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ZNF397 acts as a transcriptional coactivator essential for AR-driven signaling. A, GSEA Pathways analysis shows cancer-related signaling pathways significantly altered in ZNF397-KO cells compared to wild-type cells, lineage specific pathways were highlighted with color: green-AR dependent and luminal lineage pathways, red-lineage plastic signaling pathways. B, GSEA analysis of androgen response gene expression in ZNF397-KO cells compared to wild-type cells. C, AR gene score based on the expression of canonical AR target genes (AR Score Gene) in ZNF397-KO and wild-type cells. mean ± SEM are presented. P values were calculated using two-tailed t test. D, Heatmap represents the relative gene expression of AR Score genes in ZNF397-KO cells compared to wild-type cells, measured by RNA-seq. E, <t>Co-IP</t> of AR (with Flag tag) and full length or the SCAN domain of ZNF397 (with TY1 tag) in HEK293T cells. F, Global distribution of ZNF397 binding peaks at known AR binding sites (as determined by AR ChIP-seq), based on ZNF397 ChIP-seq in LNCaP/AR cells. Reads from two independently cultured cell samples were plotted and matching input controls were used for analysis. G, Representative AR-binding sites (as determined by AR ChIP-seq) and ZNF397-binding sites (as determined by ZNF397 ChIP-seq) in the genomic loci of canonical AR gene loci in the LNCaP/AR cell. The binding peak distances (kilo base pair) to TSS (transcriptional start site) are annotated in green. H, ZNF397-binding peak score (CPM, see “Methods”) in the genomic loci of AR Score genes (14 of 20) in LNCaP/AR cells. Reads from two independent cell cultures/guide were plotted, matching input controls were used for analysis. I, Relative gene expression levels of AR target genes in LNCaP/AR cells transduced with Cas9 and annotated guide RNAs, and treated with Veh (EtOH) or 10 nmol/L DHT for 12 hours, normalized and compared to sgNT + Veh group. For all panels unless otherwise noted, mean ± SEM are presented. P values were calculated using two-way ANOVA with Bonferroni multiple-comparison test. See also Supplementary Fig. S4 and Supplementary Table S2.
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ZNF397 acts as a transcriptional coactivator essential for AR-driven signaling. A, GSEA Pathways analysis shows cancer-related signaling pathways significantly altered in ZNF397-KO cells compared to wild-type cells, lineage specific pathways were highlighted with color: green-AR dependent and luminal lineage pathways, red-lineage plastic signaling pathways. B, GSEA analysis of androgen response gene expression in ZNF397-KO cells compared to wild-type cells. C, AR gene score based on the expression of canonical AR target genes (AR Score Gene) in ZNF397-KO and wild-type cells. mean ± SEM are presented. P values were calculated using two-tailed t test. D, Heatmap represents the relative gene expression of AR Score genes in ZNF397-KO cells compared to wild-type cells, measured by RNA-seq. E, <t>Co-IP</t> of AR (with Flag tag) and full length or the SCAN domain of ZNF397 (with TY1 tag) in HEK293T cells. F, Global distribution of ZNF397 binding peaks at known AR binding sites (as determined by AR ChIP-seq), based on ZNF397 ChIP-seq in LNCaP/AR cells. Reads from two independently cultured cell samples were plotted and matching input controls were used for analysis. G, Representative AR-binding sites (as determined by AR ChIP-seq) and ZNF397-binding sites (as determined by ZNF397 ChIP-seq) in the genomic loci of canonical AR gene loci in the LNCaP/AR cell. The binding peak distances (kilo base pair) to TSS (transcriptional start site) are annotated in green. H, ZNF397-binding peak score (CPM, see “Methods”) in the genomic loci of AR Score genes (14 of 20) in LNCaP/AR cells. Reads from two independent cell cultures/guide were plotted, matching input controls were used for analysis. I, Relative gene expression levels of AR target genes in LNCaP/AR cells transduced with Cas9 and annotated guide RNAs, and treated with Veh (EtOH) or 10 nmol/L DHT for 12 hours, normalized and compared to sgNT + Veh group. For all panels unless otherwise noted, mean ± SEM are presented. P values were calculated using two-way ANOVA with Bonferroni multiple-comparison test. See also Supplementary Fig. S4 and Supplementary Table S2.
