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electroporation buffer  (Amaxa)

 
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    Structured Review

    Amaxa electroporation buffer
    (A) Schematic of CRISPR/Cas9-mediated BAP1 knockout (BKO) in patient-derived normal (PDON) and tumour (PDOT) organoids. The cross indicates unsuccessful expansion. (B) Tracking of variant allelic frequency (VAF) in normal kidney organoids following <t>electroporation</t> with guide RNAs targeting PBRM1 or BAP1 . (C) Schematic of CRISPR/Cas9-mediated BAP1 knockout (BKO) in normal organoids (K1088N1_GN1) with concurrent CDKN2A and VHL loss (CV background). (D) Principal-component analysis (PCA) of bulk transcriptomes from parental and BAP1 -engineered organoid lines. (E) GSEA of BAP1 -KO tumour organoids versus parental controls using the Hallmark E2F Targets gene set. (F) Comparison of normalised expression (DESeq2 VST) of selected genes between BAP1 -KO and parental tumour organoids ( n = 5 PDOT, n = 6 PDOT-BKO). Unpaired t -test; *: p < 0.01. (G) GSEA of BAP1 -KO tumour organoids versus parental controls using the Gene Ontology Biological Process (GOBP) Chromosome Segregation gene set. (H) Representative DAPI staining showing micronucleus presence in BAP1 -KO and parental tumour organoids. Scale bar, 50 µm. (I) Violin plot showing the number of clonal copy-number variants (CNVs), excluding chromosome 3p loss, in tumours with clonal BAP1 or PBRM1 mutations. Unpaired t -test; p = 0.0703. Clonal PBRM1 , n = 25; clonal BAP1 , n = 7. (J) Heatmap showing normalised accessibility scores for the top 1000 differentially accessible regions (DARs) between BAP1 -WT and BAP1 -KO organoids. (K) Genomic annotation of regions with increased (top) or decreased (bottom) chromatin accessibility following BAP1 loss. UTR, untranslated region. (L) Volcano plot showing differential transcription-factor binding activities between BAP1 -WT and BAP1 -KO tumour organoids. Significance was defined by −log10(p-value) above the 95% quantile and differential binding scores in top 5% in each direction. See also Figure S8 and Table S7.
    Electroporation Buffer, supplied by Amaxa, 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/product/electroporation+buffer/bio_rxiv__64898__2026__04__30__721837-302-14-16?v=Amaxa
    Average 86 stars, based on 1 article reviews
    electroporation buffer - by Bioz Stars, 2026-08
    86/100 stars

    Images

    1) Product Images from "Distinct functions of PBRM1 and BAP1 reconcile the course of kidney cancer evolution and disease progression"

    Article Title: Distinct functions of PBRM1 and BAP1 reconcile the course of kidney cancer evolution and disease progression

