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chip-seq spike in chromatin  (Active Motif)


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    Active Motif chip-seq spike in chromatin
    Chip Seq Spike In Chromatin, supplied by Active Motif, 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/product/chip+seq+spike/chip+seq+spike+in+chromatin/pmc12022051-293-5-9
    Average 90 stars, based on 1 article reviews
    chip-seq spike in chromatin - by Bioz Stars, 2026-11
    90/100 stars

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    Article Title: MYCN and KAT2A form a feedforward loop to drive an oncogenic transcriptional program in neuroblastoma
    Article Snippet: ChIP experiments included Active Motif ChIP-seq spike in chromatin (Active Motif Cat No. 53083) and Drosophila -specific histone variant H2Ac (Active Motif Cat No. 61686).

    Article Title: Targeting SWI/SNF ATPases reduces neuroblastoma cell plasticity.
    Article Snippet: Tumor cell heterogeneity defines therapy responsiveness in neuroblastoma (NB), a cancer derived from neural crest cells.. NB consists of two primary subtypes: adrenergic and mesenchymal.. Adrenergic traits predominate in NB tumors, while mesenchymal features becomes enriched post-chemotherapy or after relapse.

    Article Title: MYCN and KAT2A form a feedforward loop to drive an oncogenic transcriptional program in neuroblastoma.
    Article Snippet: ChIP experiments included Active Motif ChIP-seq spike in chromatin (Active Motif Cat No. 53083) and Drosophila-specific histone variant H2Ac (Active Motif Cat No. 61686).

    Article Title: CASZ1 induces skeletal muscle and rhabdomyosarcoma differentiation through a feed-forward loop with MYOD and MYOG
    Article Snippet: To normalize ChIP-seq signal, we employed Active Motif ChIP-seq spike in using Drosophila chromatin (Active Motif catalog # 53083) and an antibody against Drosophila specific histone variant H2Av (Active Motif, catalog #61686) according to the manufacturer’s instructions.

    Article Title: HAND2 Assists MYCN Enhancer Invasion to Regulate a Noradrenergic Neuroblastoma Phenotype
    Article Snippet: To normalize ChIP-seq signal, we employed Active Motif ChIP-seq spike-in using Drosophila chromatin (Active Motif catalogue # 53083) and an antibody against Drosophila specific histone variant H2Av (Active Motif, catalogue # 61686) according to the manufacturer’s instructions.

    Article Title: Selective Roles of Vertebrate PCF11 in Premature and Full-Length Transcript Termination
    Article Snippet: Rabbit polyclonal anti-H2Av (used for: ChIP-seq spike-in) , Active motif , Cat# 61686; RRID: AB_2737370.

    Chromatin Immunoprecipitation:

    Article Title: Recruitment of the CoREST transcription repressor complexes by Nerve Growth factor IB-like receptor (Nurr1/NR4A2) mediates silencing of HIV in microglial cells
    Article Snippet: .. Did the authors use a normalization approach, i.e spike in a known quantity of a certain DNA to standardized between samples (e.g., ChIP seq spike in normalization by Active Motif). ..