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ZNF397 acts as a transcriptional coactivator essential for AR-driven signaling. A, GSEA Pathways analysis shows cancer-related signaling pathways significantly altered in ZNF397-KO cells compared to wild-type cells, lineage specific pathways were highlighted with color: green-AR dependent and luminal lineage pathways, red-lineage plastic signaling pathways. B, GSEA analysis of androgen response gene expression in ZNF397-KO cells compared to wild-type cells. C, AR gene score based on the expression of canonical AR target genes (AR Score Gene) in ZNF397-KO and wild-type cells. mean ± SEM are presented. P values were calculated using two-tailed t test. D, Heatmap represents the relative gene expression of AR Score genes in ZNF397-KO cells compared to wild-type cells, measured by RNA-seq. E, <t>Co-IP</t> of AR (with Flag tag) and full length or the SCAN domain of ZNF397 (with TY1 tag) in HEK293T cells. F, Global distribution of ZNF397 binding peaks at known AR binding sites (as determined by AR ChIP-seq), based on ZNF397 ChIP-seq in LNCaP/AR cells. Reads from two independently cultured cell samples were plotted and matching input controls were used for analysis. G, Representative AR-binding sites (as determined by AR ChIP-seq) and ZNF397-binding sites (as determined by ZNF397 ChIP-seq) in the genomic loci of canonical AR gene loci in the LNCaP/AR cell. The binding peak distances (kilo base pair) to TSS (transcriptional start site) are annotated in green. H, ZNF397-binding peak score (CPM, see “Methods”) in the genomic loci of AR Score genes (14 of 20) in LNCaP/AR cells. Reads from two independent cell cultures/guide were plotted, matching input controls were used for analysis. I, Relative gene expression levels of AR target genes in LNCaP/AR cells transduced with Cas9 and annotated guide RNAs, and treated with Veh (EtOH) or 10 nmol/L DHT for 12 hours, normalized and compared to sgNT + Veh group. For all panels unless otherwise noted, mean ± SEM are presented. P values were calculated using two-way ANOVA with Bonferroni multiple-comparison test. See also Supplementary Fig. S4 and Supplementary Table S2.
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ZNF397 acts as a transcriptional coactivator essential for AR-driven signaling. A, GSEA Pathways analysis shows cancer-related signaling pathways significantly altered in ZNF397-KO cells compared to wild-type cells, lineage specific pathways were highlighted with color: green-AR dependent and luminal lineage pathways, red-lineage plastic signaling pathways. B, GSEA analysis of androgen response gene expression in ZNF397-KO cells compared to wild-type cells. C, AR gene score based on the expression of canonical AR target genes (AR Score Gene) in ZNF397-KO and wild-type cells. mean ± SEM are presented. P values were calculated using two-tailed t test. D, Heatmap represents the relative gene expression of AR Score genes in ZNF397-KO cells compared to wild-type cells, measured by RNA-seq. E, <t>Co-IP</t> of AR (with Flag tag) and full length or the SCAN domain of ZNF397 (with TY1 tag) in HEK293T cells. F, Global distribution of ZNF397 binding peaks at known AR binding sites (as determined by AR ChIP-seq), based on ZNF397 ChIP-seq in LNCaP/AR cells. Reads from two independently cultured cell samples were plotted and matching input controls were used for analysis. G, Representative AR-binding sites (as determined by AR ChIP-seq) and ZNF397-binding sites (as determined by ZNF397 ChIP-seq) in the genomic loci of canonical AR gene loci in the LNCaP/AR cell. The binding peak distances (kilo base pair) to TSS (transcriptional start site) are annotated in green. H, ZNF397-binding peak score (CPM, see “Methods”) in the genomic loci of AR Score genes (14 of 20) in LNCaP/AR cells. Reads from two independent cell cultures/guide were plotted, matching input controls were used for analysis. I, Relative gene expression levels of AR target genes in LNCaP/AR cells transduced with Cas9 and annotated guide RNAs, and treated with Veh (EtOH) or 10 nmol/L DHT for 12 hours, normalized and compared to sgNT + Veh group. For all panels unless otherwise noted, mean ± SEM are presented. P values were calculated using two-way ANOVA with Bonferroni multiple-comparison test. See also Supplementary Fig. S4 and Supplementary Table S2.