    Journal: bioRxiv

    doi: 10.64898/2026.04.30.721837

    (A) Schematic of CRISPR/Cas9-mediated BAP1 knockout (BKO) in patient-derived normal (PDON) and tumour (PDOT) organoids. The cross indicates unsuccessful expansion. (B) Tracking of variant allelic frequency (VAF) in normal kidney organoids following electroporation with guide RNAs targeting PBRM1 or BAP1 . (C) Schematic of CRISPR/Cas9-mediated BAP1 knockout (BKO) in normal organoids (K1088N1_GN1) with concurrent CDKN2A and VHL loss (CV background). (D) Principal-component analysis (PCA) of bulk transcriptomes from parental and BAP1 -engineered organoid lines. (E) GSEA of BAP1 -KO tumour organoids versus parental controls using the Hallmark E2F Targets gene set. (F) Comparison of normalised expression (DESeq2 VST) of selected genes between BAP1 -KO and parental tumour organoids ( n = 5 PDOT, n = 6 PDOT-BKO). Unpaired t -test; *: p < 0.01. (G) GSEA of BAP1 -KO tumour organoids versus parental controls using the Gene Ontology Biological Process (GOBP) Chromosome Segregation gene set. (H) Representative DAPI staining showing micronucleus presence in BAP1 -KO and parental tumour organoids. Scale bar, 50 µm. (I) Violin plot showing the number of clonal copy-number variants (CNVs), excluding chromosome 3p loss, in tumours with clonal BAP1 or PBRM1 mutations. Unpaired t -test; p = 0.0703. Clonal PBRM1 , n = 25; clonal BAP1 , n = 7. (J) Heatmap showing normalised accessibility scores for the top 1000 differentially accessible regions (DARs) between BAP1 -WT and BAP1 -KO organoids. (K) Genomic annotation of regions with increased (top) or decreased (bottom) chromatin accessibility following BAP1 loss. UTR, untranslated region. (L) Volcano plot showing differential transcription-factor binding activities between BAP1 -WT and BAP1 -KO tumour organoids. Significance was defined by −log10(p-value) above the 95% quantile and differential binding scores in top 5% in each direction. See also Figure S8 and Table S7.
    Figure Legend Snippet: (A) Schematic of CRISPR/Cas9-mediated BAP1 knockout (BKO) in patient-derived normal (PDON) and tumour (PDOT) organoids. The cross indicates unsuccessful expansion. (B) Tracking of variant allelic frequency (VAF) in normal kidney organoids following electroporation with guide RNAs targeting PBRM1 or BAP1 . (C) Schematic of CRISPR/Cas9-mediated BAP1 knockout (BKO) in normal organoids (K1088N1_GN1) with concurrent CDKN2A and VHL loss (CV background). (D) Principal-component analysis (PCA) of bulk transcriptomes from parental and BAP1 -engineered organoid lines. (E) GSEA of BAP1 -KO tumour organoids versus parental controls using the Hallmark E2F Targets gene set. (F) Comparison of normalised expression (DESeq2 VST) of selected genes between BAP1 -KO and parental tumour organoids ( n = 5 PDOT, n = 6 PDOT-BKO). Unpaired t -test; *: p < 0.01. (G) GSEA of BAP1 -KO tumour organoids versus parental controls using the Gene Ontology Biological Process (GOBP) Chromosome Segregation gene set. (H) Representative DAPI staining showing micronucleus presence in BAP1 -KO and parental tumour organoids. Scale bar, 50 µm. (I) Violin plot showing the number of clonal copy-number variants (CNVs), excluding chromosome 3p loss, in tumours with clonal BAP1 or PBRM1 mutations. Unpaired t -test; p = 0.0703. Clonal PBRM1 , n = 25; clonal BAP1 , n = 7. (J) Heatmap showing normalised accessibility scores for the top 1000 differentially accessible regions (DARs) between BAP1 -WT and BAP1 -KO organoids. (K) Genomic annotation of regions with increased (top) or decreased (bottom) chromatin accessibility following BAP1 loss. UTR, untranslated region. (L) Volcano plot showing differential transcription-factor binding activities between BAP1 -WT and BAP1 -KO tumour organoids. Significance was defined by −log10(p-value) above the 95% quantile and differential binding scores in top 5% in each direction. See also Figure S8 and Table S7.

    Techniques Used: CRISPR, Knock-Out, Derivative Assay, Variant Assay, Electroporation, Comparison, Expressing, Staining, Binding Assay



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    (A) Schematic of CRISPR/Cas9-mediated BAP1 knockout (BKO) in patient-derived normal (PDON) and tumour (PDOT) organoids. The cross indicates unsuccessful expansion. (B) Tracking of variant allelic frequency (VAF) in normal kidney organoids following <t>electroporation</t> with guide RNAs targeting PBRM1 or BAP1 . (C) Schematic of CRISPR/Cas9-mediated BAP1 knockout (BKO) in normal organoids (K1088N1_GN1) with concurrent CDKN2A and VHL loss (CV background). (D) Principal-component analysis (PCA) of bulk transcriptomes from parental and BAP1 -engineered organoid lines. (E) GSEA of BAP1 -KO tumour organoids versus parental controls using the Hallmark E2F Targets gene set. (F) Comparison of normalised expression (DESeq2 VST) of selected genes between BAP1 -KO and parental tumour organoids ( n = 5 PDOT, n = 6 PDOT-BKO). Unpaired t -test; *: p < 0.01. (G) GSEA of BAP1 -KO tumour organoids versus parental controls using the Gene Ontology Biological Process (GOBP) Chromosome Segregation gene set. (H) Representative DAPI staining showing micronucleus presence in BAP1 -KO and parental tumour organoids. Scale bar, 50 µm. (I) Violin plot showing the number of clonal copy-number variants (CNVs), excluding chromosome 3p loss, in tumours with clonal BAP1 or PBRM1 mutations. Unpaired t -test; p = 0.0703. Clonal PBRM1 , n = 25; clonal BAP1 , n = 7. (J) Heatmap showing normalised accessibility scores for the top 1000 differentially accessible regions (DARs) between BAP1 -WT and BAP1 -KO organoids. (K) Genomic annotation of regions with increased (top) or decreased (bottom) chromatin accessibility following BAP1 loss. UTR, untranslated region. (L) Volcano plot showing differential transcription-factor binding activities between BAP1 -WT and BAP1 -KO tumour organoids. Significance was defined by −log10(p-value) above the 95% quantile and differential binding scores in top 5% in each direction. See also Figure S8 and Table S7.
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    Image Search Results