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    A) Immunofluorescence for bromouridine (BrU) after cardiomyocytes were cultured with BrU for 2 hr to label nascent RNAs. One binucleated cardiomyocyte per image, with nuclei zoomed in. Texts and icons below images indicate nuclear states. Scale bar: 5 μm. All data in , except , are from cardiomyocytes freshly isolated from mice at day 14 post tamoxifen. B) Nuclear BrU intensity by nuclear states after 1-hr BrU incubation. Density and box plots: BrU intensity distribution and interquartile range. Circles: mean intensity within biological replicates (color coded). Asterisks: P < 0.05 from t -tests on linear regression-estimated means with mouse-clustered standard errors. Underlying data: 244 intact nuclei from 4 WT mice, 275 intact, 111 ruptured, 104 resealed nuclei from 3 Lmna CKO mice. C) Relationship between nuclear BrU intensity and nuclear NLS–tdTomato intensity in all types of nuclei in Lmna CKO cardiomyocytes (519 nuclei from 3 mice). Line: simple linear regression fit with 95% confidence interval. R: Pearson correlation coefficient. P: t -test p -value on linear regression-estimated means with mouse-clustered standard errors. See for individual replicates. D) Immunofluorescence for RNA polymerase II (Pol II) in cardiomyocytes. Scale bar: 5 μm. E) Nuclear Pol II intensity by nuclear states. Underlying data: 285 intact nuclei from 3 WT mice, 180 intact, 133 ruptured, 136 resealed nuclei from 3 Lmna CKO mice. Graph annotations and statistics as in (B) . F) Relationship between Pol II intensity and NLS–tdTomato intensity in all types of nuclei in Lmna CKO cardiomyocytes (495 nuclei from 3 mice). Graph annotations and statistics as in (C) . G) Pol <t>II</t> <t>ChIP-seq</t> and input read coverage in WT and Lmna CKO cardiomyocytes (3 mice per genotype). ChIP-seq signals are normalized to <t>internal</t> <t>spike-in</t> controls. H) Average Pol II ChIP-seq signals across 21,177 protein-coding genes. X-axis: 100 equally-spaced bins in gene bodies, 5 bins for 1 kb-upstream regions, and 10 bins for 2 kb-downstream regions. I) Statistical comparison of gene-body Pol II signals in Lmna CKO versus WT cardiomyocytes for 11,942 Pol II-bound genes. Pol II-lost or gained genes are defined at limma p -value < 0.05. J) Ten most enriched Gene Ontology terms among the 1,759 Pol II-lost genes in Lmna CKO cardiomyocytes, with three representative genes for each term. P: Metascape p -value. K) Gene expression state of Pol II-lost, Pol II-gained, and all other genes in Lmna CKO (n=5) versus WT (n=7) hearts. P, DESeq2 p -value. RNA-seq data from En et al. 2024. L) Summary of . Nuclear rupture causes transcriptional deficiency due to RNA Pol II loss.
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    A) Immunofluorescence for bromouridine (BrU) after cardiomyocytes were cultured with BrU for 2 hr to label nascent RNAs. One binucleated cardiomyocyte per image, with nuclei zoomed in. Texts and icons below images indicate nuclear states. Scale bar: 5 μm. All data in , except , are from cardiomyocytes freshly isolated from mice at day 14 post tamoxifen. B) Nuclear BrU intensity by nuclear states after 1-hr BrU incubation. Density and box plots: BrU intensity distribution and interquartile range. Circles: mean intensity within biological replicates (color coded). Asterisks: P < 0.05 from t -tests on linear regression-estimated means with mouse-clustered standard errors. Underlying data: 244 intact nuclei from 4 WT mice, 275 intact, 111 ruptured, 104 resealed nuclei from 3 Lmna CKO mice. C) Relationship between nuclear BrU intensity and nuclear NLS–tdTomato intensity in all types of nuclei in Lmna CKO cardiomyocytes (519 nuclei from 3 mice). Line: simple linear regression fit with 95% confidence interval. R: Pearson correlation coefficient. P: t -test p -value on linear regression-estimated means with mouse-clustered standard errors. See for individual replicates. D) Immunofluorescence for RNA polymerase II (Pol II) in cardiomyocytes. Scale bar: 5 μm. E) Nuclear Pol II intensity by nuclear states. Underlying data: 285 intact nuclei from 3 WT mice, 180 intact, 133 ruptured, 136 resealed nuclei from 3 Lmna CKO mice. Graph annotations and statistics as in (B) . F) Relationship between Pol II intensity and NLS–tdTomato intensity in all types of nuclei in Lmna CKO cardiomyocytes (495 nuclei from 3 mice). Graph annotations and statistics as in (C) . G) Pol <t>II</t> <t>ChIP-seq</t> and input read coverage in WT and Lmna CKO cardiomyocytes (3 mice per genotype). ChIP-seq signals are normalized to <t>internal</t> <t>spike-in</t> controls. H) Average Pol II ChIP-seq signals across 21,177 protein-coding genes. X-axis: 100 equally-spaced bins in gene bodies, 5 bins for 1 kb-upstream regions, and 10 bins for 2 kb-downstream regions. I) Statistical comparison of gene-body Pol II signals in Lmna CKO versus WT cardiomyocytes for 11,942 Pol II-bound genes. Pol II-lost or gained genes are defined at limma p -value < 0.05. J) Ten most enriched Gene Ontology terms among the 1,759 Pol II-lost genes in Lmna CKO cardiomyocytes, with three representative genes for each term. P: Metascape p -value. K) Gene expression state of Pol II-lost, Pol II-gained, and all other genes in Lmna CKO (n=5) versus WT (n=7) hearts. P, DESeq2 p -value. RNA-seq data from En et al. 2024. L) Summary of . Nuclear rupture causes transcriptional deficiency due to RNA Pol II loss.
