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k562 human chronic myelogenous leukemia cell line  (ATCC)
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ATCC k562 human chronic myelogenous leukemia cell line
K562 Human Chronic Myelogenous Leukemia Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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k562 human chronic myelogenous leukemia cell line - by Bioz Stars, 2026-02
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k562 human myeloid leukemia cell line  (ATCC)
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ATCC k562 human myeloid leukemia cell line
( A ) Venn diagrams showing the overlap of genes with CEs, CE circles, with the DEGs, DE circles, per genotype as compared to WT samples. ( B ) Venn diagram showing the enrichment of DNA binding protein motifs at the promoters of the DEGs. ( C ) Bubble plot showing the enrichment of DNA binding proteins unique to the double-mutant expression signature and interacting with genes with CEs. The binary matrix on the right side shows which protein (row of the heatmap) physically interacts with which protein coded in a mis-spliced gene (columns of the matrix). ( D ) Bar plot showing the percentage of DNA binding proteins interacting with proteins that contain CEs. ( E ) Bar plot showing the number of chromatin modifiers found with CEs at each genotype. ( F ) Bar plot showing the relative survival of <t>K562</t> cells carrying IDH2 R140Q and/or SRSF2 P95H mutations in response to treatment with different doses of romidepsin. Asterisks indicate statistical significance [ P adj < 0.05 as per analysis of variance (ANOVA) followed by Tukey’s post hoc; shown are only the significant results with respect to the double mutant; N = 3 replicates]. ( G ) Graphical summary of the results of our whole study. Mutations in both IDH2 and SRSF2 genes cause the abnormal promotion of CCNG-rich exons, which code for proteins physically interacting with TFs or complexes that, in turn, regulate the expression of downstream genes, including signaling genes.
K562 Human Myeloid Leukemia Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/k562 human myeloid leukemia cell line/product/ATCC
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k562 human myeloid leukemia cell line - by Bioz Stars, 2026-02
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human leukemia k562 cells  (ATCC)
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ATCC human leukemia k562 cells
( A ) Venn diagrams showing the overlap of genes with CEs, CE circles, with the DEGs, DE circles, per genotype as compared to WT samples. ( B ) Venn diagram showing the enrichment of DNA binding protein motifs at the promoters of the DEGs. ( C ) Bubble plot showing the enrichment of DNA binding proteins unique to the double-mutant expression signature and interacting with genes with CEs. The binary matrix on the right side shows which protein (row of the heatmap) physically interacts with which protein coded in a mis-spliced gene (columns of the matrix). ( D ) Bar plot showing the percentage of DNA binding proteins interacting with proteins that contain CEs. ( E ) Bar plot showing the number of chromatin modifiers found with CEs at each genotype. ( F ) Bar plot showing the relative survival of <t>K562</t> cells carrying IDH2 R140Q and/or SRSF2 P95H mutations in response to treatment with different doses of romidepsin. Asterisks indicate statistical significance [ P adj < 0.05 as per analysis of variance (ANOVA) followed by Tukey’s post hoc; shown are only the significant results with respect to the double mutant; N = 3 replicates]. ( G ) Graphical summary of the results of our whole study. Mutations in both IDH2 and SRSF2 genes cause the abnormal promotion of CCNG-rich exons, which code for proteins physically interacting with TFs or complexes that, in turn, regulate the expression of downstream genes, including signaling genes.
Human Leukemia K562 Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/human leukemia k562 cells/product/ATCC
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human leukemia k562 cells - by Bioz Stars, 2026-02
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human leukemia cancer cell line k 562  (ATCC)
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ATCC human leukemia cancer cell line k 562
( A ) Venn diagrams showing the overlap of genes with CEs, CE circles, with the DEGs, DE circles, per genotype as compared to WT samples. ( B ) Venn diagram showing the enrichment of DNA binding protein motifs at the promoters of the DEGs. ( C ) Bubble plot showing the enrichment of DNA binding proteins unique to the double-mutant expression signature and interacting with genes with CEs. The binary matrix on the right side shows which protein (row of the heatmap) physically interacts with which protein coded in a mis-spliced gene (columns of the matrix). ( D ) Bar plot showing the percentage of DNA binding proteins interacting with proteins that contain CEs. ( E ) Bar plot showing the number of chromatin modifiers found with CEs at each genotype. ( F ) Bar plot showing the relative survival of <t>K562</t> cells carrying IDH2 R140Q and/or SRSF2 P95H mutations in response to treatment with different doses of romidepsin. Asterisks indicate statistical significance [ P adj < 0.05 as per analysis of variance (ANOVA) followed by Tukey’s post hoc; shown are only the significant results with respect to the double mutant; N = 3 replicates]. ( G ) Graphical summary of the results of our whole study. Mutations in both IDH2 and SRSF2 genes cause the abnormal promotion of CCNG-rich exons, which code for proteins physically interacting with TFs or complexes that, in turn, regulate the expression of downstream genes, including signaling genes.
Human Leukemia Cancer Cell Line K 562, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/human leukemia cancer cell line k 562/product/ATCC
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human leukemia cancer cell line k 562 - by Bioz Stars, 2026-02
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human chronic myeloid leukemia k562 cells  (DSMZ)
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DSMZ human chronic myeloid leukemia k562 cells
( A ) Venn diagrams showing the overlap of genes with CEs, CE circles, with the DEGs, DE circles, per genotype as compared to WT samples. ( B ) Venn diagram showing the enrichment of DNA binding protein motifs at the promoters of the DEGs. ( C ) Bubble plot showing the enrichment of DNA binding proteins unique to the double-mutant expression signature and interacting with genes with CEs. The binary matrix on the right side shows which protein (row of the heatmap) physically interacts with which protein coded in a mis-spliced gene (columns of the matrix). ( D ) Bar plot showing the percentage of DNA binding proteins interacting with proteins that contain CEs. ( E ) Bar plot showing the number of chromatin modifiers found with CEs at each genotype. ( F ) Bar plot showing the relative survival of <t>K562</t> cells carrying IDH2 R140Q and/or SRSF2 P95H mutations in response to treatment with different doses of romidepsin. Asterisks indicate statistical significance [ P adj < 0.05 as per analysis of variance (ANOVA) followed by Tukey’s post hoc; shown are only the significant results with respect to the double mutant; N = 3 replicates]. ( G ) Graphical summary of the results of our whole study. Mutations in both IDH2 and SRSF2 genes cause the abnormal promotion of CCNG-rich exons, which code for proteins physically interacting with TFs or complexes that, in turn, regulate the expression of downstream genes, including signaling genes.
Human Chronic Myeloid Leukemia K562 Cells, supplied by DSMZ, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/human chronic myeloid leukemia k562 cells/product/DSMZ
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human chronic myeloid leukemia k562 cells - by Bioz Stars, 2026-02
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( A ) Venn diagrams showing the overlap of genes with CEs, CE circles, with the DEGs, DE circles, per genotype as compared to WT samples. ( B ) Venn diagram showing the enrichment of DNA binding protein motifs at the promoters of the DEGs. ( C ) Bubble plot showing the enrichment of DNA binding proteins unique to the double-mutant expression signature and interacting with genes with CEs. The binary matrix on the right side shows which protein (row of the heatmap) physically interacts with which protein coded in a mis-spliced gene (columns of the matrix). ( D ) Bar plot showing the percentage of DNA binding proteins interacting with proteins that contain CEs. ( E ) Bar plot showing the number of chromatin modifiers found with CEs at each genotype. ( F ) Bar plot showing the relative survival of K562 cells carrying IDH2 R140Q and/or SRSF2 P95H mutations in response to treatment with different doses of romidepsin. Asterisks indicate statistical significance [ P adj < 0.05 as per analysis of variance (ANOVA) followed by Tukey’s post hoc; shown are only the significant results with respect to the double mutant; N = 3 replicates]. ( G ) Graphical summary of the results of our whole study. Mutations in both IDH2 and SRSF2 genes cause the abnormal promotion of CCNG-rich exons, which code for proteins physically interacting with TFs or complexes that, in turn, regulate the expression of downstream genes, including signaling genes.

