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hi c  (Arima Genomics Inc)


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    Structured Review

    Arima Genomics Inc hi c
    Hi C, supplied by Arima Genomics Inc, 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/hi c/product/Arima Genomics Inc
    Average 99 stars, based on 1 article reviews
    hi c - by Bioz Stars, 2025-05
    99/100 stars

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    Arima Genomics Inc lncap cells
    A. Schematic overview of the experimental design. <t>LNCaP</t> <t>cells</t> were treated with 10nM DHT and samples were collected at five time-points for the androgen-stimulation time-course (30mins, 2hrs, 4hrs, 16hrs and EtOH (control)) for mRNA-seq, AR ChIP-seq and Promoter Capture Hi-C (PCHi-C). B. Principal component analyses showing the relationship among the AR binding ChIP-seq profiles upon DHT stimulation in the androgen-stimulation time-course. Data plotted for normalised read counts. The number of differentially bound AR peaks between each DHT time-point and EtOH is shown. C. Heatmap and average profiles of AR ChIP-Seq (n=3 merged replicates) signal intensity at AR binding sites for differentially bound AR peaks for each time-point of DHT stimulation compared to EtOH control. D. Overlap of differentially bound AR peaks at each time-point of DHT stimulation compared to EtOH control presented in an upset plot. E. Transcription factor motifs enriched at differentially bound AR peaks (FDR < 0.05 and logFC > 0.6) identified by two-way analyses between each DHT treatment time-point and EtOH control. Percent of AR peaks with motif was compared to matched random regions across the genome.
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    Image Search Results


    A. Schematic overview of the experimental design. LNCaP cells were treated with 10nM DHT and samples were collected at five time-points for the androgen-stimulation time-course (30mins, 2hrs, 4hrs, 16hrs and EtOH (control)) for mRNA-seq, AR ChIP-seq and Promoter Capture Hi-C (PCHi-C). B. Principal component analyses showing the relationship among the AR binding ChIP-seq profiles upon DHT stimulation in the androgen-stimulation time-course. Data plotted for normalised read counts. The number of differentially bound AR peaks between each DHT time-point and EtOH is shown. C. Heatmap and average profiles of AR ChIP-Seq (n=3 merged replicates) signal intensity at AR binding sites for differentially bound AR peaks for each time-point of DHT stimulation compared to EtOH control. D. Overlap of differentially bound AR peaks at each time-point of DHT stimulation compared to EtOH control presented in an upset plot. E. Transcription factor motifs enriched at differentially bound AR peaks (FDR < 0.05 and logFC > 0.6) identified by two-way analyses between each DHT treatment time-point and EtOH control. Percent of AR peaks with motif was compared to matched random regions across the genome.

    Journal: bioRxiv

    Article Title: Androgen stimulation rapidly reorganizes temporal 3D genome and epigenome states to trigger AR-mediated transcription in prostate cancer

    doi: 10.1101/2024.12.17.628805

    Figure Lengend Snippet: A. Schematic overview of the experimental design. LNCaP cells were treated with 10nM DHT and samples were collected at five time-points for the androgen-stimulation time-course (30mins, 2hrs, 4hrs, 16hrs and EtOH (control)) for mRNA-seq, AR ChIP-seq and Promoter Capture Hi-C (PCHi-C). B. Principal component analyses showing the relationship among the AR binding ChIP-seq profiles upon DHT stimulation in the androgen-stimulation time-course. Data plotted for normalised read counts. The number of differentially bound AR peaks between each DHT time-point and EtOH is shown. C. Heatmap and average profiles of AR ChIP-Seq (n=3 merged replicates) signal intensity at AR binding sites for differentially bound AR peaks for each time-point of DHT stimulation compared to EtOH control. D. Overlap of differentially bound AR peaks at each time-point of DHT stimulation compared to EtOH control presented in an upset plot. E. Transcription factor motifs enriched at differentially bound AR peaks (FDR < 0.05 and logFC > 0.6) identified by two-way analyses between each DHT treatment time-point and EtOH control. Percent of AR peaks with motif was compared to matched random regions across the genome.

    Article Snippet: Hi-C in LNCaP cells was performed using the Arima-HiC kit, according to the manufacturer’s protocols (Arima HiC Cat. #A510008, Arima Capture-HiC+ Kit, cat#A510008, cat#A303010 and cat#A311025).

    Techniques: Control, ChIP-sequencing, Hi-C, Binding Assay

    A. Heatmap showing change in expression (Z-scores of logFC vs. EtOH) of genes belonging Androgen Response (GSEA) Hallmark in Factor 3 (“Progressive Transcription”). B. Schematic overview of the experimental design for the “early” DHT time-course. LNCaP cells were treated with 10nM DHT and samples were collected at five time-points for the androgen-stimulation time-course (5mins, 10mins, 20mins, 30mins and EtOH (control) for CUT&RUN (AR, FOXA1, CTCF, c-MYC, H3K27ac, replicates = 3), Promoter Capture Hi-C (PCHi-C, replicates = 2) and TT-seq (replicates = 2). C. Heatmap showing nascent expression (Z-scores of logFC 4sU labelled TT-Seq vs. unlabelled Total RNA-Seq) across “early” DHT treatment time-course of genes in the Androgen Response Hallmark and with top weights in Factor 3 (“Progressive Transcription”). D. Representative examples demonstrating the association between FOXA1 and AR binding as compared across DHT time-points and nascent expression of top weighted androgen response hallmark genes: TPD52 (left panel) and INPP4B (right panel). FOXA1 and AR CUT&RUN signal tracks (replicates merged) are shown. Arrow indicates the initial AR co-binding event with FOXA1 induced by the androgen stimulation.

    Journal: bioRxiv

    Article Title: Androgen stimulation rapidly reorganizes temporal 3D genome and epigenome states to trigger AR-mediated transcription in prostate cancer

    doi: 10.1101/2024.12.17.628805

    Figure Lengend Snippet: A. Heatmap showing change in expression (Z-scores of logFC vs. EtOH) of genes belonging Androgen Response (GSEA) Hallmark in Factor 3 (“Progressive Transcription”). B. Schematic overview of the experimental design for the “early” DHT time-course. LNCaP cells were treated with 10nM DHT and samples were collected at five time-points for the androgen-stimulation time-course (5mins, 10mins, 20mins, 30mins and EtOH (control) for CUT&RUN (AR, FOXA1, CTCF, c-MYC, H3K27ac, replicates = 3), Promoter Capture Hi-C (PCHi-C, replicates = 2) and TT-seq (replicates = 2). C. Heatmap showing nascent expression (Z-scores of logFC 4sU labelled TT-Seq vs. unlabelled Total RNA-Seq) across “early” DHT treatment time-course of genes in the Androgen Response Hallmark and with top weights in Factor 3 (“Progressive Transcription”). D. Representative examples demonstrating the association between FOXA1 and AR binding as compared across DHT time-points and nascent expression of top weighted androgen response hallmark genes: TPD52 (left panel) and INPP4B (right panel). FOXA1 and AR CUT&RUN signal tracks (replicates merged) are shown. Arrow indicates the initial AR co-binding event with FOXA1 induced by the androgen stimulation.

    Article Snippet: Hi-C in LNCaP cells was performed using the Arima-HiC kit, according to the manufacturer’s protocols (Arima HiC Cat. #A510008, Arima Capture-HiC+ Kit, cat#A510008, cat#A303010 and cat#A311025).

    Techniques: Expressing, Control, Hi-C, RNA Sequencing Assay, Binding Assay