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rabbit anti human glut3  (Bio-Rad)


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    Structured Review

    Bio-Rad rabbit anti human glut3
    Figure 1. <t>GLUT3</t> is required for the effector function of Th17 cells (A) Immunoblot analysis of murine GLUT3, ACLY, IRF4, NFATc1, and GAPDH expression. (B) Analysis of Slc2a3 (GLUT3) gene expression in naive CD4+ T cells and T helper (Th) cell subsets by qRT-PCR; mean ± SEM of 5–6 mice. (C and D) Glycolytic proton efflux rate (glycoPER) analyses of WT and GLUT3-deficient Th1 (C) and Th17 (D) cells using a Seahorse extracellular flux analyzer; mean ± SEM of 5 mice. (E) Proliferation analysis of WT and GLUT3-deficient Th1 and Th17 cells.
    Rabbit Anti Human Glut3, supplied by Bio-Rad, used in various techniques. Bioz Stars score: 91/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/rabbit+anti+human+glut3/Rabbit+anti+Human+Glut-1/pm35316657-373-13-15
    Average 91 stars, based on 6 article reviews
    rabbit anti human glut3 - by Bioz Stars, 2026-10
    91/100 stars

    Images

    1) Product Images from "The glucose transporter GLUT3 controls T helper 17 cell responses through glycolytic-epigenetic reprogramming."

    Article Title: The glucose transporter GLUT3 controls T helper 17 cell responses through glycolytic-epigenetic reprogramming.

    Journal: Cell metabolism

    doi: 10.1016/j.cmet.2022.02.015

    Figure 1. GLUT3 is required for the effector function of Th17 cells (A) Immunoblot analysis of murine GLUT3, ACLY, IRF4, NFATc1, and GAPDH expression. (B) Analysis of Slc2a3 (GLUT3) gene expression in naive CD4+ T cells and T helper (Th) cell subsets by qRT-PCR; mean ± SEM of 5–6 mice. (C and D) Glycolytic proton efflux rate (glycoPER) analyses of WT and GLUT3-deficient Th1 (C) and Th17 (D) cells using a Seahorse extracellular flux analyzer; mean ± SEM of 5 mice. (E) Proliferation analysis of WT and GLUT3-deficient Th1 and Th17 cells.
    Figure Legend Snippet: Figure 1. GLUT3 is required for the effector function of Th17 cells (A) Immunoblot analysis of murine GLUT3, ACLY, IRF4, NFATc1, and GAPDH expression. (B) Analysis of Slc2a3 (GLUT3) gene expression in naive CD4+ T cells and T helper (Th) cell subsets by qRT-PCR; mean ± SEM of 5–6 mice. (C and D) Glycolytic proton efflux rate (glycoPER) analyses of WT and GLUT3-deficient Th1 (C) and Th17 (D) cells using a Seahorse extracellular flux analyzer; mean ± SEM of 5 mice. (E) Proliferation analysis of WT and GLUT3-deficient Th1 and Th17 cells.

    Techniques Used: Western Blot, Expressing, Gene Expression, Quantitative RT-PCR

    Figure 2. Ablation of GLUT3 in T cells prevents autoimmunity (A–D) Slc2a3fl/flCd4Cre mice are protected from experimental autoimmune encephalomyelitis (EAE). (A) Clinical EAE scores of WT and Slc2a3fl/flCd4Cre mice after immunization with MOG35-55 peptide emulsified in CFA; mean ± SEM of 9 mice per cohort.
    Figure Legend Snippet: Figure 2. Ablation of GLUT3 in T cells prevents autoimmunity (A–D) Slc2a3fl/flCd4Cre mice are protected from experimental autoimmune encephalomyelitis (EAE). (A) Clinical EAE scores of WT and Slc2a3fl/flCd4Cre mice after immunization with MOG35-55 peptide emulsified in CFA; mean ± SEM of 9 mice per cohort.

