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anti programmed cell death protein 1 pd 1 monoclonal antibody  (Bio X Cell)


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    Bio X Cell anti programmed cell death protein 1 pd 1 monoclonal antibody
    B4GALT2-mediated regulation of immune microenvironment and neoplastic growth. ( A ) The correlation matrix revealed inverse associations between B4GALT2 levels and immune-related transcripts, with prominent immune gene clusters (highlighted by black margins) exhibiting the strongest negative correlations. ( B ) The spatial distribution of CD8 and CD20 lymphocytes was visualized via multiplexed immunofluorescence in regions displaying differential B4GALT2 abundance. ( C, D ) Successful B4GALT2 suppression in LUAD cell lines was validated through immunoblotting and quantitative PCR analyses. ( E–G ) Cellular viability and colony formation capacity following B4GALT2 manipulation were assessed via CCK8 and clonogenic methodologies. ( H ) Experimental design involved subcutaneous inoculation of C57BL/6 mice with 1×10 6 sh-B4galt2 or control LLC cells, followed by administration of <t>either</t> <t>PD-1</t> specific antibody or corresponding IgG2a control. ( I ) Temporal monitoring of tumor progression across treatment groups demonstrated optimal therapeutic efficacy in the shB4galt2+anti-PD1 cohort, manifesting as significantly attenuated tumor expansion. B4GALT2, beta-1,4-galactosyltransferase 2; LUAD, lung adenocarcinoma; PD-1, programmed cell death protein 1.
    Anti Programmed Cell Death Protein 1 Pd 1 Monoclonal Antibody, supplied by Bio X Cell, used in various techniques. Bioz Stars score: 95/100, based on 62 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti programmed cell death protein 1 pd 1 monoclonal antibody/product/Bio X Cell
    Average 95 stars, based on 62 article reviews
    anti programmed cell death protein 1 pd 1 monoclonal antibody - by Bioz Stars, 2026-04
    95/100 stars

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    1) Product Images from "Novel post-translational modification learning signature reveals B4GALT2 as an immune exclusion regulator in lung adenocarcinoma"

    Article Title: Novel post-translational modification learning signature reveals B4GALT2 as an immune exclusion regulator in lung adenocarcinoma

    Journal: Journal for Immunotherapy of Cancer

    doi: 10.1136/jitc-2024-010787

    B4GALT2-mediated regulation of immune microenvironment and neoplastic growth. ( A ) The correlation matrix revealed inverse associations between B4GALT2 levels and immune-related transcripts, with prominent immune gene clusters (highlighted by black margins) exhibiting the strongest negative correlations. ( B ) The spatial distribution of CD8 and CD20 lymphocytes was visualized via multiplexed immunofluorescence in regions displaying differential B4GALT2 abundance. ( C, D ) Successful B4GALT2 suppression in LUAD cell lines was validated through immunoblotting and quantitative PCR analyses. ( E–G ) Cellular viability and colony formation capacity following B4GALT2 manipulation were assessed via CCK8 and clonogenic methodologies. ( H ) Experimental design involved subcutaneous inoculation of C57BL/6 mice with 1×10 6 sh-B4galt2 or control LLC cells, followed by administration of either PD-1 specific antibody or corresponding IgG2a control. ( I ) Temporal monitoring of tumor progression across treatment groups demonstrated optimal therapeutic efficacy in the shB4galt2+anti-PD1 cohort, manifesting as significantly attenuated tumor expansion. B4GALT2, beta-1,4-galactosyltransferase 2; LUAD, lung adenocarcinoma; PD-1, programmed cell death protein 1.
    Figure Legend Snippet: B4GALT2-mediated regulation of immune microenvironment and neoplastic growth. ( A ) The correlation matrix revealed inverse associations between B4GALT2 levels and immune-related transcripts, with prominent immune gene clusters (highlighted by black margins) exhibiting the strongest negative correlations. ( B ) The spatial distribution of CD8 and CD20 lymphocytes was visualized via multiplexed immunofluorescence in regions displaying differential B4GALT2 abundance. ( C, D ) Successful B4GALT2 suppression in LUAD cell lines was validated through immunoblotting and quantitative PCR analyses. ( E–G ) Cellular viability and colony formation capacity following B4GALT2 manipulation were assessed via CCK8 and clonogenic methodologies. ( H ) Experimental design involved subcutaneous inoculation of C57BL/6 mice with 1×10 6 sh-B4galt2 or control LLC cells, followed by administration of either PD-1 specific antibody or corresponding IgG2a control. ( I ) Temporal monitoring of tumor progression across treatment groups demonstrated optimal therapeutic efficacy in the shB4galt2+anti-PD1 cohort, manifesting as significantly attenuated tumor expansion. B4GALT2, beta-1,4-galactosyltransferase 2; LUAD, lung adenocarcinoma; PD-1, programmed cell death protein 1.

