay, Dissection, Sequencing, Real-time Polymerase Chain Reaction

    Gene symbols and TaqMan primers for mRNAs assayed.

    Journal: Schizophrenia Research: Cognition

    Article Title: Relationship of cognitive measures to mRNA levels in lymphocytes from patients with schizophrenia and controls

    doi: 10.1016/j.scog.2024.100321

    Figure Lengend Snippet: Gene symbols and TaqMan primers for mRNAs assayed.

    Article Snippet: FPRL2 , Hs00266666_s1 , Formyl peptide receptor 3.

    Techniques: TaqMan Assay, Gene Expression, Sequencing, Variant Assay, Derivative Assay, Protein Binding