    Techniques Used:

    Figure 3. GLUT3 controls a complex metabolic-transcriptional network in Th17 cells (A) Principal component (PC) analysis of WT and GLUT3-deficient (Slc2a3fl/flCd4Cre) Th1 and Th17 cell RNA-seq data; n = 3 biological replicates per T cell subset and genotype. (B and C) MA plots of differentially expressed genes (DEGs) in WT versus GLUT3-deficient Th1 (B) and Th17 cells (C); genes significantly (p adjusted < 0.01) upregulated and downregulated are depicted in red and blue, respectively. (D) Venn diagram analyses of >4-fold DEGs (p adjusted < 0.01) of GLUT3-deficient Th1 and Th17 cells. (E) Gene set enrichment analysis (GSEA) of WT versus GLUT3-deficient Th17 cells. (F) Network clustering of significantly (p < 0.005) enriched gene expression signatures to identify dysregulated physiological processes in GLUT3-deficient Th17 cells. Downegulated and upregulated gene sets in GLUT3-deficient Th17 cells compared with WT are shown in blue and red, respectively. (G) Heatmap analysis of selected genes in GLUT3-deficient and WT Th1 and Th17 cells. (H) GSEAs of WT versus GLUT3-deficient Th17 cells highlight impaired mitochondrial gene expression and function.
    Figure Legend Snippet: Figure 3. GLUT3 controls a complex metabolic-transcriptional network in Th17 cells (A) Principal component (PC) analysis of WT and GLUT3-deficient (Slc2a3fl/flCd4Cre) Th1 and Th17 cell RNA-seq data; n = 3 biological replicates per T cell subset and genotype. (B and C) MA plots of differentially expressed genes (DEGs) in WT versus GLUT3-deficient Th1 (B) and Th17 cells (C); genes significantly (p adjusted < 0.01) upregulated and downregulated are depicted in red and blue, respectively. (D) Venn diagram analyses of >4-fold DEGs (p adjusted < 0.01) of GLUT3-deficient Th1 and Th17 cells. (E) Gene set enrichment analysis (GSEA) of WT versus GLUT3-deficient Th17 cells. (F) Network clustering of significantly (p < 0.005) enriched gene expression signatures to identify dysregulated physiological processes in GLUT3-deficient Th17 cells. Downegulated and upregulated gene sets in GLUT3-deficient Th17 cells compared with WT are shown in blue and red, respectively. (G) Heatmap analysis of selected genes in GLUT3-deficient and WT Th1 and Th17 cells. (H) GSEAs of WT versus GLUT3-deficient Th17 cells highlight impaired mitochondrial gene expression and function.

    Techniques Used: RNA Sequencing, Gene Expression

    Related Articles

    Incubation:

    Article Title: The glucose transporter GLUT3 controls T helper 17 cell responses through glycolytic-epigenetic reprogramming.
    Article Snippet: For immunofluorescence staining, Jurkat T cells were spun on Superfrost slides (Roth), dried and fixed with 4% PFA. .. After an 1 h incubation at RT with mouse-anti-Tom20 (Abcam, clone EPR15581-39) and rabbit-anti-human GLUT3 (BioRad), the samples were washed and stained for 1 h with secondary donkey anti-rabbit IgG (H+L) Alexa Fluor 488 and donkey anti-mouse IgG (H+L) Alexa Fluor 647 antibodies (both Invitrogen). .. To detect T cell infiltration in tissues, sections were deparaffinized and re-hydrated before antigen retrieval was achieved by heating in 10 mM citric acid buffer (pH 6.0) in a high-pressure cooker (Deni) for 20 min, followed by blocking with antibody diluent (Dako) for 1 h. After an overnight incubation with a rabbit anti-mouse CD3 (1:1000, Dako) at 4 C, the slides were washed and stained for 1 h with a donkey anti-rabbit IgG (H+L) Alexa Fluor 546 (1:800; Invitrogen).

    Staining:

    Article Title: The glucose transporter GLUT3 controls T helper 17 cell responses through glycolytic-epigenetic reprogramming.
    Article Snippet: For immunofluorescence staining, Jurkat T cells were spun on Superfrost slides (Roth), dried and fixed with 4% PFA. .. After an 1 h incubation at RT with mouse-anti-Tom20 (Abcam, clone EPR15581-39) and rabbit-anti-human GLUT3 (BioRad), the samples were washed and stained for 1 h with secondary donkey anti-rabbit IgG (H+L) Alexa Fluor 488 and donkey anti-mouse IgG (H+L) Alexa Fluor 647 antibodies (both Invitrogen). .. To detect T cell infiltration in tissues, sections were deparaffinized and re-hydrated before antigen retrieval was achieved by heating in 10 mM citric acid buffer (pH 6.0) in a high-pressure cooker (Deni) for 20 min, followed by blocking with antibody diluent (Dako) for 1 h. After an overnight incubation with a rabbit anti-mouse CD3 (1:1000, Dako) at 4 C, the slides were washed and stained for 1 h with a donkey anti-rabbit IgG (H+L) Alexa Fluor 546 (1:800; Invitrogen).



