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rabbit anti fancd2 antibody  (Novus Biologicals)


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    Structured Review

    Novus Biologicals rabbit anti fancd2 antibody
    (A) Western blot illustrating FANCA protein loss in FANCA-deficient cell lines. (B,C) Lack of <t>FANCD2</t> monoubiquitination, a hallmark of FA pathway activation, in FANCA-deficient cells. (D,E) FANCA-deficient cells show increased vulnerability to MMC: drug response curves for CCH-SCC-FA1 ( FANCA -/- ) vs CCH-SCC-FA1 ( FANCA Compl ) (D) and DU145 WT vs DU145_ FANCA KO (E) are illustrated. (F,G) FANCA-deficient cells show increased vulnerability to cisplatin: drug response curves for CCH-SCC-FA1 ( FANCA -/- ) vs CCH-SCC-FA1 ( FANCA Compl ) (F) and DU145 WT vs DU145_ FANCA KO (G) are illustrated.
    Rabbit Anti Fancd2 Antibody, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 95/100, based on 187 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/rabbit+anti+fancd2+nb100+182/FANCD2+Antibody+-+BSA+Free/bio_rxiv__64898__2026__02__04__703705-167-13-16
    Average 95 stars, based on 187 article reviews
    rabbit anti fancd2 antibody - by Bioz Stars, 2026-09
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    Images

    1) Product Images from "Aurora kinase A is a synthetic lethal target in FANCA-deficient cancers"

    Article Title: Aurora kinase A is a synthetic lethal target in FANCA-deficient cancers

    Journal: bioRxiv

    doi: 10.64898/2026.02.04.703705

    (A) Western blot illustrating FANCA protein loss in FANCA-deficient cell lines. (B,C) Lack of FANCD2 monoubiquitination, a hallmark of FA pathway activation, in FANCA-deficient cells. (D,E) FANCA-deficient cells show increased vulnerability to MMC: drug response curves for CCH-SCC-FA1 ( FANCA -/- ) vs CCH-SCC-FA1 ( FANCA Compl ) (D) and DU145 WT vs DU145_ FANCA KO (E) are illustrated. (F,G) FANCA-deficient cells show increased vulnerability to cisplatin: drug response curves for CCH-SCC-FA1 ( FANCA -/- ) vs CCH-SCC-FA1 ( FANCA Compl ) (F) and DU145 WT vs DU145_ FANCA KO (G) are illustrated.
    Figure Legend Snippet: (A) Western blot illustrating FANCA protein loss in FANCA-deficient cell lines. (B,C) Lack of FANCD2 monoubiquitination, a hallmark of FA pathway activation, in FANCA-deficient cells. (D,E) FANCA-deficient cells show increased vulnerability to MMC: drug response curves for CCH-SCC-FA1 ( FANCA -/- ) vs CCH-SCC-FA1 ( FANCA Compl ) (D) and DU145 WT vs DU145_ FANCA KO (E) are illustrated. (F,G) FANCA-deficient cells show increased vulnerability to cisplatin: drug response curves for CCH-SCC-FA1 ( FANCA -/- ) vs CCH-SCC-FA1 ( FANCA Compl ) (F) and DU145 WT vs DU145_ FANCA KO (G) are illustrated.

    Techniques Used: Western Blot, Activation Assay

    Cells were exposed to 1 µM MMC for 24 hours vs control conditions (DMSO) and imaged via confocal microscopy using Zeiss LSM 710 or Zeiss LSM 980 (63x). (A,C,E) Representative immunofluorescence images for CCH-SCC-FA1 ( FANCA Compl ) vs CCH-SCC-FA1 ( FANCA -/- ) (A), DU145 WT vs DU145_ FANCA KO (C), and RPE1 WT vs RPE1_ FANCA KD (E); scale represents 20 µm. (B, D, F) FANCD2 foci quantification for the same FANCA-deficient vs proficient cell lines. The number of foci per cell are represented, and statistical significance was calculated with the unpaired t-test.
    Figure Legend Snippet: Cells were exposed to 1 µM MMC for 24 hours vs control conditions (DMSO) and imaged via confocal microscopy using Zeiss LSM 710 or Zeiss LSM 980 (63x). (A,C,E) Representative immunofluorescence images for CCH-SCC-FA1 ( FANCA Compl ) vs CCH-SCC-FA1 ( FANCA -/- ) (A), DU145 WT vs DU145_ FANCA KO (C), and RPE1 WT vs RPE1_ FANCA KD (E); scale represents 20 µm. (B, D, F) FANCD2 foci quantification for the same FANCA-deficient vs proficient cell lines. The number of foci per cell are represented, and statistical significance was calculated with the unpaired t-test.

