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stable gene knockdown cells  (Genechem)

 
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    Genechem stable gene knockdown cells
    PYCR1 <t>knockdown</t> impairs proline synthesis and suppresses the PI3K/AKT/mTOR signaling pathway in BLCA <t>cells.</t> ( A ) Quantification of intracellular proline levels in T24 and J82 cells after PYCR1 knockdown. ( B ) Correlation analysis showing positive associations between PYCR1 expression and SLC1A5 (left) and P5CS (right) in BLCA samples. ( C ) Western blot analysis confirming that knockdown of PYCR1 reduces protein expression levels of P5CS and SLC1A5. ( D ) Heatmap of differentially expressed <t>genes</t> in BLCA cells following PYCR1 knockdown from RNA-seq data. ( E - F ) Pathway enrichment analyses of downregulated ( E ) and upregulated ( F ) genes after PYCR1 knockdown, indicating involvement in PI3K-AKT and immune-related signaling pathways. ( G ) Western blot analysis validating the downregulation of PI3K, AKT, and mTOR pathway components upon PYCR1 knockdown in T24 and J82 cells. ( H ) Western blot analysis of PI3K/AKT/mTOR pathway activation following PYCR1 overexpression with or without LY294002 treatment in T24 and J82 cells. PYCR1 overexpression increased phosphorylation of PI3K, AKT, and mTOR, which was reversed by the PI3K inhibitor. Vinculin served as the loading control. Data are presented as mean ± SD from three independent experiments. * P < 0.05, ** P < 0.01; oe: Overexpression
    Stable Gene Knockdown Cells, supplied by Genechem, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/stable gene knockdown cells/product/Genechem
    Average 86 stars, based on 1 article reviews
    stable gene knockdown cells - by Bioz Stars, 2026-06
    86/100 stars

    Images

    1) Product Images from "Glutamine metabolism reprogramming promotes bladder cancer progression via PYCR1: a multi-omics and functional validation study"

    Article Title: Glutamine metabolism reprogramming promotes bladder cancer progression via PYCR1: a multi-omics and functional validation study

    Journal: Journal of Translational Medicine

    doi: 10.1186/s12967-025-07386-2

    PYCR1 knockdown impairs proline synthesis and suppresses the PI3K/AKT/mTOR signaling pathway in BLCA cells. ( A ) Quantification of intracellular proline levels in T24 and J82 cells after PYCR1 knockdown. ( B ) Correlation analysis showing positive associations between PYCR1 expression and SLC1A5 (left) and P5CS (right) in BLCA samples. ( C ) Western blot analysis confirming that knockdown of PYCR1 reduces protein expression levels of P5CS and SLC1A5. ( D ) Heatmap of differentially expressed genes in BLCA cells following PYCR1 knockdown from RNA-seq data. ( E - F ) Pathway enrichment analyses of downregulated ( E ) and upregulated ( F ) genes after PYCR1 knockdown, indicating involvement in PI3K-AKT and immune-related signaling pathways. ( G ) Western blot analysis validating the downregulation of PI3K, AKT, and mTOR pathway components upon PYCR1 knockdown in T24 and J82 cells. ( H ) Western blot analysis of PI3K/AKT/mTOR pathway activation following PYCR1 overexpression with or without LY294002 treatment in T24 and J82 cells. PYCR1 overexpression increased phosphorylation of PI3K, AKT, and mTOR, which was reversed by the PI3K inhibitor. Vinculin served as the loading control. Data are presented as mean ± SD from three independent experiments. * P < 0.05, ** P < 0.01; oe: Overexpression
    Figure Legend Snippet: PYCR1 knockdown impairs proline synthesis and suppresses the PI3K/AKT/mTOR signaling pathway in BLCA cells. ( A ) Quantification of intracellular proline levels in T24 and J82 cells after PYCR1 knockdown. ( B ) Correlation analysis showing positive associations between PYCR1 expression and SLC1A5 (left) and P5CS (right) in BLCA samples. ( C ) Western blot analysis confirming that knockdown of PYCR1 reduces protein expression levels of P5CS and SLC1A5. ( D ) Heatmap of differentially expressed genes in BLCA cells following PYCR1 knockdown from RNA-seq data. ( E - F ) Pathway enrichment analyses of downregulated ( E ) and upregulated ( F ) genes after PYCR1 knockdown, indicating involvement in PI3K-AKT and immune-related signaling pathways. ( G ) Western blot analysis validating the downregulation of PI3K, AKT, and mTOR pathway components upon PYCR1 knockdown in T24 and J82 cells. ( H ) Western blot analysis of PI3K/AKT/mTOR pathway activation following PYCR1 overexpression with or without LY294002 treatment in T24 and J82 cells. PYCR1 overexpression increased phosphorylation of PI3K, AKT, and mTOR, which was reversed by the PI3K inhibitor. Vinculin served as the loading control. Data are presented as mean ± SD from three independent experiments. * P < 0.05, ** P < 0.01; oe: Overexpression