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ZNF397 acts as a transcriptional coactivator essential for AR-driven signaling. A, GSEA Pathways analysis shows cancer-related signaling pathways significantly altered in ZNF397-KO cells compared to wild-type cells, lineage specific pathways were highlighted with color: green-AR dependent and luminal lineage pathways, red-lineage plastic signaling pathways. B, GSEA analysis of androgen response gene expression in ZNF397-KO cells compared to wild-type cells. C, AR gene score based on the expression of canonical AR target genes (AR Score Gene) in ZNF397-KO and wild-type cells. mean ± SEM are presented. P values were calculated using two-tailed t test. D, Heatmap represents the relative gene expression of AR Score genes in ZNF397-KO cells compared to wild-type cells, measured by RNA-seq. E, <t>Co-IP</t> of AR (with Flag tag) and full length or the SCAN domain of ZNF397 (with TY1 tag) in HEK293T cells. F, Global distribution of ZNF397 binding peaks at known AR binding sites (as determined by AR ChIP-seq), based on ZNF397 ChIP-seq in LNCaP/AR cells. Reads from two independently cultured cell samples were plotted and matching input controls were used for analysis. G, Representative AR-binding sites (as determined by AR ChIP-seq) and ZNF397-binding sites (as determined by ZNF397 ChIP-seq) in the genomic loci of canonical AR gene loci in the LNCaP/AR cell. The binding peak distances (kilo base pair) to TSS (transcriptional start site) are annotated in green. H, ZNF397-binding peak score (CPM, see “Methods”) in the genomic loci of AR Score genes (14 of 20) in LNCaP/AR cells. Reads from two independent cell cultures/guide were plotted, matching input controls were used for analysis. I, Relative gene expression levels of AR target genes in LNCaP/AR cells transduced with Cas9 and annotated guide RNAs, and treated with Veh (EtOH) or 10 nmol/L DHT for 12 hours, normalized and compared to sgNT + Veh group. For all panels unless otherwise noted, mean ± SEM are presented. P values were calculated using two-way ANOVA with Bonferroni multiple-comparison test. See also Supplementary Fig. S4 and Supplementary Table S2.
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ZNF397 acts as a transcriptional coactivator essential for AR-driven signaling. A, GSEA Pathways analysis shows cancer-related signaling pathways significantly altered in ZNF397-KO cells compared to wild-type cells, lineage specific pathways were highlighted with color: green-AR dependent and luminal lineage pathways, red-lineage plastic signaling pathways. B, GSEA analysis of androgen response gene expression in ZNF397-KO cells compared to wild-type cells. C, AR gene score based on the expression of canonical AR target genes (AR Score Gene) in ZNF397-KO and wild-type cells. mean ± SEM are presented. P values were calculated using two-tailed t test. D, Heatmap represents the relative gene expression of AR Score genes in ZNF397-KO cells compared to wild-type cells, measured by RNA-seq. E, <t>Co-IP</t> of AR (with Flag tag) and full length or the SCAN domain of ZNF397 (with TY1 tag) in HEK293T cells. F, Global distribution of ZNF397 binding peaks at known AR binding sites (as determined by AR ChIP-seq), based on ZNF397 ChIP-seq in LNCaP/AR cells. Reads from two independently cultured cell samples were plotted and matching input controls were used for analysis. G, Representative AR-binding sites (as determined by AR ChIP-seq) and ZNF397-binding sites (as determined by ZNF397 ChIP-seq) in the genomic loci of canonical AR gene loci in the LNCaP/AR cell. The binding peak distances (kilo base pair) to TSS (transcriptional start site) are annotated in green. H, ZNF397-binding peak score (CPM, see “Methods”) in the genomic loci of AR Score genes (14 of 20) in LNCaP/AR cells. Reads from two independent cell cultures/guide were plotted, matching input controls were used for analysis. I, Relative gene expression levels of AR target genes in LNCaP/AR cells transduced with Cas9 and annotated guide RNAs, and treated with Veh (EtOH) or 10 nmol/L DHT for 12 hours, normalized and compared to sgNT + Veh group. For all panels unless otherwise noted, mean ± SEM are presented. P values were calculated using two-way ANOVA with Bonferroni multiple-comparison test. See also Supplementary Fig. S4 and Supplementary Table S2.