    Techniques Used: Control, Confocal Microscopy, Immunofluorescence



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    Novus Biologicals rabbit anti fancd2 antibody
    (A) Western blot illustrating FANCA protein loss in FANCA-deficient cell lines. (B,C) Lack of <t>FANCD2</t> monoubiquitination, a hallmark of FA pathway activation, in FANCA-deficient cells. (D,E) FANCA-deficient cells show increased vulnerability to MMC: drug response curves for CCH-SCC-FA1 ( FANCA -/- ) vs CCH-SCC-FA1 ( FANCA Compl ) (D) and DU145 WT vs DU145_ FANCA KO (E) are illustrated. (F,G) FANCA-deficient cells show increased vulnerability to cisplatin: drug response curves for CCH-SCC-FA1 ( FANCA -/- ) vs CCH-SCC-FA1 ( FANCA Compl ) (F) and DU145 WT vs DU145_ FANCA KO (G) are illustrated.
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    Novus Biologicals rabbit anti fancd2
    (A) Western blot illustrating FANCA protein loss in FANCA-deficient cell lines. (B,C) Lack of <t>FANCD2</t> monoubiquitination, a hallmark of FA pathway activation, in FANCA-deficient cells. (D,E) FANCA-deficient cells show increased vulnerability to MMC: drug response curves for CCH-SCC-FA1 ( FANCA -/- ) vs CCH-SCC-FA1 ( FANCA Compl ) (D) and DU145 WT vs DU145_ FANCA KO (E) are illustrated. (F,G) FANCA-deficient cells show increased vulnerability to cisplatin: drug response curves for CCH-SCC-FA1 ( FANCA -/- ) vs CCH-SCC-FA1 ( FANCA Compl ) (F) and DU145 WT vs DU145_ FANCA KO (G) are illustrated.
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    (A) Western blot illustrating FANCA protein loss in FANCA-deficient cell lines. (B,C) Lack of <t>FANCD2</t> monoubiquitination, a hallmark of FA pathway activation, in FANCA-deficient cells. (D,E) FANCA-deficient cells show increased vulnerability to MMC: drug response curves for CCH-SCC-FA1 ( FANCA -/- ) vs CCH-SCC-FA1 ( FANCA Compl ) (D) and DU145 WT vs DU145_ FANCA KO (E) are illustrated. (F,G) FANCA-deficient cells show increased vulnerability to cisplatin: drug response curves for CCH-SCC-FA1 ( FANCA -/- ) vs CCH-SCC-FA1 ( FANCA Compl ) (F) and DU145 WT vs DU145_ FANCA KO (G) are illustrated.
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    Novus Biologicals anti resource source identifier rabbit polyclonal fancd2 novus biologicals nb100-182
    (A) Western blot illustrating FANCA protein loss in FANCA-deficient cell lines. (B,C) Lack of <t>FANCD2</t> monoubiquitination, a hallmark of FA pathway activation, in FANCA-deficient cells. (D,E) FANCA-deficient cells show increased vulnerability to MMC: drug response curves for CCH-SCC-FA1 ( FANCA -/- ) vs CCH-SCC-FA1 ( FANCA Compl ) (D) and DU145 WT vs DU145_ FANCA KO (E) are illustrated. (F,G) FANCA-deficient cells show increased vulnerability to cisplatin: drug response curves for CCH-SCC-FA1 ( FANCA -/- ) vs CCH-SCC-FA1 ( FANCA Compl ) (F) and DU145 WT vs DU145_ FANCA KO (G) are illustrated.
    Anti Resource Source Identifier Rabbit Polyclonal Fancd2 Novus Biologicals Nb100 182, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    SLX4IP localizes to stressed CFSs . A , representative images of SLX4IP foci. SLX4IP forms distinct nuclear foci induced by APH (0,2 μM). B , for cell cycle analysis, U2OS cells are sorted by mean EdU and total DAPI content. This allows for quantification of SLX4IP foci in each cell cycle stage (mean ± SD; n = 3 biological replicates; >260 cells analyzed per condition). C , representative images of SLX4IP colocalization with <t>FANCD2</t> in U2OS prometaphase cells. D , quantification of foci in ( C ) (mean ± SD; n = 3 biological replicates; 50 cells analyzed per condition). E , ChIP-qPCR analysis of GFP-SLX4IP or GFP localization to GAPDH or FRA7H in cells treated with DMSO or APH (0,2 μM) (mean ± SD; n = 2 biological replicates). Significance was assessed by Student’s unpaired t -tests. Scale bars: 10 μM.
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    <t>FANCD2</t> binding is non-random and enriched at transcription start sites. ( A ) Heatmaps of FANCD2 ChIP-seq data from U2OS (OK), HCT116 (FE), and FA-D2 + FANCD2 (BL) cells, before and after aphidicolin (APH) treatment. ( B ) Heatmaps from ENCODE ChIP-seq datasets of DNA binding proteins CTCF, POLR2A, and RAD21 and post-translationally modified histones H3K27ac, H3K27me3, and H4K20me1. Heatmaps were generated relative to the transcription start sites (TSS) (5,000 bp upstream and downstream) of UCSC genes and gene predictions from the GRCh37/hg19 genome assembly. ( C ) Read density plots of CTCF, POLR2A, RAD21, H3K27ac, H3K27me3, H4K20me1(left) and OK, FE and BL ChIP-seq data before and after (APH) treatment (right). Plots were generated relative to TSS. An asterisk (*) and hash (#) symbol are used to clearly distinguish the darker blue lines
    Rabbit Polyclonal Anti Fancd2 Antibody, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    <t>FANCD2</t> binding is non-random and enriched at transcription start sites. ( A ) Heatmaps of FANCD2 ChIP-seq data from U2OS (OK), HCT116 (FE), and FA-D2 + FANCD2 (BL) cells, before and after aphidicolin (APH) treatment. ( B ) Heatmaps from ENCODE ChIP-seq datasets of DNA binding proteins CTCF, POLR2A, and RAD21 and post-translationally modified histones H3K27ac, H3K27me3, and H4K20me1. Heatmaps were generated relative to the transcription start sites (TSS) (5,000 bp upstream and downstream) of UCSC genes and gene predictions from the GRCh37/hg19 genome assembly. ( C ) Read density plots of CTCF, POLR2A, RAD21, H3K27ac, H3K27me3, H4K20me1(left) and OK, FE and BL ChIP-seq data before and after (APH) treatment (right). Plots were generated relative to TSS. An asterisk (*) and hash (#) symbol are used to clearly distinguish the darker blue lines
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    Image Search Results