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    A) Immunofluorescence for bromouridine (BrU) after cardiomyocytes were cultured with BrU for 2 hr to label nascent RNAs. One binucleated cardiomyocyte per image, with nuclei zoomed in. Texts and icons below images indicate nuclear states. Scale bar: 5 μm. All data in , except , are from cardiomyocytes freshly isolated from mice at day 14 post tamoxifen. B) Nuclear BrU intensity by nuclear states after 1-hr BrU incubation. Density and box plots: BrU intensity distribution and interquartile range. Circles: mean intensity within biological replicates (color coded). Asterisks: P < 0.05 from t -tests on linear regression-estimated means with mouse-clustered standard errors. Underlying data: 244 intact nuclei from 4 WT mice, 275 intact, 111 ruptured, 104 resealed nuclei from 3 Lmna CKO mice. C) Relationship between nuclear BrU intensity and nuclear NLS–tdTomato intensity in all types of nuclei in Lmna CKO cardiomyocytes (519 nuclei from 3 mice). Line: simple linear regression fit with 95% confidence interval. R: Pearson correlation coefficient. P: t -test p -value on linear regression-estimated means with mouse-clustered standard errors. See for individual replicates. D) Immunofluorescence for RNA polymerase II (Pol II) in cardiomyocytes. Scale bar: 5 μm. E) Nuclear Pol II intensity by nuclear states. Underlying data: 285 intact nuclei from 3 WT mice, 180 intact, 133 ruptured, 136 resealed nuclei from 3 Lmna CKO mice. Graph annotations and statistics as in (B) . F) Relationship between Pol II intensity and NLS–tdTomato intensity in all types of nuclei in Lmna CKO cardiomyocytes (495 nuclei from 3 mice). Graph annotations and statistics as in (C) . G) Pol <t>II</t> <t>ChIP-seq</t> and input read coverage in WT and Lmna CKO cardiomyocytes (3 mice per genotype). ChIP-seq signals are normalized to <t>internal</t> <t>spike-in</t> controls. H) Average Pol II ChIP-seq signals across 21,177 protein-coding genes. X-axis: 100 equally-spaced bins in gene bodies, 5 bins for 1 kb-upstream regions, and 10 bins for 2 kb-downstream regions. I) Statistical comparison of gene-body Pol II signals in Lmna CKO versus WT cardiomyocytes for 11,942 Pol II-bound genes. Pol II-lost or gained genes are defined at limma p -value < 0.05. J) Ten most enriched Gene Ontology terms among the 1,759 Pol II-lost genes in Lmna CKO cardiomyocytes, with three representative genes for each term. P: Metascape p -value. K) Gene expression state of Pol II-lost, Pol II-gained, and all other genes in Lmna CKO (n=5) versus WT (n=7) hearts. P, DESeq2 p -value. RNA-seq data from En et al. 2024. L) Summary of . Nuclear rupture causes transcriptional deficiency due to RNA Pol II loss.
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    A) Immunofluorescence for bromouridine (BrU) after cardiomyocytes were cultured with BrU for 2 hr to label nascent RNAs. One binucleated cardiomyocyte per image, with nuclei zoomed in. Texts and icons below images indicate nuclear states. Scale bar: 5 μm. All data in , except , are from cardiomyocytes freshly isolated from mice at day 14 post tamoxifen. B) Nuclear BrU intensity by nuclear states after 1-hr BrU incubation. Density and box plots: BrU intensity distribution and interquartile range. Circles: mean intensity within biological replicates (color coded). Asterisks: P < 0.05 from t -tests on linear regression-estimated means with mouse-clustered standard errors. Underlying data: 244 intact nuclei from 4 WT mice, 275 intact, 111 ruptured, 104 resealed nuclei from 3 Lmna CKO mice. C) Relationship between nuclear BrU intensity and nuclear NLS–tdTomato intensity in all types of nuclei in Lmna CKO cardiomyocytes (519 nuclei from 3 mice). Line: simple linear regression fit with 95% confidence interval. R: Pearson correlation coefficient. P: t -test p -value on linear regression-estimated means with mouse-clustered standard errors. See for individual replicates. D) Immunofluorescence for RNA polymerase II (Pol II) in cardiomyocytes. Scale bar: 5 μm. E) Nuclear Pol II intensity by nuclear states. Underlying data: 285 intact nuclei from 3 WT mice, 180 intact, 133 ruptured, 136 resealed nuclei from 3 Lmna CKO mice. Graph annotations and statistics as in (B) . F) Relationship between Pol II intensity and NLS–tdTomato intensity in all types of nuclei in Lmna CKO cardiomyocytes (495 nuclei from 3 mice). Graph annotations and statistics as in (C) . G) Pol <t>II</t> <t>ChIP-seq</t> and input read coverage in WT and Lmna CKO cardiomyocytes (3 mice per genotype). ChIP-seq signals are normalized to <t>internal</t> <t>spike-in</t> controls. H) Average Pol II ChIP-seq signals across 21,177 protein-coding genes. X-axis: 100 equally-spaced bins in gene bodies, 5 bins for 1 kb-upstream regions, and 10 bins for 2 kb-downstream regions. I) Statistical comparison of gene-body Pol II signals in Lmna CKO versus WT cardiomyocytes for 11,942 Pol II-bound genes. Pol II-lost or gained genes are defined at limma p -value < 0.05. J) Ten most enriched Gene Ontology terms among the 1,759 Pol II-lost genes in Lmna CKO cardiomyocytes, with three representative genes for each term. P: Metascape p -value. K) Gene expression state of Pol II-lost, Pol II-gained, and all other genes in Lmna CKO (n=5) versus WT (n=7) hearts. P, DESeq2 p -value. RNA-seq data from En et al. 2024. L) Summary of . Nuclear rupture causes transcriptional deficiency due to RNA Pol II loss.