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ZNF397 acts as a transcriptional coactivator essential for AR-driven signaling. A, GSEA Pathways analysis shows cancer-related signaling pathways significantly altered in ZNF397-KO cells compared to wild-type cells, lineage specific pathways were highlighted with color: green-AR dependent and luminal lineage pathways, red-lineage plastic signaling pathways. B, GSEA analysis of androgen response gene expression in ZNF397-KO cells compared to wild-type cells. C, AR gene score based on the expression of canonical AR target genes (AR Score Gene) in ZNF397-KO and wild-type cells. mean ± SEM are presented. P values were calculated using two-tailed t test. D, Heatmap represents the relative gene expression of AR Score genes in ZNF397-KO cells compared to wild-type cells, measured by RNA-seq. E, <t>Co-IP</t> of AR (with Flag tag) and full length or the SCAN domain of ZNF397 (with TY1 tag) in HEK293T cells. F, Global distribution of ZNF397 binding peaks at known AR binding sites (as determined by AR ChIP-seq), based on ZNF397 ChIP-seq in LNCaP/AR cells. Reads from two independently cultured cell samples were plotted and matching input controls were used for analysis. G, Representative AR-binding sites (as determined by AR ChIP-seq) and ZNF397-binding sites (as determined by ZNF397 ChIP-seq) in the genomic loci of canonical AR gene loci in the LNCaP/AR cell. The binding peak distances (kilo base pair) to TSS (transcriptional start site) are annotated in green. H, ZNF397-binding peak score (CPM, see “Methods”) in the genomic loci of AR Score genes (14 of 20) in LNCaP/AR cells. Reads from two independent cell cultures/guide were plotted, matching input controls were used for analysis. I, Relative gene expression levels of AR target genes in LNCaP/AR cells transduced with Cas9 and annotated guide RNAs, and treated with Veh (EtOH) or 10 nmol/L DHT for 12 hours, normalized and compared to sgNT + Veh group. For all panels unless otherwise noted, mean ± SEM are presented. P values were calculated using two-way ANOVA with Bonferroni multiple-comparison test. See also Supplementary Fig. S4 and Supplementary Table S2.
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ZNF397 acts as a transcriptional coactivator essential for AR-driven signaling. A, GSEA Pathways analysis shows cancer-related signaling pathways significantly altered in ZNF397-KO cells compared to wild-type cells, lineage specific pathways were highlighted with color: green-AR dependent and luminal lineage pathways, red-lineage plastic signaling pathways. B, GSEA analysis of androgen response gene expression in ZNF397-KO cells compared to wild-type cells. C, AR gene score based on the expression of canonical AR target genes (AR Score Gene) in ZNF397-KO and wild-type cells. mean ± SEM are presented. P values were calculated using two-tailed t test. D, Heatmap represents the relative gene expression of AR Score genes in ZNF397-KO cells compared to wild-type cells, measured by RNA-seq. E, Co-IP of AR (with Flag tag) and full length or the SCAN domain of ZNF397 (with TY1 tag) in HEK293T cells. F, Global distribution of ZNF397 binding peaks at known AR binding sites (as determined by AR ChIP-seq), based on ZNF397 ChIP-seq in LNCaP/AR cells. Reads from two independently cultured cell samples were plotted and matching input controls were used for analysis. G, Representative AR-binding sites (as determined by AR ChIP-seq) and ZNF397-binding sites (as determined by ZNF397 ChIP-seq) in the genomic loci of canonical AR gene loci in the LNCaP/AR cell. The binding peak distances (kilo base pair) to TSS (transcriptional start site) are annotated in green. H, ZNF397-binding peak score (CPM, see “Methods”) in the genomic loci of AR Score genes (14 of 20) in LNCaP/AR cells. Reads from two independent cell cultures/guide were plotted, matching input controls were used for analysis. I, Relative gene expression levels of AR target genes in LNCaP/AR cells transduced with Cas9 and annotated guide RNAs, and treated with Veh (EtOH) or 10 nmol/L DHT for 12 hours, normalized and compared to sgNT + Veh group. For all panels unless otherwise noted, mean ± SEM are presented. P values were calculated using two-way ANOVA with Bonferroni multiple-comparison test. See also Supplementary Fig. S4 and Supplementary Table S2.

