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gm csfr  (Bio-Techne corporation)


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    Structured Review

    Bio-Techne corporation gm csfr
    Gm Csfr, supplied by Bio-Techne corporation, used in various techniques. Bioz Stars score: 90/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/gm csfr/product/Bio-Techne corporation
    Average 90 stars, based on 2 article reviews
    gm csfr - by Bioz Stars, 2026-03
    90/100 stars

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    Image Search Results


    Gene and protein expression of GM-CSF alpha (GM-CSFR-α) and beta-common (GM-CSFR-β c ) receptors in 7-month-old mice. ( a ) UMAP of PNF from 7-month-old Nf1 f/f ; DhhCre mice compared to aged-match wild-type (WT) control DRG. ( b ) Dot plot showing gene expression in various cell types (y-axis: Identity). ( c ) Representative pictures of immunostaining for GM-CSFR-α and GM-CSFR-β c in WT DRG and PNF tissue sections. ( d ) Frequency of non-immune (CD45-) and immune (CD45+) cells in WT DRG (n = 6) and PNF (n = 8)and ( e ) subtypes of CD45+ immune cells expressing GM-CSFR-α ((WT DRG (n = 4) and PNF (n = 4)) and GM-CSFR-β c ((WT DRG (n = 6) and PNF (n = 8)).Unpaired t -test or 2-way ANOVA multiple comparison test, * p < 0.05, ** p < 0.001, *** p < 0.0001, **** p < 0.00001.

    Journal: Cancers

    Article Title: Granulocyte-Macrophage Colony Stimulating Factor Receptor Contributes to Plexiform Neurofibroma Initiation

    doi: 10.3390/cancers17050905

    Figure Lengend Snippet: Gene and protein expression of GM-CSF alpha (GM-CSFR-α) and beta-common (GM-CSFR-β c ) receptors in 7-month-old mice. ( a ) UMAP of PNF from 7-month-old Nf1 f/f ; DhhCre mice compared to aged-match wild-type (WT) control DRG. ( b ) Dot plot showing gene expression in various cell types (y-axis: Identity). ( c ) Representative pictures of immunostaining for GM-CSFR-α and GM-CSFR-β c in WT DRG and PNF tissue sections. ( d ) Frequency of non-immune (CD45-) and immune (CD45+) cells in WT DRG (n = 6) and PNF (n = 8)and ( e ) subtypes of CD45+ immune cells expressing GM-CSFR-α ((WT DRG (n = 4) and PNF (n = 4)) and GM-CSFR-β c ((WT DRG (n = 6) and PNF (n = 8)).Unpaired t -test or 2-way ANOVA multiple comparison test, * p < 0.05, ** p < 0.001, *** p < 0.0001, **** p < 0.00001.

    Article Snippet: For immunohistochemistry (IHC), the procedure was as for immunofluorescence (IF), except that following overnight incubation with anti-GM-CSFR beta rabbit polyclonal antibody (Bioss; cat# bs-3689R, Woburn, MA, USA) or anti-GM-CSFR alpha rabbit polyclonal antibody (Bioss; cat# bs-1457R, USA) at 4 °C, the sections were subsequently incubated with biotinylated goat anti-rabbit secondary antibody (VectorLabs; cat#BA-1000, Newark, CA, USA) for 1 h and rinsed three times in TBST for 5 min each.

    Techniques: Expressing, Control, Gene Expression, Immunostaining, Comparison

    Effects of GM-CSFR-α and GM-CSFR β c genetic deletion on survival and nerve pathology. ( a ) Kaplan–Meier survival curve of Nf1 f/f ; DhhCre (control) (n = 9) and mice bearing deletion of the receptor GM-CSFR-α (GM-CSFR-α-/-; Nf1 f/f ; DhhCre (n = 18)) or GM-CSFR-β c (GM-CSFR-β c -/-; Nf1 f/f ; DhhCre (n = 16)). ( b ) representative pictures of aged-matched gross dissection of spinal cord from each mouse (Nf1 f/f ; DhhCre (control) (n = 5), GM-CSFR-α-/-; Nf1 f/f ; DhhCre (n = 6) and GM-CSFR-β c -/-; Nf1 f/f ; DhhCre (n = 6)) and quantification of tumor number and size (diameter). White arrows indicate PNF. ( c ) Representative images of tissue sections stained with H&E and ( d ) electromicrographs of saphenous nerve showing the ultrastructure of an intact Schwann cell Remak bundle (blue margin) in WT mice compared to the disrupted Remak structure (blue arrows) in tumor mice in the presence or loss of GM-CSF receptors. ( e ) High percentage (6 or more) of grouped axons indicate a normal Remak bundle. Two-way ANOVA multiple comparison test, * p < 0.05, **** p < 0.00001.