    Techniques Used: Knockdown, Expressing, Western Blot, RNA Sequencing, Protein-Protein interactions, Activation Assay, Over Expression, Phospho-proteomics, Control



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    stable gene knockdown cells  (Genechem)
    86
    Genechem stable gene knockdown cells
    PYCR1 <t>knockdown</t> impairs proline synthesis and suppresses the PI3K/AKT/mTOR signaling pathway in BLCA <t>cells.</t> ( A ) Quantification of intracellular proline levels in T24 and J82 cells after PYCR1 knockdown. ( B ) Correlation analysis showing positive associations between PYCR1 expression and SLC1A5 (left) and P5CS (right) in BLCA samples. ( C ) Western blot analysis confirming that knockdown of PYCR1 reduces protein expression levels of P5CS and SLC1A5. ( D ) Heatmap of differentially expressed <t>genes</t> in BLCA cells following PYCR1 knockdown from RNA-seq data. ( E - F ) Pathway enrichment analyses of downregulated ( E ) and upregulated ( F ) genes after PYCR1 knockdown, indicating involvement in PI3K-AKT and immune-related signaling pathways. ( G ) Western blot analysis validating the downregulation of PI3K, AKT, and mTOR pathway components upon PYCR1 knockdown in T24 and J82 cells. ( H ) Western blot analysis of PI3K/AKT/mTOR pathway activation following PYCR1 overexpression with or without LY294002 treatment in T24 and J82 cells. PYCR1 overexpression increased phosphorylation of PI3K, AKT, and mTOR, which was reversed by the PI3K inhibitor. Vinculin served as the loading control. Data are presented as mean ± SD from three independent experiments. * P < 0.05, ** P < 0.01; oe: Overexpression
    Stable Gene Knockdown Cells, supplied by Genechem, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/stable gene knockdown cells/product/Genechem
    Average 86 stars, based on 1 article reviews
    stable gene knockdown cells - by Bioz Stars, 2026-06
    86/100 stars
    		  Buy from Supplier
    plasmids constructing stable cells overexpression knockdown target genes  (Thermo Fisher)
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    Thermo Fisher plasmids constructing stable cells overexpression knockdown target genes
    PYCR1 <t>knockdown</t> impairs proline synthesis and suppresses the PI3K/AKT/mTOR signaling pathway in BLCA <t>cells.</t> ( A ) Quantification of intracellular proline levels in T24 and J82 cells after PYCR1 knockdown. ( B ) Correlation analysis showing positive associations between PYCR1 expression and SLC1A5 (left) and P5CS (right) in BLCA samples. ( C ) Western blot analysis confirming that knockdown of PYCR1 reduces protein expression levels of P5CS and SLC1A5. ( D ) Heatmap of differentially expressed <t>genes</t> in BLCA cells following PYCR1 knockdown from RNA-seq data. ( E - F ) Pathway enrichment analyses of downregulated ( E ) and upregulated ( F ) genes after PYCR1 knockdown, indicating involvement in PI3K-AKT and immune-related signaling pathways. ( G ) Western blot analysis validating the downregulation of PI3K, AKT, and mTOR pathway components upon PYCR1 knockdown in T24 and J82 cells. ( H ) Western blot analysis of PI3K/AKT/mTOR pathway activation following PYCR1 overexpression with or without LY294002 treatment in T24 and J82 cells. PYCR1 overexpression increased phosphorylation of PI3K, AKT, and mTOR, which was reversed by the PI3K inhibitor. Vinculin served as the loading control. Data are presented as mean ± SD from three independent experiments. * P < 0.05, ** P < 0.01; oe: Overexpression
    Plasmids Constructing Stable Cells Overexpression Knockdown Target Genes, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/plasmids constructing stable cells overexpression knockdown target genes/product/Thermo Fisher
    Average 90 stars, based on 1 article reviews
    plasmids constructing stable cells overexpression knockdown target genes - by Bioz Stars, 2026-06
    90/100 stars
    		  Buy from Supplier