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    A) Immunofluorescence for bromouridine (BrU) after cardiomyocytes were cultured with BrU for 2 hr to label nascent RNAs. One binucleated cardiomyocyte per image, with nuclei zoomed in. Texts and icons below images indicate nuclear states. Scale bar: 5 μm. All data in , except , are from cardiomyocytes freshly isolated from mice at day 14 post tamoxifen. B) Nuclear BrU intensity by nuclear states after 1-hr BrU incubation. Density and box plots: BrU intensity distribution and interquartile range. Circles: mean intensity within biological replicates (color coded). Asterisks: P < 0.05 from t -tests on linear regression-estimated means with mouse-clustered standard errors. Underlying data: 244 intact nuclei from 4 WT mice, 275 intact, 111 ruptured, 104 resealed nuclei from 3 Lmna CKO mice. C) Relationship between nuclear BrU intensity and nuclear NLS–tdTomato intensity in all types of nuclei in Lmna CKO cardiomyocytes (519 nuclei from 3 mice). Line: simple linear regression fit with 95% confidence interval. R: Pearson correlation coefficient. P: t -test p -value on linear regression-estimated means with mouse-clustered standard errors. See for individual replicates. D) Immunofluorescence for RNA polymerase II (Pol II) in cardiomyocytes. Scale bar: 5 μm. E) Nuclear Pol II intensity by nuclear states. Underlying data: 285 intact nuclei from 3 WT mice, 180 intact, 133 ruptured, 136 resealed nuclei from 3 Lmna CKO mice. Graph annotations and statistics as in (B) . F) Relationship between Pol II intensity and NLS–tdTomato intensity in all types of nuclei in Lmna CKO cardiomyocytes (495 nuclei from 3 mice). Graph annotations and statistics as in (C) . G) Pol <t>II</t> <t>ChIP-seq</t> and input read coverage in WT and Lmna CKO cardiomyocytes (3 mice per genotype). ChIP-seq signals are normalized to <t>internal</t> <t>spike-in</t> controls. H) Average Pol II ChIP-seq signals across 21,177 protein-coding genes. X-axis: 100 equally-spaced bins in gene bodies, 5 bins for 1 kb-upstream regions, and 10 bins for 2 kb-downstream regions. I) Statistical comparison of gene-body Pol II signals in Lmna CKO versus WT cardiomyocytes for 11,942 Pol II-bound genes. Pol II-lost or gained genes are defined at limma p -value < 0.05. J) Ten most enriched Gene Ontology terms among the 1,759 Pol II-lost genes in Lmna CKO cardiomyocytes, with three representative genes for each term. P: Metascape p -value. K) Gene expression state of Pol II-lost, Pol II-gained, and all other genes in Lmna CKO (n=5) versus WT (n=7) hearts. P, DESeq2 p -value. RNA-seq data from En et al. 2024. L) Summary of . Nuclear rupture causes transcriptional deficiency due to RNA Pol II loss.
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    A) Immunofluorescence for bromouridine (BrU) after cardiomyocytes were cultured with BrU for 2 hr to label nascent RNAs. One binucleated cardiomyocyte per image, with nuclei zoomed in. Texts and icons below images indicate nuclear states. Scale bar: 5 μm. All data in , except , are from cardiomyocytes freshly isolated from mice at day 14 post tamoxifen. B) Nuclear BrU intensity by nuclear states after 1-hr BrU incubation. Density and box plots: BrU intensity distribution and interquartile range. Circles: mean intensity within biological replicates (color coded). Asterisks: P < 0.05 from t -tests on linear regression-estimated means with mouse-clustered standard errors. Underlying data: 244 intact nuclei from 4 WT mice, 275 intact, 111 ruptured, 104 resealed nuclei from 3 Lmna CKO mice. C) Relationship between nuclear BrU intensity and nuclear NLS–tdTomato intensity in all types of nuclei in Lmna CKO cardiomyocytes (519 nuclei from 3 mice). Line: simple linear regression fit with 95% confidence interval. R: Pearson correlation coefficient. P: t -test p -value on linear regression-estimated means with mouse-clustered standard errors. See for individual replicates. D) Immunofluorescence for RNA polymerase II (Pol II) in cardiomyocytes. Scale bar: 5 μm. E) Nuclear Pol II intensity by nuclear states. Underlying data: 285 intact nuclei from 3 WT mice, 180 intact, 133 ruptured, 136 resealed nuclei from 3 Lmna CKO mice. Graph annotations and statistics as in (B) . F) Relationship between Pol II intensity and NLS–tdTomato intensity in all types of nuclei in Lmna CKO cardiomyocytes (495 nuclei from 3 mice). Graph annotations and statistics as in (C) . G) Pol <t>II</t> <t>ChIP-seq</t> and input read coverage in WT and Lmna CKO cardiomyocytes (3 mice per genotype). ChIP-seq signals are normalized to <t>internal</t> <t>spike-in</t> controls. H) Average Pol II ChIP-seq signals across 21,177 protein-coding genes. X-axis: 100 equally-spaced bins in gene bodies, 5 bins for 1 kb-upstream regions, and 10 bins for 2 kb-downstream regions. I) Statistical comparison of gene-body Pol II signals in Lmna CKO versus WT cardiomyocytes for 11,942 Pol II-bound genes. Pol II-lost or gained genes are defined at limma p -value < 0.05. J) Ten most enriched Gene Ontology terms among the 1,759 Pol II-lost genes in Lmna CKO cardiomyocytes, with three representative genes for each term. P: Metascape p -value. K) Gene expression state of Pol II-lost, Pol II-gained, and all other genes in Lmna CKO (n=5) versus WT (n=7) hearts. P, DESeq2 p -value. RNA-seq data from En et al. 2024. L) Summary of . Nuclear rupture causes transcriptional deficiency due to RNA Pol II loss.