    Techniques Used: Immunofluorescence, Western Blot, Real-time Polymerase Chain Reaction, Control

    Synergistic enhancement of anti-PD-1 response via B4GALT2 suppression: modulation of CD8+ T cell phenotypes. ( A ) Flow cytometric analysis demonstrated augmented CD8+ T lymphocyte infiltration following both B4GALT2 suppression and PD-1 blockade, with maximal infiltration observed in the combination therapy cohort. ( B ) Representative cytometric profiles validated that dual intervention (shB4galt2+anti-PD1) substantially elevated activated CD8+ T cell populations while diminishing naive subset abundance. Technical annotation: GZMB serves as a cytolytic activity indicator, CD44/CD69 function as activation status markers, and CD62L identifies naive populations within CD8+ T lymphocytes; statistical significance: *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001, ns, not significant. B4GALT2, beta-1,4-galactosyltransferase 2; LUAD, lung adenocarcinoma; PD-1, programmed cell death protein 1.
    Figure Legend Snippet: Synergistic enhancement of anti-PD-1 response via B4GALT2 suppression: modulation of CD8+ T cell phenotypes. ( A ) Flow cytometric analysis demonstrated augmented CD8+ T lymphocyte infiltration following both B4GALT2 suppression and PD-1 blockade, with maximal infiltration observed in the combination therapy cohort. ( B ) Representative cytometric profiles validated that dual intervention (shB4galt2+anti-PD1) substantially elevated activated CD8+ T cell populations while diminishing naive subset abundance. Technical annotation: GZMB serves as a cytolytic activity indicator, CD44/CD69 function as activation status markers, and CD62L identifies naive populations within CD8+ T lymphocytes; statistical significance: *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001, ns, not significant. B4GALT2, beta-1,4-galactosyltransferase 2; LUAD, lung adenocarcinoma; PD-1, programmed cell death protein 1.

    Techniques Used: Activity Assay, Activation Assay



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    Image Search Results


    B4GALT2-mediated regulation of immune microenvironment and neoplastic growth. ( A ) The correlation matrix revealed inverse associations between B4GALT2 levels and immune-related transcripts, with prominent immune gene clusters (highlighted by black margins) exhibiting the strongest negative correlations. ( B ) The spatial distribution of CD8 and CD20 lymphocytes was visualized via multiplexed immunofluorescence in regions displaying differential B4GALT2 abundance. ( C, D ) Successful B4GALT2 suppression in LUAD cell lines was validated through immunoblotting and quantitative PCR analyses. ( E–G ) Cellular viability and colony formation capacity following B4GALT2 manipulation were assessed via CCK8 and clonogenic methodologies. ( H ) Experimental design involved subcutaneous inoculation of C57BL/6 mice with 1×10 6 sh-B4galt2 or control LLC cells, followed by administration of either PD-1 specific antibody or corresponding IgG2a control. ( I ) Temporal monitoring of tumor progression across treatment groups demonstrated optimal therapeutic efficacy in the shB4galt2+anti-PD1 cohort, manifesting as significantly attenuated tumor expansion. B4GALT2, beta-1,4-galactosyltransferase 2; LUAD, lung adenocarcinoma; PD-1, programmed cell death protein 1.