Journal: Cancer Discovery

Article Title: ZNF397 Deficiency Triggers TET2-Driven Lineage Plasticity and AR-Targeted Therapy Resistance in Prostate Cancer

doi: 10.1158/2159-8290.CD-23-0539

Figure Lengend Snippet: ZNF397 acts as a transcriptional coactivator essential for AR-driven signaling. A, GSEA Pathways analysis shows cancer-related signaling pathways significantly altered in ZNF397-KO cells compared to wild-type cells, lineage specific pathways were highlighted with color: green-AR dependent and luminal lineage pathways, red-lineage plastic signaling pathways. B, GSEA analysis of androgen response gene expression in ZNF397-KO cells compared to wild-type cells. C, AR gene score based on the expression of canonical AR target genes (AR Score Gene) in ZNF397-KO and wild-type cells. mean ± SEM are presented. P values were calculated using two-tailed t test. D, Heatmap represents the relative gene expression of AR Score genes in ZNF397-KO cells compared to wild-type cells, measured by RNA-seq. E, Co-IP of AR (with Flag tag) and full length or the SCAN domain of ZNF397 (with TY1 tag) in HEK293T cells. F, Global distribution of ZNF397 binding peaks at known AR binding sites (as determined by AR ChIP-seq), based on ZNF397 ChIP-seq in LNCaP/AR cells. Reads from two independently cultured cell samples were plotted and matching input controls were used for analysis. G, Representative AR-binding sites (as determined by AR ChIP-seq) and ZNF397-binding sites (as determined by ZNF397 ChIP-seq) in the genomic loci of canonical AR gene loci in the LNCaP/AR cell. The binding peak distances (kilo base pair) to TSS (transcriptional start site) are annotated in green. H, ZNF397-binding peak score (CPM, see “Methods”) in the genomic loci of AR Score genes (14 of 20) in LNCaP/AR cells. Reads from two independent cell cultures/guide were plotted, matching input controls were used for analysis. I, Relative gene expression levels of AR target genes in LNCaP/AR cells transduced with Cas9 and annotated guide RNAs, and treated with Veh (EtOH) or 10 nmol/L DHT for 12 hours, normalized and compared to sgNT + Veh group. For all panels unless otherwise noted, mean ± SEM are presented. P values were calculated using two-way ANOVA with Bonferroni multiple-comparison test. See also Supplementary Fig. S4 and Supplementary Table S2.

Article Snippet: The following antibodies were used for Co-IP: DYKDDDDK Tag (D6W5B) Rabbit mAb, CST#14793 RRID: AB_2572291; Ty1 monoclonal antibody, Diagenode#C15200054, RRID: AB_2104842; Myc Antibody (9E10), Santa Cruz Biotechnology# sc-40, RRID: AB_627268.

Techniques: Protein-Protein interactions, Gene Expression, Expressing, Two Tailed Test, RNA Sequencing, Co-Immunoprecipitation Assay, FLAG-tag, Binding Assay, ChIP-sequencing, Cell Culture, Transduction, Comparison

ZNF397-KO results in TET2-driven epigenetic and 5hmC rewiring. A, Volcano plot represents the genomic loci with most significantly enriched or depleted 5hmC modification, in ZNF397-KO cells compared to the control sgNT cells, according to genomic 5hmC-seal seq. Significantly changed gene loci were annotated as dark blue dots, and lineage-plastic signature genes with most significantly enriched 5hmC were annotated as yellow dots. Reads from two independently cultured cell samples were pooled for analysis. B, Volcano plot represents the genomic loci with most significantly enriched or depleted 5hmC modifications, in ZNF397/TET2-double-KO (sgZNF397 + sgTET2) cells compared to the ZNF397-KO (sgZNF397) cells, according to genomic 5hmC–seal seq. Significantly changed gene loci were annotated as dark blue, and lineage-plastic signature genes with most significantly depleted 5hmC were annotated as yellow dots. Reads from two independently cultured cell samples were pooled for analysis. C, Heatmap represents the 5hmC enrichment score (CPM, see “Methods”) in the genomic loci of lineage plastic marker genes in the sgNT, sgZNF397 and sgZNF397 + sgTET2 cells. D, Bar plot presents the lineage gene signatures with most enriched or depleted 5hmC modification in patients with AR-independent mCRPC and t-SCNC compared to patients with AR-dependent adenocarcinoma in a cohort of patients with prostate cancer, based on the results of genomic 5hmC-seq. E, Bar plot presents the lineage gene signatures with most enriched or depleted 5hmC modifications in patients with ZNF397 -high ( ZNF397 expression above median) compared to patients with ZNF397 -low ( ZNF397 expression below median) in a cohort of patients with prostate cancer, based on the results of genomic 5hmC-seq. F, Heatmap represents the correlation between ZNF397 expression and the 5hmC modification in the genomic loci of those marker genes of lineage-specific gene signatures, based on the results of genomic 5hmC-seq. G, Co-IP of ZNF397 SCAN domain and the TET2 CD domain with a Flag or Myc tag in HEK293T cells. H, Global distribution of ZNF397 binding peaks at known lineage-plastic and multilineage signature gene loci, based on ZNF397 ChIP-seq in LNCaP/AR cells. Reads from two independently cultured cell samples were plotted and matching input controls were used for analysis. Schematic figure was created with BioRender.com.See also Supplementary Figs. S8, S9 and Supplementary Table S5.