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    A) Immunofluorescence for bromouridine (BrU) after cardiomyocytes were cultured with BrU for 2 hr to label nascent RNAs. One binucleated cardiomyocyte per image, with nuclei zoomed in. Texts and icons below images indicate nuclear states. Scale bar: 5 μm. All data in , except , are from cardiomyocytes freshly isolated from mice at day 14 post tamoxifen. B) Nuclear BrU intensity by nuclear states after 1-hr BrU incubation. Density and box plots: BrU intensity distribution and interquartile range. Circles: mean intensity within biological replicates (color coded). Asterisks: P < 0.05 from t -tests on linear regression-estimated means with mouse-clustered standard errors. Underlying data: 244 intact nuclei from 4 WT mice, 275 intact, 111 ruptured, 104 resealed nuclei from 3 Lmna CKO mice. C) Relationship between nuclear BrU intensity and nuclear NLS–tdTomato intensity in all types of nuclei in Lmna CKO cardiomyocytes (519 nuclei from 3 mice). Line: simple linear regression fit with 95% confidence interval. R: Pearson correlation coefficient. P: t -test p -value on linear regression-estimated means with mouse-clustered standard errors. See for individual replicates. D) Immunofluorescence for RNA polymerase II (Pol II) in cardiomyocytes. Scale bar: 5 μm. E) Nuclear Pol II intensity by nuclear states. Underlying data: 285 intact nuclei from 3 WT mice, 180 intact, 133 ruptured, 136 resealed nuclei from 3 Lmna CKO mice. Graph annotations and statistics as in (B) . F) Relationship between Pol II intensity and NLS–tdTomato intensity in all types of nuclei in Lmna CKO cardiomyocytes (495 nuclei from 3 mice). Graph annotations and statistics as in (C) . G) Pol <t>II</t> <t>ChIP-seq</t> and input read coverage in WT and Lmna CKO cardiomyocytes (3 mice per genotype). ChIP-seq signals are normalized to <t>internal</t> <t>spike-in</t> controls. H) Average Pol II ChIP-seq signals across 21,177 protein-coding genes. X-axis: 100 equally-spaced bins in gene bodies, 5 bins for 1 kb-upstream regions, and 10 bins for 2 kb-downstream regions. I) Statistical comparison of gene-body Pol II signals in Lmna CKO versus WT cardiomyocytes for 11,942 Pol II-bound genes. Pol II-lost or gained genes are defined at limma p -value < 0.05. J) Ten most enriched Gene Ontology terms among the 1,759 Pol II-lost genes in Lmna CKO cardiomyocytes, with three representative genes for each term. P: Metascape p -value. K) Gene expression state of Pol II-lost, Pol II-gained, and all other genes in Lmna CKO (n=5) versus WT (n=7) hearts. P, DESeq2 p -value. RNA-seq data from En et al. 2024. L) Summary of . Nuclear rupture causes transcriptional deficiency due to RNA Pol II loss.
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    chip seq spike  (Danaher Inc)
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    A) Immunofluorescence for bromouridine (BrU) after cardiomyocytes were cultured with BrU for 2 hr to label nascent RNAs. One binucleated cardiomyocyte per image, with nuclei zoomed in. Texts and icons below images indicate nuclear states. Scale bar: 5 μm. All data in , except , are from cardiomyocytes freshly isolated from mice at day 14 post tamoxifen. B) Nuclear BrU intensity by nuclear states after 1-hr BrU incubation. Density and box plots: BrU intensity distribution and interquartile range. Circles: mean intensity within biological replicates (color coded). Asterisks: P < 0.05 from t -tests on linear regression-estimated means with mouse-clustered standard errors. Underlying data: 244 intact nuclei from 4 WT mice, 275 intact, 111 ruptured, 104 resealed nuclei from 3 Lmna CKO mice. C) Relationship between nuclear BrU intensity and nuclear NLS–tdTomato intensity in all types of nuclei in Lmna CKO cardiomyocytes (519 nuclei from 3 mice). Line: simple linear regression fit with 95% confidence interval. R: Pearson correlation coefficient. P: t -test p -value on linear regression-estimated means with mouse-clustered standard errors. See for individual replicates. D) Immunofluorescence for RNA polymerase II (Pol II) in cardiomyocytes. Scale bar: 5 μm. E) Nuclear Pol II intensity by nuclear states. Underlying data: 285 intact nuclei from 3 WT mice, 180 intact, 133 ruptured, 136 resealed nuclei from 3 Lmna CKO mice. Graph annotations and statistics as in (B) . F) Relationship between Pol II intensity and NLS–tdTomato intensity in all types of nuclei in Lmna CKO cardiomyocytes (495 nuclei from 3 mice). Graph annotations and statistics as in (C) . G) Pol <t>II</t> <t>ChIP-seq</t> and input read coverage in WT and Lmna CKO cardiomyocytes (3 mice per genotype). ChIP-seq signals are normalized to <t>internal</t> <t>spike-in</t> controls. H) Average Pol II ChIP-seq signals across 21,177 protein-coding genes. X-axis: 100 equally-spaced bins in gene bodies, 5 bins for 1 kb-upstream regions, and 10 bins for 2 kb-downstream regions. I) Statistical comparison of gene-body Pol II signals in Lmna CKO versus WT cardiomyocytes for 11,942 Pol II-bound genes. Pol II-lost or gained genes are defined at limma p -value < 0.05. J) Ten most enriched Gene Ontology terms among the 1,759 Pol II-lost genes in Lmna CKO cardiomyocytes, with three representative genes for each term. P: Metascape p -value. K) Gene expression state of Pol II-lost, Pol II-gained, and all other genes in Lmna CKO (n=5) versus WT (n=7) hearts. P, DESeq2 p -value. RNA-seq data from En et al. 2024. L) Summary of . Nuclear rupture causes transcriptional deficiency due to RNA Pol II loss.
    Chip Seq Spike, supplied by Danaher Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    deposited data calibrated spike in chip seq  (Zymo Research)