    (A) Western blot illustrating FANCA protein loss in FANCA-deficient cell lines. (B,C) Lack of FANCD2 monoubiquitination, a hallmark of FA pathway activation, in FANCA-deficient cells. (D,E) FANCA-deficient cells show increased vulnerability to MMC: drug response curves for CCH-SCC-FA1 ( FANCA -/- ) vs CCH-SCC-FA1 ( FANCA Compl ) (D) and DU145 WT vs DU145_ FANCA KO (E) are illustrated. (F,G) FANCA-deficient cells show increased vulnerability to cisplatin: drug response curves for CCH-SCC-FA1 ( FANCA -/- ) vs CCH-SCC-FA1 ( FANCA Compl ) (F) and DU145 WT vs DU145_ FANCA KO (G) are illustrated.

    Journal: bioRxiv

    Article Title: Aurora kinase A is a synthetic lethal target in FANCA-deficient cancers

    doi: 10.64898/2026.02.04.703705

    Figure Lengend Snippet: (A) Western blot illustrating FANCA protein loss in FANCA-deficient cell lines. (B,C) Lack of FANCD2 monoubiquitination, a hallmark of FA pathway activation, in FANCA-deficient cells. (D,E) FANCA-deficient cells show increased vulnerability to MMC: drug response curves for CCH-SCC-FA1 ( FANCA -/- ) vs CCH-SCC-FA1 ( FANCA Compl ) (D) and DU145 WT vs DU145_ FANCA KO (E) are illustrated. (F,G) FANCA-deficient cells show increased vulnerability to cisplatin: drug response curves for CCH-SCC-FA1 ( FANCA -/- ) vs CCH-SCC-FA1 ( FANCA Compl ) (F) and DU145 WT vs DU145_ FANCA KO (G) are illustrated.