    (A) Schematic of CRISPR/Cas9-mediated BAP1 knockout (BKO) in patient-derived normal (PDON) and tumour (PDOT) organoids. The cross indicates unsuccessful expansion. (B) Tracking of variant allelic frequency (VAF) in normal kidney organoids following electroporation with guide RNAs targeting PBRM1 or BAP1 . (C) Schematic of CRISPR/Cas9-mediated BAP1 knockout (BKO) in normal organoids (K1088N1_GN1) with concurrent CDKN2A and VHL loss (CV background). (D) Principal-component analysis (PCA) of bulk transcriptomes from parental and BAP1 -engineered organoid lines. (E) GSEA of BAP1 -KO tumour organoids versus parental controls using the Hallmark E2F Targets gene set. (F) Comparison of normalised expression (DESeq2 VST) of selected genes between BAP1 -KO and parental tumour organoids ( n = 5 PDOT, n = 6 PDOT-BKO). Unpaired t -test; *: p < 0.01. (G) GSEA of BAP1 -KO tumour organoids versus parental controls using the Gene Ontology Biological Process (GOBP) Chromosome Segregation gene set. (H) Representative DAPI staining showing micronucleus presence in BAP1 -KO and parental tumour organoids. Scale bar, 50 µm. (I) Violin plot showing the number of clonal copy-number variants (CNVs), excluding chromosome 3p loss, in tumours with clonal BAP1 or PBRM1 mutations. Unpaired t -test; p = 0.0703. Clonal PBRM1 , n = 25; clonal BAP1 , n = 7. (J) Heatmap showing normalised accessibility scores for the top 1000 differentially accessible regions (DARs) between BAP1 -WT and BAP1 -KO organoids. (K) Genomic annotation of regions with increased (top) or decreased (bottom) chromatin accessibility following BAP1 loss. UTR, untranslated region. (L) Volcano plot showing differential transcription-factor binding activities between BAP1 -WT and BAP1 -KO tumour organoids. Significance was defined by −log10(p-value) above the 95% quantile and differential binding scores in top 5% in each direction. See also Figure S8 and Table S7.

    Journal: bioRxiv

    Article Title: Distinct functions of PBRM1 and BAP1 reconcile the course of kidney cancer evolution and disease progression

    doi: 10.64898/2026.04.30.721837

    Figure Lengend Snippet: (A) Schematic of CRISPR/Cas9-mediated BAP1 knockout (BKO) in patient-derived normal (PDON) and tumour (PDOT) organoids. The cross indicates unsuccessful expansion. (B) Tracking of variant allelic frequency (VAF) in normal kidney organoids following electroporation with guide RNAs targeting PBRM1 or BAP1 . (C) Schematic of CRISPR/Cas9-mediated BAP1 knockout (BKO) in normal organoids (K1088N1_GN1) with concurrent CDKN2A and VHL loss (CV background). (D) Principal-component analysis (PCA) of bulk transcriptomes from parental and BAP1 -engineered organoid lines. (E) GSEA of BAP1 -KO tumour organoids versus parental controls using the Hallmark E2F Targets gene set. (F) Comparison of normalised expression (DESeq2 VST) of selected genes between BAP1 -KO and parental tumour organoids ( n = 5 PDOT, n = 6 PDOT-BKO). Unpaired t -test; *: p < 0.01. (G) GSEA of BAP1 -KO tumour organoids versus parental controls using the Gene Ontology Biological Process (GOBP) Chromosome Segregation gene set. (H) Representative DAPI staining showing micronucleus presence in BAP1 -KO and parental tumour organoids. Scale bar, 50 µm. (I) Violin plot showing the number of clonal copy-number variants (CNVs), excluding chromosome 3p loss, in tumours with clonal BAP1 or PBRM1 mutations. Unpaired t -test; p = 0.0703. Clonal PBRM1 , n = 25; clonal BAP1 , n = 7. (J) Heatmap showing normalised accessibility scores for the top 1000 differentially accessible regions (DARs) between BAP1 -WT and BAP1 -KO organoids. (K) Genomic annotation of regions with increased (top) or decreased (bottom) chromatin accessibility following BAP1 loss. UTR, untranslated region. (L) Volcano plot showing differential transcription-factor binding activities between BAP1 -WT and BAP1 -KO tumour organoids. Significance was defined by −log10(p-value) above the 95% quantile and differential binding scores in top 5% in each direction. See also Figure S8 and Table S7.

    Article Snippet: A total of one million single cells were pelleted and resuspended in 100 μL electroporation buffer (Amaxa P3 Primary Cell Solution, Lonza), prepared by adding 18 μL of Supplement to 82 μL P3 Solution.

    Techniques: CRISPR, Knock-Out, Derivative Assay, Variant Assay, Electroporation, Comparison, Expressing, Staining, Binding Assay