    93
    Zymo Research deposited data calibrated spike in chip seq
    A) Immunofluorescence for bromouridine (BrU) after cardiomyocytes were cultured with BrU for 2 hr to label nascent RNAs. One binucleated cardiomyocyte per image, with nuclei zoomed in. Texts and icons below images indicate nuclear states. Scale bar: 5 μm. All data in , except , are from cardiomyocytes freshly isolated from mice at day 14 post tamoxifen. B) Nuclear BrU intensity by nuclear states after 1-hr BrU incubation. Density and box plots: BrU intensity distribution and interquartile range. Circles: mean intensity within biological replicates (color coded). Asterisks: P < 0.05 from t -tests on linear regression-estimated means with mouse-clustered standard errors. Underlying data: 244 intact nuclei from 4 WT mice, 275 intact, 111 ruptured, 104 resealed nuclei from 3 Lmna CKO mice. C) Relationship between nuclear BrU intensity and nuclear NLS–tdTomato intensity in all types of nuclei in Lmna CKO cardiomyocytes (519 nuclei from 3 mice). Line: simple linear regression fit with 95% confidence interval. R: Pearson correlation coefficient. P: t -test p -value on linear regression-estimated means with mouse-clustered standard errors. See for individual replicates. D) Immunofluorescence for RNA polymerase II (Pol II) in cardiomyocytes. Scale bar: 5 μm. E) Nuclear Pol II intensity by nuclear states. Underlying data: 285 intact nuclei from 3 WT mice, 180 intact, 133 ruptured, 136 resealed nuclei from 3 Lmna CKO mice. Graph annotations and statistics as in (B) . F) Relationship between Pol II intensity and NLS–tdTomato intensity in all types of nuclei in Lmna CKO cardiomyocytes (495 nuclei from 3 mice). Graph annotations and statistics as in (C) . G) Pol <t>II</t> <t>ChIP-seq</t> and input read coverage in WT and Lmna CKO cardiomyocytes (3 mice per genotype). ChIP-seq signals are normalized to <t>internal</t> <t>spike-in</t> controls. H) Average Pol II ChIP-seq signals across 21,177 protein-coding genes. X-axis: 100 equally-spaced bins in gene bodies, 5 bins for 1 kb-upstream regions, and 10 bins for 2 kb-downstream regions. I) Statistical comparison of gene-body Pol II signals in Lmna CKO versus WT cardiomyocytes for 11,942 Pol II-bound genes. Pol II-lost or gained genes are defined at limma p -value < 0.05. J) Ten most enriched Gene Ontology terms among the 1,759 Pol II-lost genes in Lmna CKO cardiomyocytes, with three representative genes for each term. P: Metascape p -value. K) Gene expression state of Pol II-lost, Pol II-gained, and all other genes in Lmna CKO (n=5) versus WT (n=7) hearts. P, DESeq2 p -value. RNA-seq data from En et al. 2024. L) Summary of . Nuclear rupture causes transcriptional deficiency due to RNA Pol II loss.
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    A) Immunofluorescence for bromouridine (BrU) after cardiomyocytes were cultured with BrU for 2 hr to label nascent RNAs. One binucleated cardiomyocyte per image, with nuclei zoomed in. Texts and icons below images indicate nuclear states. Scale bar: 5 μm. All data in , except , are from cardiomyocytes freshly isolated from mice at day 14 post tamoxifen. B) Nuclear BrU intensity by nuclear states after 1-hr BrU incubation. Density and box plots: BrU intensity distribution and interquartile range. Circles: mean intensity within biological replicates (color coded). Asterisks: P < 0.05 from t -tests on linear regression-estimated means with mouse-clustered standard errors. Underlying data: 244 intact nuclei from 4 WT mice, 275 intact, 111 ruptured, 104 resealed nuclei from 3 Lmna CKO mice. C) Relationship between nuclear BrU intensity and nuclear NLS–tdTomato intensity in all types of nuclei in Lmna CKO cardiomyocytes (519 nuclei from 3 mice). Line: simple linear regression fit with 95% confidence interval. R: Pearson correlation coefficient. P: t -test p -value on linear regression-estimated means with mouse-clustered standard errors. See for individual replicates. D) Immunofluorescence for RNA polymerase II (Pol II) in cardiomyocytes. Scale bar: 5 μm. E) Nuclear Pol II intensity by nuclear states. Underlying data: 285 intact nuclei from 3 WT mice, 180 intact, 133 ruptured, 136 resealed nuclei from 3 Lmna CKO mice. Graph annotations and statistics as in (B) . F) Relationship between Pol II intensity and NLS–tdTomato intensity in all types of nuclei in Lmna CKO cardiomyocytes (495 nuclei from 3 mice). Graph annotations and statistics as in (C) . G) Pol II ChIP-seq and input read coverage in WT and Lmna CKO cardiomyocytes (3 mice per genotype). ChIP-seq signals are normalized to internal spike-in controls. H) Average Pol II ChIP-seq signals across 21,177 protein-coding genes. X-axis: 100 equally-spaced bins in gene bodies, 5 bins for 1 kb-upstream regions, and 10 bins for 2 kb-downstream regions. I) Statistical comparison of gene-body Pol II signals in Lmna CKO versus WT cardiomyocytes for 11,942 Pol II-bound genes. Pol II-lost or gained genes are defined at limma p -value < 0.05. J) Ten most enriched Gene Ontology terms among the 1,759 Pol II-lost genes in Lmna CKO cardiomyocytes, with three representative genes for each term. P: Metascape p -value. K) Gene expression state of Pol II-lost, Pol II-gained, and all other genes in Lmna CKO (n=5) versus WT (n=7) hearts. P, DESeq2 p -value. RNA-seq data from En et al. 2024. L) Summary of . Nuclear rupture causes transcriptional deficiency due to RNA Pol II loss.