    Journal: Journal for Immunotherapy of Cancer

    Article Title: Novel post-translational modification learning signature reveals B4GALT2 as an immune exclusion regulator in lung adenocarcinoma

    doi: 10.1136/jitc-2024-010787

    Figure Lengend Snippet: B4GALT2-mediated regulation of immune microenvironment and neoplastic growth. ( A ) The correlation matrix revealed inverse associations between B4GALT2 levels and immune-related transcripts, with prominent immune gene clusters (highlighted by black margins) exhibiting the strongest negative correlations. ( B ) The spatial distribution of CD8 and CD20 lymphocytes was visualized via multiplexed immunofluorescence in regions displaying differential B4GALT2 abundance. ( C, D ) Successful B4GALT2 suppression in LUAD cell lines was validated through immunoblotting and quantitative PCR analyses. ( E–G ) Cellular viability and colony formation capacity following B4GALT2 manipulation were assessed via CCK8 and clonogenic methodologies. ( H ) Experimental design involved subcutaneous inoculation of C57BL/6 mice with 1×10 6 sh-B4galt2 or control LLC cells, followed by administration of either PD-1 specific antibody or corresponding IgG2a control. ( I ) Temporal monitoring of tumor progression across treatment groups demonstrated optimal therapeutic efficacy in the shB4galt2+anti-PD1 cohort, manifesting as significantly attenuated tumor expansion. B4GALT2, beta-1,4-galactosyltransferase 2; LUAD, lung adenocarcinoma; PD-1, programmed cell death protein 1.

    Article Snippet: The study groups were administered either anti-programmed cell death protein 1 (PD-1) monoclonal antibody (BioXcell, BE0146) or isotype-matched IgG control (BioXcell, BE0089) via intraperitoneal route.

    Techniques: Immunofluorescence, Western Blot, Real-time Polymerase Chain Reaction, Control

    Synergistic enhancement of anti-PD-1 response via B4GALT2 suppression: modulation of CD8+ T cell phenotypes. ( A ) Flow cytometric analysis demonstrated augmented CD8+ T lymphocyte infiltration following both B4GALT2 suppression and PD-1 blockade, with maximal infiltration observed in the combination therapy cohort. ( B ) Representative cytometric profiles validated that dual intervention (shB4galt2+anti-PD1) substantially elevated activated CD8+ T cell populations while diminishing naive subset abundance. Technical annotation: GZMB serves as a cytolytic activity indicator, CD44/CD69 function as activation status markers, and CD62L identifies naive populations within CD8+ T lymphocytes; statistical significance: *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001, ns, not significant. B4GALT2, beta-1,4-galactosyltransferase 2; LUAD, lung adenocarcinoma; PD-1, programmed cell death protein 1.

    Journal: Journal for Immunotherapy of Cancer

    Article Title: Novel post-translational modification learning signature reveals B4GALT2 as an immune exclusion regulator in lung adenocarcinoma

    doi: 10.1136/jitc-2024-010787

    Figure Lengend Snippet: Synergistic enhancement of anti-PD-1 response via B4GALT2 suppression: modulation of CD8+ T cell phenotypes. ( A ) Flow cytometric analysis demonstrated augmented CD8+ T lymphocyte infiltration following both B4GALT2 suppression and PD-1 blockade, with maximal infiltration observed in the combination therapy cohort. ( B ) Representative cytometric profiles validated that dual intervention (shB4galt2+anti-PD1) substantially elevated activated CD8+ T cell populations while diminishing naive subset abundance. Technical annotation: GZMB serves as a cytolytic activity indicator, CD44/CD69 function as activation status markers, and CD62L identifies naive populations within CD8+ T lymphocytes; statistical significance: *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001, ns, not significant. B4GALT2, beta-1,4-galactosyltransferase 2; LUAD, lung adenocarcinoma; PD-1, programmed cell death protein 1.

    Article Snippet: The study groups were administered either anti-programmed cell death protein 1 (PD-1) monoclonal antibody (BioXcell, BE0146) or isotype-matched IgG control (BioXcell, BE0089) via intraperitoneal route.

    Techniques: Activity Assay, Activation Assay