    Article Snippet: Cells were then incubated with the primary antibody for 1 hour at RT, rabbit anti-FANCD2 antibody (Novus Biologicals, NB100-182, 1:500 in SB) or mouse anti-FANCD2 antibody (Novus Biologicals, NB100-316, 1:500 in SB).

    Techniques: Western Blot, Activation Assay

    Cells were exposed to 1 µM MMC for 24 hours vs control conditions (DMSO) and imaged via confocal microscopy using Zeiss LSM 710 or Zeiss LSM 980 (63x). (A,C,E) Representative immunofluorescence images for CCH-SCC-FA1 ( FANCA Compl ) vs CCH-SCC-FA1 ( FANCA -/- ) (A), DU145 WT vs DU145_ FANCA KO (C), and RPE1 WT vs RPE1_ FANCA KD (E); scale represents 20 µm. (B, D, F) FANCD2 foci quantification for the same FANCA-deficient vs proficient cell lines. The number of foci per cell are represented, and statistical significance was calculated with the unpaired t-test.

    Journal: bioRxiv

    Article Title: Aurora kinase A is a synthetic lethal target in FANCA-deficient cancers

    doi: 10.64898/2026.02.04.703705

    Figure Lengend Snippet: Cells were exposed to 1 µM MMC for 24 hours vs control conditions (DMSO) and imaged via confocal microscopy using Zeiss LSM 710 or Zeiss LSM 980 (63x). (A,C,E) Representative immunofluorescence images for CCH-SCC-FA1 ( FANCA Compl ) vs CCH-SCC-FA1 ( FANCA -/- ) (A), DU145 WT vs DU145_ FANCA KO (C), and RPE1 WT vs RPE1_ FANCA KD (E); scale represents 20 µm. (B, D, F) FANCD2 foci quantification for the same FANCA-deficient vs proficient cell lines. The number of foci per cell are represented, and statistical significance was calculated with the unpaired t-test.

    Article Snippet: Cells were then incubated with the primary antibody for 1 hour at RT, rabbit anti-FANCD2 antibody (Novus Biologicals, NB100-182, 1:500 in SB) or mouse anti-FANCD2 antibody (Novus Biologicals, NB100-316, 1:500 in SB).

    Techniques: Control, Confocal Microscopy, Immunofluorescence

    SLX4IP localizes to stressed CFSs . A , representative images of SLX4IP foci. SLX4IP forms distinct nuclear foci induced by APH (0,2 μM). B , for cell cycle analysis, U2OS cells are sorted by mean EdU and total DAPI content. This allows for quantification of SLX4IP foci in each cell cycle stage (mean ± SD; n = 3 biological replicates; >260 cells analyzed per condition). C , representative images of SLX4IP colocalization with FANCD2 in U2OS prometaphase cells. D , quantification of foci in ( C ) (mean ± SD; n = 3 biological replicates; 50 cells analyzed per condition). E , ChIP-qPCR analysis of GFP-SLX4IP or GFP localization to GAPDH or FRA7H in cells treated with DMSO or APH (0,2 μM) (mean ± SD; n = 2 biological replicates). Significance was assessed by Student’s unpaired t -tests. Scale bars: 10 μM.

    Journal: The Journal of Biological Chemistry

    Article Title: Loss of SLX4IP leads to common fragile site instability and compromises DNA interstrand crosslink repair in vivo

    doi: 10.1016/j.jbc.2025.110244

    Figure Lengend Snippet: SLX4IP localizes to stressed CFSs . A , representative images of SLX4IP foci. SLX4IP forms distinct nuclear foci induced by APH (0,2 μM). B , for cell cycle analysis, U2OS cells are sorted by mean EdU and total DAPI content. This allows for quantification of SLX4IP foci in each cell cycle stage (mean ± SD; n = 3 biological replicates; >260 cells analyzed per condition). C , representative images of SLX4IP colocalization with FANCD2 in U2OS prometaphase cells. D , quantification of foci in ( C ) (mean ± SD; n = 3 biological replicates; 50 cells analyzed per condition). E , ChIP-qPCR analysis of GFP-SLX4IP or GFP localization to GAPDH or FRA7H in cells treated with DMSO or APH (0,2 μM) (mean ± SD; n = 2 biological replicates). Significance was assessed by Student’s unpaired t -tests. Scale bars: 10 μM.