    Journal: bioRxiv

    Article Title: RNA polymerase loss by nuclear rupture drives LMNA cardiomyopathy

    doi: 10.64898/2026.04.03.716433

    Figure Lengend Snippet: A) Immunofluorescence for bromouridine (BrU) after cardiomyocytes were cultured with BrU for 2 hr to label nascent RNAs. One binucleated cardiomyocyte per image, with nuclei zoomed in. Texts and icons below images indicate nuclear states. Scale bar: 5 μm. All data in , except , are from cardiomyocytes freshly isolated from mice at day 14 post tamoxifen. B) Nuclear BrU intensity by nuclear states after 1-hr BrU incubation. Density and box plots: BrU intensity distribution and interquartile range. Circles: mean intensity within biological replicates (color coded). Asterisks: P < 0.05 from t -tests on linear regression-estimated means with mouse-clustered standard errors. Underlying data: 244 intact nuclei from 4 WT mice, 275 intact, 111 ruptured, 104 resealed nuclei from 3 Lmna CKO mice. C) Relationship between nuclear BrU intensity and nuclear NLS–tdTomato intensity in all types of nuclei in Lmna CKO cardiomyocytes (519 nuclei from 3 mice). Line: simple linear regression fit with 95% confidence interval. R: Pearson correlation coefficient. P: t -test p -value on linear regression-estimated means with mouse-clustered standard errors. See for individual replicates. D) Immunofluorescence for RNA polymerase II (Pol II) in cardiomyocytes. Scale bar: 5 μm. E) Nuclear Pol II intensity by nuclear states. Underlying data: 285 intact nuclei from 3 WT mice, 180 intact, 133 ruptured, 136 resealed nuclei from 3 Lmna CKO mice. Graph annotations and statistics as in (B) . F) Relationship between Pol II intensity and NLS–tdTomato intensity in all types of nuclei in Lmna CKO cardiomyocytes (495 nuclei from 3 mice). Graph annotations and statistics as in (C) . G) Pol II ChIP-seq and input read coverage in WT and Lmna CKO cardiomyocytes (3 mice per genotype). ChIP-seq signals are normalized to internal spike-in controls. H) Average Pol II ChIP-seq signals across 21,177 protein-coding genes. X-axis: 100 equally-spaced bins in gene bodies, 5 bins for 1 kb-upstream regions, and 10 bins for 2 kb-downstream regions. I) Statistical comparison of gene-body Pol II signals in Lmna CKO versus WT cardiomyocytes for 11,942 Pol II-bound genes. Pol II-lost or gained genes are defined at limma p -value < 0.05. J) Ten most enriched Gene Ontology terms among the 1,759 Pol II-lost genes in Lmna CKO cardiomyocytes, with three representative genes for each term. P: Metascape p -value. K) Gene expression state of Pol II-lost, Pol II-gained, and all other genes in Lmna CKO (n=5) versus WT (n=7) hearts. P, DESeq2 p -value. RNA-seq data from En et al. 2024. L) Summary of . Nuclear rupture causes transcriptional deficiency due to RNA Pol II loss.