    Image Search Results


    PYCR1 knockdown impairs proline synthesis and suppresses the PI3K/AKT/mTOR signaling pathway in BLCA cells. ( A ) Quantification of intracellular proline levels in T24 and J82 cells after PYCR1 knockdown. ( B ) Correlation analysis showing positive associations between PYCR1 expression and SLC1A5 (left) and P5CS (right) in BLCA samples. ( C ) Western blot analysis confirming that knockdown of PYCR1 reduces protein expression levels of P5CS and SLC1A5. ( D ) Heatmap of differentially expressed genes in BLCA cells following PYCR1 knockdown from RNA-seq data. ( E - F ) Pathway enrichment analyses of downregulated ( E ) and upregulated ( F ) genes after PYCR1 knockdown, indicating involvement in PI3K-AKT and immune-related signaling pathways. ( G ) Western blot analysis validating the downregulation of PI3K, AKT, and mTOR pathway components upon PYCR1 knockdown in T24 and J82 cells. ( H ) Western blot analysis of PI3K/AKT/mTOR pathway activation following PYCR1 overexpression with or without LY294002 treatment in T24 and J82 cells. PYCR1 overexpression increased phosphorylation of PI3K, AKT, and mTOR, which was reversed by the PI3K inhibitor. Vinculin served as the loading control. Data are presented as mean ± SD from three independent experiments. * P < 0.05, ** P < 0.01; oe: Overexpression

    Journal: Journal of Translational Medicine

    Article Title: Glutamine metabolism reprogramming promotes bladder cancer progression via PYCR1: a multi-omics and functional validation study

    doi: 10.1186/s12967-025-07386-2

    Figure Lengend Snippet: PYCR1 knockdown impairs proline synthesis and suppresses the PI3K/AKT/mTOR signaling pathway in BLCA cells. ( A ) Quantification of intracellular proline levels in T24 and J82 cells after PYCR1 knockdown. ( B ) Correlation analysis showing positive associations between PYCR1 expression and SLC1A5 (left) and P5CS (right) in BLCA samples. ( C ) Western blot analysis confirming that knockdown of PYCR1 reduces protein expression levels of P5CS and SLC1A5. ( D ) Heatmap of differentially expressed genes in BLCA cells following PYCR1 knockdown from RNA-seq data. ( E - F ) Pathway enrichment analyses of downregulated ( E ) and upregulated ( F ) genes after PYCR1 knockdown, indicating involvement in PI3K-AKT and immune-related signaling pathways. ( G ) Western blot analysis validating the downregulation of PI3K, AKT, and mTOR pathway components upon PYCR1 knockdown in T24 and J82 cells. ( H ) Western blot analysis of PI3K/AKT/mTOR pathway activation following PYCR1 overexpression with or without LY294002 treatment in T24 and J82 cells. PYCR1 overexpression increased phosphorylation of PI3K, AKT, and mTOR, which was reversed by the PI3K inhibitor. Vinculin served as the loading control. Data are presented as mean ± SD from three independent experiments. * P < 0.05, ** P < 0.01; oe: Overexpression

    Article Snippet: To generate stable gene knockdown cells, lentiviral vectors expressing specific short hairpin RNA (shRNA) sequences targeting the desired gene, along with corresponding negative controls, were sourced from Genechem (Shanghai, China).

    Techniques: Knockdown, Expressing, Western Blot, RNA Sequencing, Protein-Protein interactions, Activation Assay, Over Expression, Phospho-proteomics, Control