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    Figure 1. <t>GLUT3</t> is required for the effector function of Th17 cells (A) Immunoblot analysis of murine GLUT3, ACLY, IRF4, NFATc1, and GAPDH expression. (B) Analysis of Slc2a3 (GLUT3) gene expression in naive CD4+ T cells and T helper (Th) cell subsets by qRT-PCR; mean ± SEM of 5–6 mice. (C and D) Glycolytic proton efflux rate (glycoPER) analyses of WT and GLUT3-deficient Th1 (C) and Th17 (D) cells using a Seahorse extracellular flux analyzer; mean ± SEM of 5 mice. (E) Proliferation analysis of WT and GLUT3-deficient Th1 and Th17 cells.
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    Figure 1. <t>GLUT3</t> is required for the effector function of Th17 cells (A) Immunoblot analysis of murine GLUT3, ACLY, IRF4, NFATc1, and GAPDH expression. (B) Analysis of Slc2a3 (GLUT3) gene expression in naive CD4+ T cells and T helper (Th) cell subsets by qRT-PCR; mean ± SEM of 5–6 mice. (C and D) Glycolytic proton efflux rate (glycoPER) analyses of WT and GLUT3-deficient Th1 (C) and Th17 (D) cells using a Seahorse extracellular flux analyzer; mean ± SEM of 5 mice. (E) Proliferation analysis of WT and GLUT3-deficient Th1 and Th17 cells.
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    A) GLUT1 membrane immunostaining in oral squamous cell carcinoma, 400×; B) GLUT1 expression in oral squamous cell carcinoma. Note both GLUT1 expression: membrane and nucleus (arrows), 200×; C) <t>GLUT3</t> membrane immunostaining in oral squamous cell carcinoma; D) No GLUT3 immunostaining. Note also GLUT3 expression in the inflammatory cells, 200×.
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    Image Search Results


    Figure 1. GLUT3 is required for the effector function of Th17 cells (A) Immunoblot analysis of murine GLUT3, ACLY, IRF4, NFATc1, and GAPDH expression. (B) Analysis of Slc2a3 (GLUT3) gene expression in naive CD4+ T cells and T helper (Th) cell subsets by qRT-PCR; mean ± SEM of 5–6 mice. (C and D) Glycolytic proton efflux rate (glycoPER) analyses of WT and GLUT3-deficient Th1 (C) and Th17 (D) cells using a Seahorse extracellular flux analyzer; mean ± SEM of 5 mice. (E) Proliferation analysis of WT and GLUT3-deficient Th1 and Th17 cells.

    Journal: Cell metabolism

    Article Title: The glucose transporter GLUT3 controls T helper 17 cell responses through glycolytic-epigenetic reprogramming.

    doi: 10.1016/j.cmet.2022.02.015

    Figure Lengend Snippet: Figure 1. GLUT3 is required for the effector function of Th17 cells (A) Immunoblot analysis of murine GLUT3, ACLY, IRF4, NFATc1, and GAPDH expression. (B) Analysis of Slc2a3 (GLUT3) gene expression in naive CD4+ T cells and T helper (Th) cell subsets by qRT-PCR; mean ± SEM of 5–6 mice. (C and D) Glycolytic proton efflux rate (glycoPER) analyses of WT and GLUT3-deficient Th1 (C) and Th17 (D) cells using a Seahorse extracellular flux analyzer; mean ± SEM of 5 mice. (E) Proliferation analysis of WT and GLUT3-deficient Th1 and Th17 cells.

    Article Snippet: After an 1 h incubation at RT with mouse-anti-Tom20 (Abcam, clone EPR15581-39) and rabbit-anti-human GLUT3 (BioRad), the samples were washed and stained for 1 h with secondary donkey anti-rabbit IgG (H+L) Alexa Fluor 488 and donkey anti-mouse IgG (H+L) Alexa Fluor 647 antibodies (both Invitrogen).

    Techniques: Western Blot, Expressing, Gene Expression, Quantitative RT-PCR

    Figure 2. Ablation of GLUT3 in T cells prevents autoimmunity (A–D) Slc2a3fl/flCd4Cre mice are protected from experimental autoimmune encephalomyelitis (EAE). (A) Clinical EAE scores of WT and Slc2a3fl/flCd4Cre mice after immunization with MOG35-55 peptide emulsified in CFA; mean ± SEM of 9 mice per cohort.

