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rechip seq  (Santa Cruz Biotechnology)
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Santa Cruz Biotechnology rechip seq
( A – C ) Circos plot representing the genome-wide co-recruitment profile <t>of</t> <t>E2F4-p53.</t> Circos plot was generated from E2F4-p53 <t>ReChip-seq</t> analysis carried out in ( A ) HCT116 p53 WT, ( B ) HCT116 p21−/−, ( C ) HCT116 p53−/− p53 TAD mutant (+Dox) cells and publicly available E2F4 ChIP seq datasets. The tracks from outside to inside sequentially represent: all the human chromosomes, E2F4-p53 Re-ChIP enrichment regions, E2F4 ChIP enrichment region, E2F4-p53 Re-ChIP intensity, and E2F4 ChIP intensity. ( D ) Heatmap representing E2F4-p53 recruitment in the presence of WT p53 near the TSS. Heatmap was generated based on E2F4-p53 Re-ChIP seq analysis carried out in HCT116 WT cells. ( E , F ) Multi-variant analysis of ChIP-seq. Analysis was done with ( E ) E2F4-p53 Re-ChIP-seq data from HCT116 p53 WT cells, Fischer DREAM targets, and E2F4 ChIP-seq data, ( F ) HCT116 p53 WT, HCT116 p21−/− and HCT116 p53−/− + p53 TAD mutant (+Dox) cells. Venn diagram was generated using peaks enriched within ±1 kb of the TSS in all cases. ( G ) E2F4, p53 Re-ChIP data overlap with E2F4 ChIP seq data. IGV browser tracks from E2F4 p53 Re-ChIP seq peaks (HCT116 p53 WT, HCT116 p21−/−, HCT116 p53−/− p53 TAD mutant (+Dox condition)), E2F4 ChIP seq peaks (HepG2, MCF7), p53 ChIP peak and respective input signals. Upstream of TSS for BLM promoter has been depicted. ( H ) Pathway analysis from E2F4-p53 Re-ChIP seq analysis indicates key pathways affected having implications during cancer progression. Pathway analysis of genes enriched in Re-ChIP-seq of HCT116 p53 WT was performed using GSEA MSigDB.
Rechip Seq, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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( A – C ) Circos plot representing the genome-wide co-recruitment profile of E2F4-p53. Circos plot was generated from E2F4-p53 ReChip-seq analysis carried out in ( A ) HCT116 p53 WT, ( B ) HCT116 p21−/−, ( C ) HCT116 p53−/− p53 TAD mutant (+Dox) cells and publicly available E2F4 ChIP seq datasets. The tracks from outside to inside sequentially represent: all the human chromosomes, E2F4-p53 Re-ChIP enrichment regions, E2F4 ChIP enrichment region, E2F4-p53 Re-ChIP intensity, and E2F4 ChIP intensity. ( D ) Heatmap representing E2F4-p53 recruitment in the presence of WT p53 near the TSS. Heatmap was generated based on E2F4-p53 Re-ChIP seq analysis carried out in HCT116 WT cells. ( E , F ) Multi-variant analysis of ChIP-seq. Analysis was done with ( E ) E2F4-p53 Re-ChIP-seq data from HCT116 p53 WT cells, Fischer DREAM targets, and E2F4 ChIP-seq data, ( F ) HCT116 p53 WT, HCT116 p21−/− and HCT116 p53−/− + p53 TAD mutant (+Dox) cells. Venn diagram was generated using peaks enriched within ±1 kb of the TSS in all cases. ( G ) E2F4, p53 Re-ChIP data overlap with E2F4 ChIP seq data. IGV browser tracks from E2F4 p53 Re-ChIP seq peaks (HCT116 p53 WT, HCT116 p21−/−, HCT116 p53−/− p53 TAD mutant (+Dox condition)), E2F4 ChIP seq peaks (HepG2, MCF7), p53 ChIP peak and respective input signals. Upstream of TSS for BLM promoter has been depicted. ( H ) Pathway analysis from E2F4-p53 Re-ChIP seq analysis indicates key pathways affected having implications during cancer progression. Pathway analysis of genes enriched in Re-ChIP-seq of HCT116 p53 WT was performed using GSEA MSigDB.

Journal: The EMBO Journal

Article Title: p53 regulates DREAM complex-mediated repression in a p21-independent manner

doi: 10.1038/s44318-025-00402-7

Figure Lengend Snippet: ( A – C ) Circos plot representing the genome-wide co-recruitment profile of E2F4-p53. Circos plot was generated from E2F4-p53 ReChip-seq analysis carried out in ( A ) HCT116 p53 WT, ( B ) HCT116 p21−/−, ( C ) HCT116 p53−/− p53 TAD mutant (+Dox) cells and publicly available E2F4 ChIP seq datasets. The tracks from outside to inside sequentially represent: all the human chromosomes, E2F4-p53 Re-ChIP enrichment regions, E2F4 ChIP enrichment region, E2F4-p53 Re-ChIP intensity, and E2F4 ChIP intensity. ( D ) Heatmap representing E2F4-p53 recruitment in the presence of WT p53 near the TSS. Heatmap was generated based on E2F4-p53 Re-ChIP seq analysis carried out in HCT116 WT cells. ( E , F ) Multi-variant analysis of ChIP-seq. Analysis was done with ( E ) E2F4-p53 Re-ChIP-seq data from HCT116 p53 WT cells, Fischer DREAM targets, and E2F4 ChIP-seq data, ( F ) HCT116 p53 WT, HCT116 p21−/− and HCT116 p53−/− + p53 TAD mutant (+Dox) cells. Venn diagram was generated using peaks enriched within ±1 kb of the TSS in all cases. ( G ) E2F4, p53 Re-ChIP data overlap with E2F4 ChIP seq data. IGV browser tracks from E2F4 p53 Re-ChIP seq peaks (HCT116 p53 WT, HCT116 p21−/−, HCT116 p53−/− p53 TAD mutant (+Dox condition)), E2F4 ChIP seq peaks (HepG2, MCF7), p53 ChIP peak and respective input signals. Upstream of TSS for BLM promoter has been depicted. ( H ) Pathway analysis from E2F4-p53 Re-ChIP seq analysis indicates key pathways affected having implications during cancer progression. Pathway analysis of genes enriched in Re-ChIP-seq of HCT116 p53 WT was performed using GSEA MSigDB.

Article Snippet: Mouse anti-p53 DO1 (used for WB in blots expressing p53 wild type and p53 R175H, ChIP, reChIP, reChIP seq) , Santa Cruz Biotechnology , Cat# sc-126, RRID: AB_628082 (WB: 1:5000, reChIP: 3 μg/reaction, reChIP seq: 4 μg/reaction).

Techniques: Genome Wide, Generated, Mutagenesis, ChIP-sequencing, Variant Assay

Reagents and tools table

Journal: The EMBO Journal

Article Title: p53 regulates DREAM complex-mediated repression in a p21-independent manner

doi: 10.1038/s44318-025-00402-7

Figure Lengend Snippet: Reagents and tools table

Article Snippet: Mouse anti-p53 DO1 (used for WB in blots expressing p53 wild type and p53 R175H, ChIP, reChIP, reChIP seq) , Santa Cruz Biotechnology , Cat# sc-126, RRID: AB_628082 (WB: 1:5000, reChIP: 3 μg/reaction, reChIP seq: 4 μg/reaction).

Techniques: Reverse Transcription, SYBR Green Assay, Extraction, Bicinchoninic Acid Protein Assay, Plasmid Preparation, Mutagenesis, Recombinant, Cloning, Expressing, Control, Sequencing, Software