Journal: Science Advances

Article Title: Synergistic intragenic epigenetic deregulation by IDH2 and SRSF2 mutations causes mis-splicing of key transcriptional regulators

doi: 10.1126/sciadv.adu8292

Figure Lengend Snippet: ( A ) Venn diagrams showing the overlap of genes with CEs, CE circles, with the DEGs, DE circles, per genotype as compared to WT samples. ( B ) Venn diagram showing the enrichment of DNA binding protein motifs at the promoters of the DEGs. ( C ) Bubble plot showing the enrichment of DNA binding proteins unique to the double-mutant expression signature and interacting with genes with CEs. The binary matrix on the right side shows which protein (row of the heatmap) physically interacts with which protein coded in a mis-spliced gene (columns of the matrix). ( D ) Bar plot showing the percentage of DNA binding proteins interacting with proteins that contain CEs. ( E ) Bar plot showing the number of chromatin modifiers found with CEs at each genotype. ( F ) Bar plot showing the relative survival of K562 cells carrying IDH2 R140Q and/or SRSF2 P95H mutations in response to treatment with different doses of romidepsin. Asterisks indicate statistical significance [ P adj < 0.05 as per analysis of variance (ANOVA) followed by Tukey’s post hoc; shown are only the significant results with respect to the double mutant; N = 3 replicates]. ( G ) Graphical summary of the results of our whole study. Mutations in both IDH2 and SRSF2 genes cause the abnormal promotion of CCNG-rich exons, which code for proteins physically interacting with TFs or complexes that, in turn, regulate the expression of downstream genes, including signaling genes.

Article Snippet: The K562 human myeloid leukemia cell line was purchased from American Type Culture Collection (ATCC; #CCL-243).

Techniques: Binding Assay, DNA Binding Assay, Mutagenesis, Expressing