    Journal: Cell metabolism

    Article Title: The glucose transporter GLUT3 controls T helper 17 cell responses through glycolytic-epigenetic reprogramming.

    doi: 10.1016/j.cmet.2022.02.015

    Figure Lengend Snippet: Figure 2. Ablation of GLUT3 in T cells prevents autoimmunity (A–D) Slc2a3fl/flCd4Cre mice are protected from experimental autoimmune encephalomyelitis (EAE). (A) Clinical EAE scores of WT and Slc2a3fl/flCd4Cre mice after immunization with MOG35-55 peptide emulsified in CFA; mean ± SEM of 9 mice per cohort.

    Article Snippet: After an 1 h incubation at RT with mouse-anti-Tom20 (Abcam, clone EPR15581-39) and rabbit-anti-human GLUT3 (BioRad), the samples were washed and stained for 1 h with secondary donkey anti-rabbit IgG (H+L) Alexa Fluor 488 and donkey anti-mouse IgG (H+L) Alexa Fluor 647 antibodies (both Invitrogen).

    Techniques:

    Figure 3. GLUT3 controls a complex metabolic-transcriptional network in Th17 cells (A) Principal component (PC) analysis of WT and GLUT3-deficient (Slc2a3fl/flCd4Cre) Th1 and Th17 cell RNA-seq data; n = 3 biological replicates per T cell subset and genotype. (B and C) MA plots of differentially expressed genes (DEGs) in WT versus GLUT3-deficient Th1 (B) and Th17 cells (C); genes significantly (p adjusted < 0.01) upregulated and downregulated are depicted in red and blue, respectively. (D) Venn diagram analyses of >4-fold DEGs (p adjusted < 0.01) of GLUT3-deficient Th1 and Th17 cells. (E) Gene set enrichment analysis (GSEA) of WT versus GLUT3-deficient Th17 cells. (F) Network clustering of significantly (p < 0.005) enriched gene expression signatures to identify dysregulated physiological processes in GLUT3-deficient Th17 cells. Downegulated and upregulated gene sets in GLUT3-deficient Th17 cells compared with WT are shown in blue and red, respectively. (G) Heatmap analysis of selected genes in GLUT3-deficient and WT Th1 and Th17 cells. (H) GSEAs of WT versus GLUT3-deficient Th17 cells highlight impaired mitochondrial gene expression and function.

    Journal: Cell metabolism

    Article Title: The glucose transporter GLUT3 controls T helper 17 cell responses through glycolytic-epigenetic reprogramming.

    doi: 10.1016/j.cmet.2022.02.015

    Figure Lengend Snippet: Figure 3. GLUT3 controls a complex metabolic-transcriptional network in Th17 cells (A) Principal component (PC) analysis of WT and GLUT3-deficient (Slc2a3fl/flCd4Cre) Th1 and Th17 cell RNA-seq data; n = 3 biological replicates per T cell subset and genotype. (B and C) MA plots of differentially expressed genes (DEGs) in WT versus GLUT3-deficient Th1 (B) and Th17 cells (C); genes significantly (p adjusted < 0.01) upregulated and downregulated are depicted in red and blue, respectively. (D) Venn diagram analyses of >4-fold DEGs (p adjusted < 0.01) of GLUT3-deficient Th1 and Th17 cells. (E) Gene set enrichment analysis (GSEA) of WT versus GLUT3-deficient Th17 cells. (F) Network clustering of significantly (p < 0.005) enriched gene expression signatures to identify dysregulated physiological processes in GLUT3-deficient Th17 cells. Downegulated and upregulated gene sets in GLUT3-deficient Th17 cells compared with WT are shown in blue and red, respectively. (G) Heatmap analysis of selected genes in GLUT3-deficient and WT Th1 and Th17 cells. (H) GSEAs of WT versus GLUT3-deficient Th17 cells highlight impaired mitochondrial gene expression and function.

    Article Snippet: After an 1 h incubation at RT with mouse-anti-Tom20 (Abcam, clone EPR15581-39) and rabbit-anti-human GLUT3 (BioRad), the samples were washed and stained for 1 h with secondary donkey anti-rabbit IgG (H+L) Alexa Fluor 488 and donkey anti-mouse IgG (H+L) Alexa Fluor 647 antibodies (both Invitrogen).