    Article Snippet: For displayed IF, following primary antibodies have been used: 1:250 mouse SLX4IP (SantaCruz, sc-377066); 1:250 sheep SLX4 (University of Dundee, S587D); 1:500 rabbit TRF2 (novus, IMG-124A); 1:1000 rabbit FANCD2 (novus, NB100–182); 1:200 mouse Cyclin A (SantaCruz, sc-271682); 1:1000 rabbit 53BP1 (novus, NB100–304).

    Techniques: Cell Cycle Assay, ChIP-qPCR

    FANCD2 binding is non-random and enriched at transcription start sites. ( A ) Heatmaps of FANCD2 ChIP-seq data from U2OS (OK), HCT116 (FE), and FA-D2 + FANCD2 (BL) cells, before and after aphidicolin (APH) treatment. ( B ) Heatmaps from ENCODE ChIP-seq datasets of DNA binding proteins CTCF, POLR2A, and RAD21 and post-translationally modified histones H3K27ac, H3K27me3, and H4K20me1. Heatmaps were generated relative to the transcription start sites (TSS) (5,000 bp upstream and downstream) of UCSC genes and gene predictions from the GRCh37/hg19 genome assembly. ( C ) Read density plots of CTCF, POLR2A, RAD21, H3K27ac, H3K27me3, H4K20me1(left) and OK, FE and BL ChIP-seq data before and after (APH) treatment (right). Plots were generated relative to TSS. An asterisk (*) and hash (#) symbol are used to clearly distinguish the darker blue lines

    Journal: Functional & Integrative Genomics

    Article Title: FANCD2 genome binding is nonrandom and is enriched at large transcriptionally active neural genes prone to copy number variation

    doi: 10.1007/s10142-024-01453-5

    Figure Lengend Snippet: FANCD2 binding is non-random and enriched at transcription start sites. ( A ) Heatmaps of FANCD2 ChIP-seq data from U2OS (OK), HCT116 (FE), and FA-D2 + FANCD2 (BL) cells, before and after aphidicolin (APH) treatment. ( B ) Heatmaps from ENCODE ChIP-seq datasets of DNA binding proteins CTCF, POLR2A, and RAD21 and post-translationally modified histones H3K27ac, H3K27me3, and H4K20me1. Heatmaps were generated relative to the transcription start sites (TSS) (5,000 bp upstream and downstream) of UCSC genes and gene predictions from the GRCh37/hg19 genome assembly. ( C ) Read density plots of CTCF, POLR2A, RAD21, H3K27ac, H3K27me3, H4K20me1(left) and OK, FE and BL ChIP-seq data before and after (APH) treatment (right). Plots were generated relative to TSS. An asterisk (*) and hash (#) symbol are used to clearly distinguish the darker blue lines

    Article Snippet: Chromatin immunoprecipitation was performed with rabbit polyclonal anti-FANCD2 antibody (NB100-182, Novus Biologicals).

    Techniques: Binding Assay, ChIP-sequencing, DNA Binding Assay, Modification, Generated

    FANCD2 binds to large genes under conditions of replication stress. ( A ) Integrated Genomics Viewer (IGV) snapshot at IMMP2L , NRG3 , DOCK1 , and LARGE1 genomic loci depicting shared and unique FANCD2 occupancy in OK, FE, and BL datasets following aphidicolin (APH) treatment. Specific genomic regions are displayed on top of the graphic. ( B ) Comparison of the gene size distribution of all genes in the human genome to the sizes of genes bound by FANCD2 in OK, FE, and BL datasets. ( C ) Venn diagram of unique and shared FANCD2 binding targets from OK, FE, and BL ChIP-seq datasets. ( D ) List of genes bound by FANCD2 in all three ChIP-seq datasets and their corresponding gene sizes

    Journal: Functional & Integrative Genomics

    Article Title: FANCD2 genome binding is nonrandom and is enriched at large transcriptionally active neural genes prone to copy number variation

    doi: 10.1007/s10142-024-01453-5

    Figure Lengend Snippet: FANCD2 binds to large genes under conditions of replication stress. ( A ) Integrated Genomics Viewer (IGV) snapshot at IMMP2L , NRG3 , DOCK1 , and LARGE1 genomic loci depicting shared and unique FANCD2 occupancy in OK, FE, and BL datasets following aphidicolin (APH) treatment. Specific genomic regions are displayed on top of the graphic. ( B ) Comparison of the gene size distribution of all genes in the human genome to the sizes of genes bound by FANCD2 in OK, FE, and BL datasets. ( C ) Venn diagram of unique and shared FANCD2 binding targets from OK, FE, and BL ChIP-seq datasets. ( D ) List of genes bound by FANCD2 in all three ChIP-seq datasets and their corresponding gene sizes

    Article Snippet: Chromatin immunoprecipitation was performed with rabbit polyclonal anti-FANCD2 antibody (NB100-182, Novus Biologicals).