    Journal: Cancers

    Article Title: Granulocyte-Macrophage Colony Stimulating Factor Receptor Contributes to Plexiform Neurofibroma Initiation

    doi: 10.3390/cancers17050905

    Figure Lengend Snippet: Effects of GM-CSFR-α and GM-CSFR β c genetic deletion on survival and nerve pathology. ( a ) Kaplan–Meier survival curve of Nf1 f/f ; DhhCre (control) (n = 9) and mice bearing deletion of the receptor GM-CSFR-α (GM-CSFR-α-/-; Nf1 f/f ; DhhCre (n = 18)) or GM-CSFR-β c (GM-CSFR-β c -/-; Nf1 f/f ; DhhCre (n = 16)). ( b ) representative pictures of aged-matched gross dissection of spinal cord from each mouse (Nf1 f/f ; DhhCre (control) (n = 5), GM-CSFR-α-/-; Nf1 f/f ; DhhCre (n = 6) and GM-CSFR-β c -/-; Nf1 f/f ; DhhCre (n = 6)) and quantification of tumor number and size (diameter). White arrows indicate PNF. ( c ) Representative images of tissue sections stained with H&E and ( d ) electromicrographs of saphenous nerve showing the ultrastructure of an intact Schwann cell Remak bundle (blue margin) in WT mice compared to the disrupted Remak structure (blue arrows) in tumor mice in the presence or loss of GM-CSF receptors. ( e ) High percentage (6 or more) of grouped axons indicate a normal Remak bundle. Two-way ANOVA multiple comparison test, * p < 0.05, **** p < 0.00001.

    Article Snippet: For immunohistochemistry (IHC), the procedure was as for immunofluorescence (IF), except that following overnight incubation with anti-GM-CSFR beta rabbit polyclonal antibody (Bioss; cat# bs-3689R, Woburn, MA, USA) or anti-GM-CSFR alpha rabbit polyclonal antibody (Bioss; cat# bs-1457R, USA) at 4 °C, the sections were subsequently incubated with biotinylated goat anti-rabbit secondary antibody (VectorLabs; cat#BA-1000, Newark, CA, USA) for 1 h and rinsed three times in TBST for 5 min each.

    Techniques: Control, Dissection, Staining, Comparison

    Loss of GM-CSFR-β c reduced the presence of myeloid cells. Representative pictures of stained tumor tissue sections and their corresponding quantifications of ( a ) toluidine blue staining for mast cells (red arrows) (representative picture from each group, n = 4), ( b ) CD11c+ dendritic cells, ( c ) Iba – 1+ macrophages and ( d ) CD3+ T cells (white arrows indicate immune cell) (representative picture from tumor tissue of PNF control (n = 5) and each GM-CSFR receptor knockout (n = 6) mice). Two-way ANOVA multiple comparison test, * p < 0.05.

    Journal: Cancers

    Article Title: Granulocyte-Macrophage Colony Stimulating Factor Receptor Contributes to Plexiform Neurofibroma Initiation

    doi: 10.3390/cancers17050905

    Figure Lengend Snippet: Loss of GM-CSFR-β c reduced the presence of myeloid cells. Representative pictures of stained tumor tissue sections and their corresponding quantifications of ( a ) toluidine blue staining for mast cells (red arrows) (representative picture from each group, n = 4), ( b ) CD11c+ dendritic cells, ( c ) Iba – 1+ macrophages and ( d ) CD3+ T cells (white arrows indicate immune cell) (representative picture from tumor tissue of PNF control (n = 5) and each GM-CSFR receptor knockout (n = 6) mice). Two-way ANOVA multiple comparison test, * p < 0.05.

    Article Snippet: For immunohistochemistry (IHC), the procedure was as for immunofluorescence (IF), except that following overnight incubation with anti-GM-CSFR beta rabbit polyclonal antibody (Bioss; cat# bs-3689R, Woburn, MA, USA) or anti-GM-CSFR alpha rabbit polyclonal antibody (Bioss; cat# bs-1457R, USA) at 4 °C, the sections were subsequently incubated with biotinylated goat anti-rabbit secondary antibody (VectorLabs; cat#BA-1000, Newark, CA, USA) for 1 h and rinsed three times in TBST for 5 min each.

    Techniques: Staining, Control, Knock-Out, Comparison

    Altered proteome profile results from lack of GM-CSFR-α and GM-CSFR-β c . ( a ) Images of scanned proteome microarray blots incubated with lysates of tumors from Nf1 f/f ; DhhCre (control) and with GM-CSFR-α or GM-CSFR-β c deletion. ( b ) Heatmap representation of proteome profile. ( c ) Cytokines that robustly increased or decreased after the loss of the GM-CSFR-β c receptor.

    Journal: Cancers

    Article Title: Granulocyte-Macrophage Colony Stimulating Factor Receptor Contributes to Plexiform Neurofibroma Initiation

    doi: 10.3390/cancers17050905

    Figure Lengend Snippet: Altered proteome profile results from lack of GM-CSFR-α and GM-CSFR-β c . ( a ) Images of scanned proteome microarray blots incubated with lysates of tumors from Nf1 f/f ; DhhCre (control) and with GM-CSFR-α or GM-CSFR-β c deletion. ( b ) Heatmap representation of proteome profile. ( c ) Cytokines that robustly increased or decreased after the loss of the GM-CSFR-β c receptor.