    Techniques: RNA Sequencing, Gene Expression

    A) GLUT1 membrane immunostaining in oral squamous cell carcinoma, 400×; B) GLUT1 expression in oral squamous cell carcinoma. Note both GLUT1 expression: membrane and nucleus (arrows), 200×; C) GLUT3 membrane immunostaining in oral squamous cell carcinoma; D) No GLUT3 immunostaining. Note also GLUT3 expression in the inflammatory cells, 200×.

    Journal: Molecules

    Article Title: Glut1 and Glut3 as Potential Prognostic Markers for Oral Squamous Cell Carcinoma

    doi: 10.3390/molecules15042374

    Figure Lengend Snippet: A) GLUT1 membrane immunostaining in oral squamous cell carcinoma, 400×; B) GLUT1 expression in oral squamous cell carcinoma. Note both GLUT1 expression: membrane and nucleus (arrows), 200×; C) GLUT3 membrane immunostaining in oral squamous cell carcinoma; D) No GLUT3 immunostaining. Note also GLUT3 expression in the inflammatory cells, 200×.

    Article Snippet: The sections were then incubated with the polyclonal rabbit anti-human GLUT1 antibody (DAKO, Carpenteria, CA, USA) used at 1/500, and with polyclonal rabbit anti-human GLUT3 antibody (Lab Vision Corporation, Fremont, CA, USA) at 1/400, for 2 h at room temperature.

    Techniques: Immunostaining, Expressing

    Association between  GLUT3  expression and clinic-pathological feature in OSCC.

    Journal: Molecules

    Article Title: Glut1 and Glut3 as Potential Prognostic Markers for Oral Squamous Cell Carcinoma

    doi: 10.3390/molecules15042374

    Figure Lengend Snippet: Association between GLUT3 expression and clinic-pathological feature in OSCC.

    Article Snippet: The sections were then incubated with the polyclonal rabbit anti-human GLUT1 antibody (DAKO, Carpenteria, CA, USA) used at 1/500, and with polyclonal rabbit anti-human GLUT3 antibody (Lab Vision Corporation, Fremont, CA, USA) at 1/400, for 2 h at room temperature.

    Techniques: Expressing

    a) Kaplan –Meier curve of overall survival at five years in patients with OSCC (52.1%); b) Overall survival as a function of GLUT1 staining pattern ( p = 0.015); c) Overall survival as a function of GLUT1 frequency, according to stratified cells ( p = 0.041); d) Overall survival as a function of GLUT3 staining pattern (negative or positive) ( p = 0.002).

    Journal: Molecules

    Article Title: Glut1 and Glut3 as Potential Prognostic Markers for Oral Squamous Cell Carcinoma

    doi: 10.3390/molecules15042374

    Figure Lengend Snippet: a) Kaplan –Meier curve of overall survival at five years in patients with OSCC (52.1%); b) Overall survival as a function of GLUT1 staining pattern ( p = 0.015); c) Overall survival as a function of GLUT1 frequency, according to stratified cells ( p = 0.041); d) Overall survival as a function of GLUT3 staining pattern (negative or positive) ( p = 0.002).

    Article Snippet: The sections were then incubated with the polyclonal rabbit anti-human GLUT1 antibody (DAKO, Carpenteria, CA, USA) used at 1/500, and with polyclonal rabbit anti-human GLUT3 antibody (Lab Vision Corporation, Fremont, CA, USA) at 1/400, for 2 h at room temperature.

    Techniques: Staining

    Kaplan – Meier curve of disease - free survival as a function of GLUT3 staining pattern ( p = 0.021).

    Journal: Molecules

    Article Title: Glut1 and Glut3 as Potential Prognostic Markers for Oral Squamous Cell Carcinoma

    doi: 10.3390/molecules15042374

    Figure Lengend Snippet: Kaplan – Meier curve of disease - free survival as a function of GLUT3 staining pattern ( p = 0.021).

    Article Snippet: The sections were then incubated with the polyclonal rabbit anti-human GLUT1 antibody (DAKO, Carpenteria, CA, USA) used at 1/500, and with polyclonal rabbit anti-human GLUT3 antibody (Lab Vision Corporation, Fremont, CA, USA) at 1/400, for 2 h at room temperature.

    Techniques: Staining