    Techniques: Comparison, Binding Assay, ChIP-sequencing

    STRINGdb network analysis reveals FANCD2 binding enrichment at neural genes. ( A ) STRINGdb analysis of FANCD2 broad binding regions (BBRs) highlighting genes implicated in nervous system development in the BL ChIP-seq dataset. ( B ) STRINGdb analysis of FANCD2 BBRs highlighting genes associated with the human phenotype (Monarch) mental or behavioral disorder biomarker in the BL ChIP-seq dataset

    Journal: Functional & Integrative Genomics

    Article Title: FANCD2 genome binding is nonrandom and is enriched at large transcriptionally active neural genes prone to copy number variation

    doi: 10.1007/s10142-024-01453-5

    Figure Lengend Snippet: STRINGdb network analysis reveals FANCD2 binding enrichment at neural genes. ( A ) STRINGdb analysis of FANCD2 broad binding regions (BBRs) highlighting genes implicated in nervous system development in the BL ChIP-seq dataset. ( B ) STRINGdb analysis of FANCD2 BBRs highlighting genes associated with the human phenotype (Monarch) mental or behavioral disorder biomarker in the BL ChIP-seq dataset

    Article Snippet: Chromatin immunoprecipitation was performed with rabbit polyclonal anti-FANCD2 antibody (NB100-182, Novus Biologicals).

    Techniques: Binding Assay, ChIP-sequencing, Biomarker Discovery

    FANCD2 broad binding regions overlap with regions of the genome prone to mitotic DNA synthesis. ( A ) IGV snapshot of FANCD2 occupancy at the IMMP2L , AUTS2 , and WWOX genes in OK, FE, and BL ChIP-seq datasets with the corresponding MiDAS-seq peaks from HeLa, U2OS, and HS68 cells at the same genomic loci from the Macheret et al. dataset (Macheret et al. ). Specific genomic regions are displayed on top of the graphic. ( B ) Bar graph depicting % region overlap between OK, FE, and BL FANCD2 ChIP-seq datasets and U2OS, HeLa, and HS68 MiDAS-seq data. ( C ) Bar graph depicting % base pair overlap between OK, FE, and BL FANCD2 ChIP-seq datasets and U2OS, HeLa, and HS68 MiDAS-seq data

    Journal: Functional & Integrative Genomics

    Article Title: FANCD2 genome binding is nonrandom and is enriched at large transcriptionally active neural genes prone to copy number variation

    doi: 10.1007/s10142-024-01453-5

    Figure Lengend Snippet: FANCD2 broad binding regions overlap with regions of the genome prone to mitotic DNA synthesis. ( A ) IGV snapshot of FANCD2 occupancy at the IMMP2L , AUTS2 , and WWOX genes in OK, FE, and BL ChIP-seq datasets with the corresponding MiDAS-seq peaks from HeLa, U2OS, and HS68 cells at the same genomic loci from the Macheret et al. dataset (Macheret et al. ). Specific genomic regions are displayed on top of the graphic. ( B ) Bar graph depicting % region overlap between OK, FE, and BL FANCD2 ChIP-seq datasets and U2OS, HeLa, and HS68 MiDAS-seq data. ( C ) Bar graph depicting % base pair overlap between OK, FE, and BL FANCD2 ChIP-seq datasets and U2OS, HeLa, and HS68 MiDAS-seq data

    Article Snippet: Chromatin immunoprecipitation was performed with rabbit polyclonal anti-FANCD2 antibody (NB100-182, Novus Biologicals).