    Article Snippet: We used AAVpro 293T cells (TaKaRa, 632273) for MyoAAV production and BJ-5ta cells (human hTERT-immortalized foreskin fibroblast; ATCC, CRL-4001) for ChIP-seq spike-in controls.

    Techniques: Immunofluorescence, Cell Culture, Isolation, Incubation, ChIP-sequencing, Comparison, Gene Expression, RNA Sequencing

    A) Number of Pol II ChIP-seq and input sequencing reads aligned to the mouse genome (experimental) or the human genome (spike-in control). Scale factors are computed by spike-in control reads and sequencing depths and used to normalize Pol II ChIP-seq signals. All data in are derived from mice at 2 weeks post tamoxifen. B) Pol II ChIP-seq read coverage in all mouse genes stratified by gene-body Pol II coverage. Genes with Pol II coverage greater than or equal to 100 (2 in Log 10 ) were considered Pol II-bound (11,942 genes). C) Pol II ChIP-seq read coverage in all human genes, derived from the spike-in control chromatin. D) Gene-body Pol II ChIP-seq read coverage between every pair of biological replicates. E) Principal Component Analysis (PCA) of gene-body Pol II coverage in 11,942 Pol II-bound protein-coding genes. F) Cumulative fraction of 1,759 Pol II-lost genes and all other genes (y-axis) along the scale of differential gene expression between Lmna CKO hearts and wild-type hearts (x-axis). P, Kolmogorov-Smirnov test p -value comparing log 2 fold change of gene expression between Pol II-lost genes and all other genes. G) Gene expression state of Pol II-lost genes, Pol II-gained genes, and all other genes in the cardiomyocyte population in Lmna CKO (n=3) versus WT (n=3) hearts derived from single-nucleus RNA-seq in En et al. 2024. P, DESeq2 p -value. H) Same as F, but along the scale of differential gene expression between Lmna CKO and wild-type pseudo-bulk cardiomyocytes from the single-nucleus RNA-seq. P, Kolmogorov-Smirnov test p -value comparing log 2 fold change of gene expression between Pol II-lost genes and all other genes.

    Journal: bioRxiv

    Article Title: RNA polymerase loss by nuclear rupture drives LMNA cardiomyopathy

    doi: 10.64898/2026.04.03.716433

    Figure Lengend Snippet: A) Number of Pol II ChIP-seq and input sequencing reads aligned to the mouse genome (experimental) or the human genome (spike-in control). Scale factors are computed by spike-in control reads and sequencing depths and used to normalize Pol II ChIP-seq signals. All data in are derived from mice at 2 weeks post tamoxifen. B) Pol II ChIP-seq read coverage in all mouse genes stratified by gene-body Pol II coverage. Genes with Pol II coverage greater than or equal to 100 (2 in Log 10 ) were considered Pol II-bound (11,942 genes). C) Pol II ChIP-seq read coverage in all human genes, derived from the spike-in control chromatin. D) Gene-body Pol II ChIP-seq read coverage between every pair of biological replicates. E) Principal Component Analysis (PCA) of gene-body Pol II coverage in 11,942 Pol II-bound protein-coding genes. F) Cumulative fraction of 1,759 Pol II-lost genes and all other genes (y-axis) along the scale of differential gene expression between Lmna CKO hearts and wild-type hearts (x-axis). P, Kolmogorov-Smirnov test p -value comparing log 2 fold change of gene expression between Pol II-lost genes and all other genes. G) Gene expression state of Pol II-lost genes, Pol II-gained genes, and all other genes in the cardiomyocyte population in Lmna CKO (n=3) versus WT (n=3) hearts derived from single-nucleus RNA-seq in En et al. 2024. P, DESeq2 p -value. H) Same as F, but along the scale of differential gene expression between Lmna CKO and wild-type pseudo-bulk cardiomyocytes from the single-nucleus RNA-seq. P, Kolmogorov-Smirnov test p -value comparing log 2 fold change of gene expression between Pol II-lost genes and all other genes.

    Article Snippet: We used AAVpro 293T cells (TaKaRa, 632273) for MyoAAV production and BJ-5ta cells (human hTERT-immortalized foreskin fibroblast; ATCC, CRL-4001) for ChIP-seq spike-in controls.

    Techniques: ChIP-sequencing, Sequencing, Control, Derivative Assay, Gene Expression, RNA Sequencing