    Article Snippet: For immunohistochemistry (IHC), the procedure was as for immunofluorescence (IF), except that following overnight incubation with anti-GM-CSFR beta rabbit polyclonal antibody (Bioss; cat# bs-3689R, Woburn, MA, USA) or anti-GM-CSFR alpha rabbit polyclonal antibody (Bioss; cat# bs-1457R, USA) at 4 °C, the sections were subsequently incubated with biotinylated goat anti-rabbit secondary antibody (VectorLabs; cat#BA-1000, Newark, CA, USA) for 1 h and rinsed three times in TBST for 5 min each.

    Techniques: Microarray, Incubation, Control

    Figure 5. G-/GM-CSF and G-/GM-CSFR in PDX and cell lines. (A) NGS, copy number, (B) G-/GM-CSF cytokine array in different samples and components, (C) mRNA expression in UC PDX, NPC-B13 served as a control. (D) Neutrophil infiltration around the tumor. (E) G-/GM-CSFR expression in UC PDX and cell line xenograft.

    Journal: American Journal of Cancer Research

    Article Title: Paraneoplastic leukocytosis induces NETosis and thrombosis in bladder cancer PDX model

    doi: 10.62347/ihio5742

    Figure Lengend Snippet: Figure 5. G-/GM-CSF and G-/GM-CSFR in PDX and cell lines. (A) NGS, copy number, (B) G-/GM-CSF cytokine array in different samples and components, (C) mRNA expression in UC PDX, NPC-B13 served as a control. (D) Neutrophil infiltration around the tumor. (E) G-/GM-CSFR expression in UC PDX and cell line xenograft.

    Article Snippet: Antibodies used in this study were as follows: G-CSF (Abcam ab197993), G-CSFR (Abcam ab126167), GM-CSF (Santa Cruz Biotechnology SC-32753), GM-CSFR (Santa Cruz Biotechnology SC-21764, SC-456), Histone 3 (citrulline R2 + R8 + R17, Abcam ab5103), Ly6G (eBioscience 17-9668-82), Cleaved PARP (Cell Signaling Technology 95465), p-FGFR1/2/3/4 (Proteintech 11935-1-AP), FGFR2 (Signalway Antibody 32586), p-STAT3 (Cell Signaling Technology 9145), STAT3 (Cell

    Techniques: Expressing, Control

    Figure 10. Summary of innovative treatment targets in paraneoplastic leukocytosis/NETosis/thrombosis in UC Pa tients: 1. Cancer cells secrete growth factors, such as G-CSF and GM-CSF, and express their cognate receptors (G-CSFR or GM-CSFR), initiating autocrine/paracrine loops that enhance tumor growth. 2. Released growth factors stimulate the bone marrow, resulting in the excessive production of neutrophils, contributing to leukocytosis/NETo sis/thrombosis. 3. Systemic NETosis/thrombosis may induce vital organ failure at distant sites, while local NETosis/ thrombosis can retain growth factors, further amplifying the autocrine/paracrine effect. Utilize a combination of cancer-killing therapies, anti-neutrophil interventions, and anti-coagulation measures to comprehensively disrupt the vicious cycle.

    Journal: American Journal of Cancer Research

    Article Title: Paraneoplastic leukocytosis induces NETosis and thrombosis in bladder cancer PDX model

    doi: 10.62347/ihio5742

    Figure Lengend Snippet: Figure 10. Summary of innovative treatment targets in paraneoplastic leukocytosis/NETosis/thrombosis in UC Pa tients: 1. Cancer cells secrete growth factors, such as G-CSF and GM-CSF, and express their cognate receptors (G-CSFR or GM-CSFR), initiating autocrine/paracrine loops that enhance tumor growth. 2. Released growth factors stimulate the bone marrow, resulting in the excessive production of neutrophils, contributing to leukocytosis/NETo sis/thrombosis. 3. Systemic NETosis/thrombosis may induce vital organ failure at distant sites, while local NETosis/ thrombosis can retain growth factors, further amplifying the autocrine/paracrine effect. Utilize a combination of cancer-killing therapies, anti-neutrophil interventions, and anti-coagulation measures to comprehensively disrupt the vicious cycle.

    Article Snippet: Antibodies used in this study were as follows: G-CSF (Abcam ab197993), G-CSFR (Abcam ab126167), GM-CSF (Santa Cruz Biotechnology SC-32753), GM-CSFR (Santa Cruz Biotechnology SC-21764, SC-456), Histone 3 (citrulline R2 + R8 + R17, Abcam ab5103), Ly6G (eBioscience 17-9668-82), Cleaved PARP (Cell Signaling Technology 95465), p-FGFR1/2/3/4 (Proteintech 11935-1-AP), FGFR2 (Signalway Antibody 32586), p-STAT3 (Cell Signaling Technology 9145), STAT3 (Cell

    Techniques: Coagulation