    Techniques: Binding Assay, DNA Synthesis, ChIP-sequencing

    FANCD2 broad binding regions overlap with regions that are hotspots for copy number variation. ( A ) IGV snapshot of FANCD2 binding at the AUTS2 , NEGR1 , and WWOX genes with copy number variation gain (green) or loss (orange, red) data from the Wilson et al. study (Wilson et al. ) shown above and below the peak regions, respectively. Specific genomic regions are displayed on top of the graphic. ( B ) Bar graphs depicting % region overlap, and % base pair overlap between the OK, FE, and BL FANCD2 ChIP-seq datasets and copy number variation regions from 090 and HF1 cells from the Wilson et al. study (Wilson et al. )

    Journal: Functional & Integrative Genomics

    Article Title: FANCD2 genome binding is nonrandom and is enriched at large transcriptionally active neural genes prone to copy number variation

    doi: 10.1007/s10142-024-01453-5

    Figure Lengend Snippet: FANCD2 broad binding regions overlap with regions that are hotspots for copy number variation. ( A ) IGV snapshot of FANCD2 binding at the AUTS2 , NEGR1 , and WWOX genes with copy number variation gain (green) or loss (orange, red) data from the Wilson et al. study (Wilson et al. ) shown above and below the peak regions, respectively. Specific genomic regions are displayed on top of the graphic. ( B ) Bar graphs depicting % region overlap, and % base pair overlap between the OK, FE, and BL FANCD2 ChIP-seq datasets and copy number variation regions from 090 and HF1 cells from the Wilson et al. study (Wilson et al. )

    Article Snippet: Chromatin immunoprecipitation was performed with rabbit polyclonal anti-FANCD2 antibody (NB100-182, Novus Biologicals).

    Techniques: Binding Assay, ChIP-sequencing

    Loss of FANCD2 impacts gene expression of FANCD2 target genes. ( A ) Morpheus heatmap analysis of RNA-seq data demonstrating differential expression of FANCD2 broad binding region (BBR) genes in FA-D2 ( FANCD2 −/− ) cells relative to FA-D2 + FANCD2 cells. Genes with increased expression in FA-D2 ( FANCD2 −/− ) cells relative to FANCD2-complemented FA-D2 cells are depicted in red and genes with decreased expression are depicted in blue. ( B ) Log2 fold change expression of FANCD2 BBR genes between FA-D2 + FANCD2 and FA-D2 ( FANCD2 −/− ) cells after APH treatment. Genes upregulated in FA-D2 + FANCD2 cells - with an adjusted P value less than 0.05 and a log2 fold change greater than 1 - are shown in red. Genes downregulated in FA-D2 + FANCD2 cells - with an adjusted P value less than 0.05 and a log2 fold change less than − 1 - are shown in green. ( C ) Normalized read counts of FANCD2 BBR genes after APH treatment. FA-D2 + FANCD2 read counts are shown in blue and FA-D2 ( FANCD2 −/− ) are shown in orange. *, P < 0.05; **, P < 0.01; ***, P < 0.001

    Journal: Functional & Integrative Genomics

    Article Title: FANCD2 genome binding is nonrandom and is enriched at large transcriptionally active neural genes prone to copy number variation

    doi: 10.1007/s10142-024-01453-5

    Figure Lengend Snippet: Loss of FANCD2 impacts gene expression of FANCD2 target genes. ( A ) Morpheus heatmap analysis of RNA-seq data demonstrating differential expression of FANCD2 broad binding region (BBR) genes in FA-D2 ( FANCD2 −/− ) cells relative to FA-D2 + FANCD2 cells. Genes with increased expression in FA-D2 ( FANCD2 −/− ) cells relative to FANCD2-complemented FA-D2 cells are depicted in red and genes with decreased expression are depicted in blue. ( B ) Log2 fold change expression of FANCD2 BBR genes between FA-D2 + FANCD2 and FA-D2 ( FANCD2 −/− ) cells after APH treatment. Genes upregulated in FA-D2 + FANCD2 cells - with an adjusted P value less than 0.05 and a log2 fold change greater than 1 - are shown in red. Genes downregulated in FA-D2 + FANCD2 cells - with an adjusted P value less than 0.05 and a log2 fold change less than − 1 - are shown in green. ( C ) Normalized read counts of FANCD2 BBR genes after APH treatment. FA-D2 + FANCD2 read counts are shown in blue and FA-D2 ( FANCD2 −/− ) are shown in orange. *, P < 0.05; **, P < 0.01; ***, P < 0.001

    Article Snippet: Chromatin immunoprecipitation was performed with rabbit polyclonal anti-FANCD2 antibody (NB100-182, Novus Biologicals).

    Techniques: Gene Expression, RNA Sequencing, Quantitative Proteomics, Binding Assay, Expressing