Journal: Cancer Discovery

Article Title: ZNF397 Deficiency Triggers TET2-Driven Lineage Plasticity and AR-Targeted Therapy Resistance in Prostate Cancer

doi: 10.1158/2159-8290.CD-23-0539

Figure Lengend Snippet: ZNF397-KO results in TET2-driven epigenetic and 5hmC rewiring. A, Volcano plot represents the genomic loci with most significantly enriched or depleted 5hmC modification, in ZNF397-KO cells compared to the control sgNT cells, according to genomic 5hmC-seal seq. Significantly changed gene loci were annotated as dark blue dots, and lineage-plastic signature genes with most significantly enriched 5hmC were annotated as yellow dots. Reads from two independently cultured cell samples were pooled for analysis. B, Volcano plot represents the genomic loci with most significantly enriched or depleted 5hmC modifications, in ZNF397/TET2-double-KO (sgZNF397 + sgTET2) cells compared to the ZNF397-KO (sgZNF397) cells, according to genomic 5hmC–seal seq. Significantly changed gene loci were annotated as dark blue, and lineage-plastic signature genes with most significantly depleted 5hmC were annotated as yellow dots. Reads from two independently cultured cell samples were pooled for analysis. C, Heatmap represents the 5hmC enrichment score (CPM, see “Methods”) in the genomic loci of lineage plastic marker genes in the sgNT, sgZNF397 and sgZNF397 + sgTET2 cells. D, Bar plot presents the lineage gene signatures with most enriched or depleted 5hmC modification in patients with AR-independent mCRPC and t-SCNC compared to patients with AR-dependent adenocarcinoma in a cohort of patients with prostate cancer, based on the results of genomic 5hmC-seq. E, Bar plot presents the lineage gene signatures with most enriched or depleted 5hmC modifications in patients with ZNF397 -high ( ZNF397 expression above median) compared to patients with ZNF397 -low ( ZNF397 expression below median) in a cohort of patients with prostate cancer, based on the results of genomic 5hmC-seq. F, Heatmap represents the correlation between ZNF397 expression and the 5hmC modification in the genomic loci of those marker genes of lineage-specific gene signatures, based on the results of genomic 5hmC-seq. G, Co-IP of ZNF397 SCAN domain and the TET2 CD domain with a Flag or Myc tag in HEK293T cells. H, Global distribution of ZNF397 binding peaks at known lineage-plastic and multilineage signature gene loci, based on ZNF397 ChIP-seq in LNCaP/AR cells. Reads from two independently cultured cell samples were plotted and matching input controls were used for analysis. Schematic figure was created with BioRender.com.See also Supplementary Figs. S8, S9 and Supplementary Table S5.

Article Snippet: The following antibodies were used for Co-IP: DYKDDDDK Tag (D6W5B) Rabbit mAb, CST#14793 RRID: AB_2572291; Ty1 monoclonal antibody, Diagenode#C15200054, RRID: AB_2104842; Myc Antibody (9E10), Santa Cruz Biotechnology# sc-40, RRID: AB_627268.

Techniques: Modification, Control, Cell Culture, Marker, Expressing, Co-Immunoprecipitation Assay, Binding Assay, ChIP-sequencing

Antibodies references used during the study.

Journal: International Journal of Molecular Sciences

Article Title: Overexpression of a Novel Noxo1 Mutant Increases Ros Production and Noxo1 Relocalisation

doi: 10.3390/ijms24054663

Figure Lengend Snippet: Antibodies references used during the study.

Article Snippet: Anti-DDK , Rabbit , D6w5b mab; Cell signaling , 1/400 , 1/1000.

Techniques: