rabbit anti ctcf  (Cell Signaling Technology Inc)

 
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    Name:
    Anti rabbit IgG H L Biotinylated Antibody
    Description:
    Affinity purified goat anti rabbit IgG H L antibody is conjugated to biotin This product has been optimized for use as a secondary antibody in western blotting applications
    Catalog Number:
    14708
    Price:
    None
    Category:
    Secondary Antibodies
    Applications:
    Western Blot
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    Structured Review

    Cell Signaling Technology Inc rabbit anti ctcf
    Foxg1Cre -mediated deletion of <t>Ctcf</t> results in a massive increase in apoptosis. A , Table of genotypes obtained during the embryonic and postnatal periods. Ratios at each time point were analyzed using a χ 2 test. Het, Ctcf flox/WT ;Foxg1-cre +/− . B , Dark-field images of control and Ctcf Foxg1-cre embryos at E13.5. (Please note limbs were taken for genotyping). C , H E staining of E13.5 sagittal cryosections demonstrates complete loss of cortex (Ctx), hippocampal hem (H), basal ganglia (BG), lens (L), and anterior retina (AR), but not the posterior retina (PR), in Ctcf Foxg1-cre embryos. D , Dark-field images of control and Ctcf Foxg1-cre embryos at E11.5. The dashed circle outlines the telencephalon, which is visibly reduced in size in the Ctcf Foxg1-cre embryos compared to littermate controls. E , Immunodetection of CTCF (red) in E11.5 sagittal cryosections confirms specific loss of CTCF expression in the forebrain neuroepithelium of Ctcf Foxg1-cre embryos. F , Pregnant females were subjected to a 1 h BrdU pulse before being killed. Immunodetection of BrdU in E11.5 control and Ctcf Foxg1-cre cortical neuroepithelium is shown. G , BrdU + cells were counted and expressed as a percentage of the total number of DAPI + cells ( n = 3). H , Immunodetection of activated <t>caspase-3</t> (red) in control and Ctcf Foxg1-cre cortical neuroepithelium at E11.5. I , AC3 + cells were counted and expressed as a percentage of the total number of DAPI + cells ( n = 3). J , TUNEL (green) detection in E11.5 control and Ctcf Foxg1-cre cortical neuroepithelium. Error bars represent the SEM. Original magnification: C , 25×; E , 50×; F , H , J , 200×. Scale bars: C , top, 1 mm; bottom, 400 μm; E , 200 μm; F , H , 50 μm; J , 100 μm.
    Affinity purified goat anti rabbit IgG H L antibody is conjugated to biotin This product has been optimized for use as a secondary antibody in western blotting applications
    https://www.bioz.com/result/rabbit anti ctcf/product/Cell Signaling Technology Inc
    Average 99 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit anti ctcf - by Bioz Stars, 2021-09
    99/100 stars

    Images

    1) Product Images from "Dual Effect of CTCF Loss on Neuroprogenitor Differentiation and Survival"

    Article Title: Dual Effect of CTCF Loss on Neuroprogenitor Differentiation and Survival

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.3769-13.2014

    Foxg1Cre -mediated deletion of Ctcf results in a massive increase in apoptosis. A , Table of genotypes obtained during the embryonic and postnatal periods. Ratios at each time point were analyzed using a χ 2 test. Het, Ctcf flox/WT ;Foxg1-cre +/− . B , Dark-field images of control and Ctcf Foxg1-cre embryos at E13.5. (Please note limbs were taken for genotyping). C , H E staining of E13.5 sagittal cryosections demonstrates complete loss of cortex (Ctx), hippocampal hem (H), basal ganglia (BG), lens (L), and anterior retina (AR), but not the posterior retina (PR), in Ctcf Foxg1-cre embryos. D , Dark-field images of control and Ctcf Foxg1-cre embryos at E11.5. The dashed circle outlines the telencephalon, which is visibly reduced in size in the Ctcf Foxg1-cre embryos compared to littermate controls. E , Immunodetection of CTCF (red) in E11.5 sagittal cryosections confirms specific loss of CTCF expression in the forebrain neuroepithelium of Ctcf Foxg1-cre embryos. F , Pregnant females were subjected to a 1 h BrdU pulse before being killed. Immunodetection of BrdU in E11.5 control and Ctcf Foxg1-cre cortical neuroepithelium is shown. G , BrdU + cells were counted and expressed as a percentage of the total number of DAPI + cells ( n = 3). H , Immunodetection of activated caspase-3 (red) in control and Ctcf Foxg1-cre cortical neuroepithelium at E11.5. I , AC3 + cells were counted and expressed as a percentage of the total number of DAPI + cells ( n = 3). J , TUNEL (green) detection in E11.5 control and Ctcf Foxg1-cre cortical neuroepithelium. Error bars represent the SEM. Original magnification: C , 25×; E , 50×; F , H , J , 200×. Scale bars: C , top, 1 mm; bottom, 400 μm; E , 200 μm; F , H , 50 μm; J , 100 μm.
    Figure Legend Snippet: Foxg1Cre -mediated deletion of Ctcf results in a massive increase in apoptosis. A , Table of genotypes obtained during the embryonic and postnatal periods. Ratios at each time point were analyzed using a χ 2 test. Het, Ctcf flox/WT ;Foxg1-cre +/− . B , Dark-field images of control and Ctcf Foxg1-cre embryos at E13.5. (Please note limbs were taken for genotyping). C , H E staining of E13.5 sagittal cryosections demonstrates complete loss of cortex (Ctx), hippocampal hem (H), basal ganglia (BG), lens (L), and anterior retina (AR), but not the posterior retina (PR), in Ctcf Foxg1-cre embryos. D , Dark-field images of control and Ctcf Foxg1-cre embryos at E11.5. The dashed circle outlines the telencephalon, which is visibly reduced in size in the Ctcf Foxg1-cre embryos compared to littermate controls. E , Immunodetection of CTCF (red) in E11.5 sagittal cryosections confirms specific loss of CTCF expression in the forebrain neuroepithelium of Ctcf Foxg1-cre embryos. F , Pregnant females were subjected to a 1 h BrdU pulse before being killed. Immunodetection of BrdU in E11.5 control and Ctcf Foxg1-cre cortical neuroepithelium is shown. G , BrdU + cells were counted and expressed as a percentage of the total number of DAPI + cells ( n = 3). H , Immunodetection of activated caspase-3 (red) in control and Ctcf Foxg1-cre cortical neuroepithelium at E11.5. I , AC3 + cells were counted and expressed as a percentage of the total number of DAPI + cells ( n = 3). J , TUNEL (green) detection in E11.5 control and Ctcf Foxg1-cre cortical neuroepithelium. Error bars represent the SEM. Original magnification: C , 25×; E , 50×; F , H , J , 200×. Scale bars: C , top, 1 mm; bottom, 400 μm; E , 200 μm; F , H , 50 μm; J , 100 μm.

    Techniques Used: Staining, Immunodetection, Expressing, TUNEL Assay

    NestinCre -mediated deletion of CTCF results in activation of caspase-mediated apoptosis. A , Table of genotype ratios obtained during the embryonic period. Ratios at each time point were analyzed by a χ 2 test. B , Immunodetection of CTCF in E12.5 control and Ctcf Nes-cre coronal forebrain sections. C , Immunodetection of CTCF in E14 control and Ctcf Nes-cre coronal forebrain sections. D , Quantification of AC3 immunostaining in E12.5, E14, and E15.5 forebrain tissue ( n = 3). AC3 + cells were counted and expressed per unit area (square millimeter). E , Immunodetection of AC3 in E15.5 control and Ctcf Nes-cre basal ganglia. F , Immunodetection of AC3 in control and Ctcf Nes-cre at 4 DIV. Het, Ctcf flox/WT ;Nestin-cre ; Ctx, cortex; BG, basal ganglia; H, hippocampal hem. Error bars represent the SEM. Original magnification: B , C , 50×; D , 100×; E , 200×. Scale bars: B , 220 μm; C , 300 μm; E , 100 μm; F , 25 μm.
    Figure Legend Snippet: NestinCre -mediated deletion of CTCF results in activation of caspase-mediated apoptosis. A , Table of genotype ratios obtained during the embryonic period. Ratios at each time point were analyzed by a χ 2 test. B , Immunodetection of CTCF in E12.5 control and Ctcf Nes-cre coronal forebrain sections. C , Immunodetection of CTCF in E14 control and Ctcf Nes-cre coronal forebrain sections. D , Quantification of AC3 immunostaining in E12.5, E14, and E15.5 forebrain tissue ( n = 3). AC3 + cells were counted and expressed per unit area (square millimeter). E , Immunodetection of AC3 in E15.5 control and Ctcf Nes-cre basal ganglia. F , Immunodetection of AC3 in control and Ctcf Nes-cre at 4 DIV. Het, Ctcf flox/WT ;Nestin-cre ; Ctx, cortex; BG, basal ganglia; H, hippocampal hem. Error bars represent the SEM. Original magnification: B , C , 50×; D , 100×; E , 200×. Scale bars: B , 220 μm; C , 300 μm; E , 100 μm; F , 25 μm.

    Techniques Used: Activation Assay, Immunodetection, Immunostaining

    2) Product Images from "DNA Methylation Activates TP73 Expression in Hepatocellular Carcinoma and Gastrointestinal Cancer"

    Article Title: DNA Methylation Activates TP73 Expression in Hepatocellular Carcinoma and Gastrointestinal Cancer

    Journal: Scientific Reports

    doi: 10.1038/s41598-019-55945-7

    Role of TP53 and CTCF in regulation of TP73 gene expression. ( A ) Ideogram representing primers used in this ChIP assay for TP73 promoter. ( B ) Regulation of TP73 gene expression in normal human liver stem cells (HepCY HepCO) and HCC GI cancer cell lines by ChIP assay. These results were produced from triplicate experiments. Note: The row of bands representing the expression of each gene and separated by white spaces as shown in the gels displayed in panel B are cropped from full-length gels of the corresponding genes . The same exposures were made for each gel . The original gels for each figure are shown in the Supplementary Information File .
    Figure Legend Snippet: Role of TP53 and CTCF in regulation of TP73 gene expression. ( A ) Ideogram representing primers used in this ChIP assay for TP73 promoter. ( B ) Regulation of TP73 gene expression in normal human liver stem cells (HepCY HepCO) and HCC GI cancer cell lines by ChIP assay. These results were produced from triplicate experiments. Note: The row of bands representing the expression of each gene and separated by white spaces as shown in the gels displayed in panel B are cropped from full-length gels of the corresponding genes . The same exposures were made for each gel . The original gels for each figure are shown in the Supplementary Information File .

    Techniques Used: Expressing, Chromatin Immunoprecipitation, Produced

    3) Product Images from "The effect of epigenetic silencing and TP53 mutation on the expression of DLL4 in human cancer stem disorder"

    Article Title: The effect of epigenetic silencing and TP53 mutation on the expression of DLL4 in human cancer stem disorder

    Journal: Oncotarget

    doi: 10.18632/oncotarget.11316

    Role of TP53 and CTCF in regulation of DLL4 gene expression A. Ideogram representing primers used in this ChIP assay for DLL4 proximal promoter region (upper panel) and regulation of DLL4 gene expression in LFS and MCF7 cells by ChIP assay. HS27 cells were used as control (lower panel). B. Ideogram representing primers used in this ChIP assay for DLL4 distal promoter region (upper panel) and regulation of DLL4 gene expression in LFS and MCF7 cells by ChIP assay in DLL4 proximal promoter region. HS27 cells were used as control (lower panel). C. TP53 and CTCF protein levels in LFS, MCF7 and IMR32 cancer cell lines. D. Determining the interaction between TP53 and CTCF by co-immunoprecipitation.
    Figure Legend Snippet: Role of TP53 and CTCF in regulation of DLL4 gene expression A. Ideogram representing primers used in this ChIP assay for DLL4 proximal promoter region (upper panel) and regulation of DLL4 gene expression in LFS and MCF7 cells by ChIP assay. HS27 cells were used as control (lower panel). B. Ideogram representing primers used in this ChIP assay for DLL4 distal promoter region (upper panel) and regulation of DLL4 gene expression in LFS and MCF7 cells by ChIP assay in DLL4 proximal promoter region. HS27 cells were used as control (lower panel). C. TP53 and CTCF protein levels in LFS, MCF7 and IMR32 cancer cell lines. D. Determining the interaction between TP53 and CTCF by co-immunoprecipitation.

    Techniques Used: Expressing, Chromatin Immunoprecipitation, Immunoprecipitation

    Role of DNA methylation, TP53 and CTCF in regulation of DLL4 gene expression A. silenced DLL4 by DNA methylation in MDA231 cell line is reactivated by inhibitor of DNA methylation 5′-aza-dC. I) DLL 4 expression level in MDA231 cell line is compared with HS27 and MCF7 by RT-PCR assay. II) Reactivation of silenced DLL4 gene in MDA231 by the DNA methylation inhibitor, 5-aza-dC. III) Methylation status of the DLL4 promoter in MDA231 cell lines treated with 5-aza-dC and detected by MS-PCR. IV) Phase-contrast photomicrographs showing morphologic changes in MDA231 cells treated with 2, 5μM, 10μM and 25μM of 5-aza-dC for 3 days, compared with untreated control cells maintained for 3 days. B. The effect of DNA methylation on interaction between CTCF and DLL4 promoter by ChIP assay C. Reactivation of DLL4 gene expression in LFS cell line, 3335, by CTCF and TP53 siRNA treatment. D. A schematic representation of presumable mechanism of regulation of DLL4 gene expression.
    Figure Legend Snippet: Role of DNA methylation, TP53 and CTCF in regulation of DLL4 gene expression A. silenced DLL4 by DNA methylation in MDA231 cell line is reactivated by inhibitor of DNA methylation 5′-aza-dC. I) DLL 4 expression level in MDA231 cell line is compared with HS27 and MCF7 by RT-PCR assay. II) Reactivation of silenced DLL4 gene in MDA231 by the DNA methylation inhibitor, 5-aza-dC. III) Methylation status of the DLL4 promoter in MDA231 cell lines treated with 5-aza-dC and detected by MS-PCR. IV) Phase-contrast photomicrographs showing morphologic changes in MDA231 cells treated with 2, 5μM, 10μM and 25μM of 5-aza-dC for 3 days, compared with untreated control cells maintained for 3 days. B. The effect of DNA methylation on interaction between CTCF and DLL4 promoter by ChIP assay C. Reactivation of DLL4 gene expression in LFS cell line, 3335, by CTCF and TP53 siRNA treatment. D. A schematic representation of presumable mechanism of regulation of DLL4 gene expression.

    Techniques Used: DNA Methylation Assay, Expressing, Reverse Transcription Polymerase Chain Reaction, Methylation, Mass Spectrometry, Polymerase Chain Reaction, Chromatin Immunoprecipitation

    4) Product Images from "The effect of epigenetic silencing and TP53 mutation on the expression of DLL4 in human cancer stem disorder"

    Article Title: The effect of epigenetic silencing and TP53 mutation on the expression of DLL4 in human cancer stem disorder

    Journal: Oncotarget

    doi: 10.18632/oncotarget.11316

    Role of TP53 and CTCF in regulation of DLL4 gene expression A. Ideogram representing primers used in this ChIP assay for DLL4 proximal promoter region (upper panel) and regulation of DLL4 gene expression in LFS and MCF7 cells by ChIP assay. HS27 cells were used as control (lower panel). B. Ideogram representing primers used in this ChIP assay for DLL4 distal promoter region (upper panel) and regulation of DLL4 gene expression in LFS and MCF7 cells by ChIP assay in DLL4 proximal promoter region. HS27 cells were used as control (lower panel). C. TP53 and CTCF protein levels in LFS, MCF7 and IMR32 cancer cell lines. D. Determining the interaction between TP53 and CTCF by co-immunoprecipitation.
    Figure Legend Snippet: Role of TP53 and CTCF in regulation of DLL4 gene expression A. Ideogram representing primers used in this ChIP assay for DLL4 proximal promoter region (upper panel) and regulation of DLL4 gene expression in LFS and MCF7 cells by ChIP assay. HS27 cells were used as control (lower panel). B. Ideogram representing primers used in this ChIP assay for DLL4 distal promoter region (upper panel) and regulation of DLL4 gene expression in LFS and MCF7 cells by ChIP assay in DLL4 proximal promoter region. HS27 cells were used as control (lower panel). C. TP53 and CTCF protein levels in LFS, MCF7 and IMR32 cancer cell lines. D. Determining the interaction between TP53 and CTCF by co-immunoprecipitation.

    Techniques Used: Expressing, Chromatin Immunoprecipitation, Immunoprecipitation

    Role of DNA methylation, TP53 and CTCF in regulation of DLL4 gene expression A. silenced DLL4 by DNA methylation in MDA231 cell line is reactivated by inhibitor of DNA methylation 5′-aza-dC. I) DLL 4 expression level in MDA231 cell line is compared with HS27 and MCF7 by RT-PCR assay. II) Reactivation of silenced DLL4 gene in MDA231 by the DNA methylation inhibitor, 5-aza-dC. III) Methylation status of the DLL4 promoter in MDA231 cell lines treated with 5-aza-dC and detected by MS-PCR. IV) Phase-contrast photomicrographs showing morphologic changes in MDA231 cells treated with 2, 5μM, 10μM and 25μM of 5-aza-dC for 3 days, compared with untreated control cells maintained for 3 days. B. The effect of DNA methylation on interaction between CTCF and DLL4 promoter by ChIP assay C. Reactivation of DLL4 gene expression in LFS cell line, 3335, by CTCF and TP53 siRNA treatment. D. A schematic representation of presumable mechanism of regulation of DLL4 gene expression.
    Figure Legend Snippet: Role of DNA methylation, TP53 and CTCF in regulation of DLL4 gene expression A. silenced DLL4 by DNA methylation in MDA231 cell line is reactivated by inhibitor of DNA methylation 5′-aza-dC. I) DLL 4 expression level in MDA231 cell line is compared with HS27 and MCF7 by RT-PCR assay. II) Reactivation of silenced DLL4 gene in MDA231 by the DNA methylation inhibitor, 5-aza-dC. III) Methylation status of the DLL4 promoter in MDA231 cell lines treated with 5-aza-dC and detected by MS-PCR. IV) Phase-contrast photomicrographs showing morphologic changes in MDA231 cells treated with 2, 5μM, 10μM and 25μM of 5-aza-dC for 3 days, compared with untreated control cells maintained for 3 days. B. The effect of DNA methylation on interaction between CTCF and DLL4 promoter by ChIP assay C. Reactivation of DLL4 gene expression in LFS cell line, 3335, by CTCF and TP53 siRNA treatment. D. A schematic representation of presumable mechanism of regulation of DLL4 gene expression.

    Techniques Used: DNA Methylation Assay, Expressing, Reverse Transcription Polymerase Chain Reaction, Methylation, Mass Spectrometry, Polymerase Chain Reaction, Chromatin Immunoprecipitation

    5) Product Images from "Neuron-specific impairment of inter-chromosomal pairing and transcription in a novel model of human 15q-duplication syndrome"

    Article Title: Neuron-specific impairment of inter-chromosomal pairing and transcription in a novel model of human 15q-duplication syndrome

    Journal: Human Molecular Genetics

    doi: 10.1093/hmg/ddr298

    Disruption of GABRB3 homologous pairing via MeCP2 and CTCF knockdown. ( A and E ) Results from western blot analysis confirming knockdown of MeCP2 (A) and CTCF (E) proteins in SH-SY5Y cells. ( B and F ) Results from western blot analysis of
    Figure Legend Snippet: Disruption of GABRB3 homologous pairing via MeCP2 and CTCF knockdown. ( A and E ) Results from western blot analysis confirming knockdown of MeCP2 (A) and CTCF (E) proteins in SH-SY5Y cells. ( B and F ) Results from western blot analysis of

    Techniques Used: Western Blot

    6) Product Images from "Identification of the elementary structural units of the DNA damage response"

    Article Title: Identification of the elementary structural units of the DNA damage response

    Journal: Nature Communications

    doi: 10.1038/ncomms15760

    CTCF depletion inhibits γH2AX nano-foci and cluster formation and diminishes the DNA repair capability. ( a ) Number of CTCF foci in esiRNA-depleted cells before and during DDR. Black dots: median number of CTCF foci in wild-type cells. ( b ) Impairment of γH2AX nano-foci and 3D-clusters formation during DDR as assessed by immunofluorescence of 3D-SIM images in CTCF-depleted cells. Scale bar, 5 μm. ( c ) γH2AX nano-foci number distributions before and after IR, in CTCF siRNA-treated cells. Black dots: median number of γH2AX nano-foci of untreated cells (from Fig. 1 ).NS: two-tailed t -test, P > 0.05. ( d ) γH2AX nano-foci DNA content distributions before and after IR, in CTCF siRNA-treated cells. Black dots: median DNA content of γH2AX nano-foci of untreated cells (from Fig. 2 ). ( e ) DNA fragmentation measured by the neutral comet assay. Boxes represent the mean of medians from four replicates (two biological replicates in duplicate), each consisting of 60 comet measurements. NS: not significant ( t -test, P > 0.05). ( f ) γH2AX cluster distributions before and after IR, in CTCF siRNA-treated cells. Black dots: median number of γH2AX clusters in untreated cells (from Fig. 6 ). All boxes and whiskers are as in Fig. 1 . Comparisons between time points (one-way ANOVA with Dunnett's correction) or between esiRNA-treated and wild-type cells (Wilcoxon/Mann–Whitney rank sum) are all statistically significant unless otherwise specified. ( g ) Model for cluster special arrangement during DDR, showing the time-dependent euchromatin-to-heterochromatin repair trend (top) and how γH2AX spreading is hampered by CTCF depletion with the concomitant loss of 3D-arrangement of chromatin loops (bottom).
    Figure Legend Snippet: CTCF depletion inhibits γH2AX nano-foci and cluster formation and diminishes the DNA repair capability. ( a ) Number of CTCF foci in esiRNA-depleted cells before and during DDR. Black dots: median number of CTCF foci in wild-type cells. ( b ) Impairment of γH2AX nano-foci and 3D-clusters formation during DDR as assessed by immunofluorescence of 3D-SIM images in CTCF-depleted cells. Scale bar, 5 μm. ( c ) γH2AX nano-foci number distributions before and after IR, in CTCF siRNA-treated cells. Black dots: median number of γH2AX nano-foci of untreated cells (from Fig. 1 ).NS: two-tailed t -test, P > 0.05. ( d ) γH2AX nano-foci DNA content distributions before and after IR, in CTCF siRNA-treated cells. Black dots: median DNA content of γH2AX nano-foci of untreated cells (from Fig. 2 ). ( e ) DNA fragmentation measured by the neutral comet assay. Boxes represent the mean of medians from four replicates (two biological replicates in duplicate), each consisting of 60 comet measurements. NS: not significant ( t -test, P > 0.05). ( f ) γH2AX cluster distributions before and after IR, in CTCF siRNA-treated cells. Black dots: median number of γH2AX clusters in untreated cells (from Fig. 6 ). All boxes and whiskers are as in Fig. 1 . Comparisons between time points (one-way ANOVA with Dunnett's correction) or between esiRNA-treated and wild-type cells (Wilcoxon/Mann–Whitney rank sum) are all statistically significant unless otherwise specified. ( g ) Model for cluster special arrangement during DDR, showing the time-dependent euchromatin-to-heterochromatin repair trend (top) and how γH2AX spreading is hampered by CTCF depletion with the concomitant loss of 3D-arrangement of chromatin loops (bottom).

    Techniques Used: esiRNA, Immunofluorescence, Two Tailed Test, Neutral Comet Assay, MANN-WHITNEY

    7) Product Images from "Downregulation of p53 by Insufficient CTCF in CD4+ T Cells Is an Important Factor Inducing Acute Graft-Versus-Host Disease"

    Article Title: Downregulation of p53 by Insufficient CTCF in CD4+ T Cells Is an Important Factor Inducing Acute Graft-Versus-Host Disease

    Journal: Frontiers in Immunology

    doi: 10.3389/fimmu.2020.568637

    CTCF downregulation results in low expression of p53 in CD4 + T cells from patients with aGVHD. (A) Relative mRNA levels of CTCF in CD4 + T cells from patients with aGVHD ( n = 15) and those without aGVHD ( n = 15), normalized to GAPDH. (B) Representative Western blotting results for CTCF protein expression in CD4 + T cells from patients with aGVHD ( n = 10) and those without aGVHD ( n = 10). (C) Quantitative analysis of band intensities for CTCF protein, normalized to GAPDH expression. (D) ChIP-qPCR analysis of CTCF enrichment in the p53 promoter in chromatin fractions extracted from CD4 + T cells from patients with aGVHD ( n = 15) and individuals without aGVHD ( n = 15). Values are relative to those obtained with input DNA prepared from untreated chromatin. (E) Correlation between CTCF enrichment and p53 mRNA levels in CD4 + T cells from aGVHD cases ( n = 15). ( ∗∗ P
    Figure Legend Snippet: CTCF downregulation results in low expression of p53 in CD4 + T cells from patients with aGVHD. (A) Relative mRNA levels of CTCF in CD4 + T cells from patients with aGVHD ( n = 15) and those without aGVHD ( n = 15), normalized to GAPDH. (B) Representative Western blotting results for CTCF protein expression in CD4 + T cells from patients with aGVHD ( n = 10) and those without aGVHD ( n = 10). (C) Quantitative analysis of band intensities for CTCF protein, normalized to GAPDH expression. (D) ChIP-qPCR analysis of CTCF enrichment in the p53 promoter in chromatin fractions extracted from CD4 + T cells from patients with aGVHD ( n = 15) and individuals without aGVHD ( n = 15). Values are relative to those obtained with input DNA prepared from untreated chromatin. (E) Correlation between CTCF enrichment and p53 mRNA levels in CD4 + T cells from aGVHD cases ( n = 15). ( ∗∗ P

    Techniques Used: Expressing, Western Blot, Chromatin Immunoprecipitation, Real-time Polymerase Chain Reaction

    CTCF is a key factor to promote p53 expression in CD4 + T cells. (A) Schematic diagram of the CTCF binding site in the p53 promoter region. (B) ChIP-PCR showing that CTCF binds to the promoter region (−694 to −515) of p53 in T cells. (C , D) p53 mRNA levels in normal CD4 + T cells after CTCF silencing or overexpression. Data are mean ± SD from three independent experiments. (E) Representative Western blotting results for p53 protein expression in CD4 + T cells after CTCF silencing or overexpression. (F , G) Quantitative analysis of band intensities for p53 protein, normalized to GAPDH expression. Data are mean ± SD from three independent experiments. ( ∗ P
    Figure Legend Snippet: CTCF is a key factor to promote p53 expression in CD4 + T cells. (A) Schematic diagram of the CTCF binding site in the p53 promoter region. (B) ChIP-PCR showing that CTCF binds to the promoter region (−694 to −515) of p53 in T cells. (C , D) p53 mRNA levels in normal CD4 + T cells after CTCF silencing or overexpression. Data are mean ± SD from three independent experiments. (E) Representative Western blotting results for p53 protein expression in CD4 + T cells after CTCF silencing or overexpression. (F , G) Quantitative analysis of band intensities for p53 protein, normalized to GAPDH expression. Data are mean ± SD from three independent experiments. ( ∗ P

    Techniques Used: Expressing, Binding Assay, Chromatin Immunoprecipitation, Polymerase Chain Reaction, Over Expression, Western Blot

    CTCF alters histone H3K9ac and H3K14ac levels in the p53 promoter. (A,B) ChIP-qPCR analysis of the enrichment of histone H3K9ac and H3K14ac levels in the p53 promoter region in normal CD4 + T cells transfected with pCMV6-CTCF (A) or pRS-CTCF (B) . Values are relative to those obtained with input DNA prepared from untreated chromatin. Data are mean ± SD from three independent experiments. (C,D) ChIP-qPCR analysis of the enrichment of histone H3K9ac (C) and H3K14ac (D) levels in the p53 promoter region in CD4 + T cells from patients with aGVHD ( n = 15) and individuals without aGVHD ( n = 15). Values are relative to those obtained with input DNA prepared from untreated chromatin. (E , F) Correlation analysis of H3K9ac (E) /H3K14ac (F) of p53 promoter and p53 expression in aGVHD CD4 + T cells ( n = 15). ∗ P
    Figure Legend Snippet: CTCF alters histone H3K9ac and H3K14ac levels in the p53 promoter. (A,B) ChIP-qPCR analysis of the enrichment of histone H3K9ac and H3K14ac levels in the p53 promoter region in normal CD4 + T cells transfected with pCMV6-CTCF (A) or pRS-CTCF (B) . Values are relative to those obtained with input DNA prepared from untreated chromatin. Data are mean ± SD from three independent experiments. (C,D) ChIP-qPCR analysis of the enrichment of histone H3K9ac (C) and H3K14ac (D) levels in the p53 promoter region in CD4 + T cells from patients with aGVHD ( n = 15) and individuals without aGVHD ( n = 15). Values are relative to those obtained with input DNA prepared from untreated chromatin. (E , F) Correlation analysis of H3K9ac (E) /H3K14ac (F) of p53 promoter and p53 expression in aGVHD CD4 + T cells ( n = 15). ∗ P

    Techniques Used: Chromatin Immunoprecipitation, Real-time Polymerase Chain Reaction, Transfection, Expressing

    CTCF recruits p300 for interaction with the p53 promoter. (A) Co-immunoprecipitation with anti-CTCF (upper panel) or anti-p300 (lower panel) antibodies in Jurkat cells after CTCF and p300 overexpression; detection of the CTCF and p300 complex was performed by Western blotting. (B) ChIP-qPCR analysis of p300 enrichment in the p53 promoter in chromatin fractions extracted from CD4 + T cells from patients with aGVHD ( n = 15) and individuals without aGVHD ( n = 15). Values are relative to those obtained with input DNA prepared from untreated chromatin. (C) Representative Western blotting results for p53 protein expression in CD4 + T cells after CTCF or p300 overexpression and CTCF silencing. Data are mean ± SD from three independent experiments. (D) ChIP-qPCR analysis of p300 enrichment in the p53 promoter in chromatin fractions extracted from CD4 + T cells after CTCF or p300 overexpression and CTCF knockdown. Values are relative to those obtained with input DNA prepared from untreated chromatin. Data are mean ± SD from three independent experiments. ∗ P
    Figure Legend Snippet: CTCF recruits p300 for interaction with the p53 promoter. (A) Co-immunoprecipitation with anti-CTCF (upper panel) or anti-p300 (lower panel) antibodies in Jurkat cells after CTCF and p300 overexpression; detection of the CTCF and p300 complex was performed by Western blotting. (B) ChIP-qPCR analysis of p300 enrichment in the p53 promoter in chromatin fractions extracted from CD4 + T cells from patients with aGVHD ( n = 15) and individuals without aGVHD ( n = 15). Values are relative to those obtained with input DNA prepared from untreated chromatin. (C) Representative Western blotting results for p53 protein expression in CD4 + T cells after CTCF or p300 overexpression and CTCF silencing. Data are mean ± SD from three independent experiments. (D) ChIP-qPCR analysis of p300 enrichment in the p53 promoter in chromatin fractions extracted from CD4 + T cells after CTCF or p300 overexpression and CTCF knockdown. Values are relative to those obtained with input DNA prepared from untreated chromatin. Data are mean ± SD from three independent experiments. ∗ P

    Techniques Used: Immunoprecipitation, Over Expression, Western Blot, Chromatin Immunoprecipitation, Real-time Polymerase Chain Reaction, Expressing

    Restoring CTCF expression in CD4 + T cells from aGVHD cases improves Treg/Th17 cell imbalance by increasing p53 expression. (A , B) ChIP-qPCR analysis of the enrichment of p300 binding (A) and H3K9/K14 (B) acetylation levels in the p53 promoter region in CD4 + T cells from three separate aGVHD cases after CTCF overexpression. Values are relative to those obtained with input DNA prepared from untreated chromatin. Data are mean ± SD from three independent experiments. (C , D) Real-time PCR analysis of p53, Foxp3, IL-10 (C) , RORγt, and IL-17A (D) expression levels in CD4 + T cells from three separate aGVHD cases after CTCF overexpression. Data are mean ± SD from three independent experiments. ∗ P
    Figure Legend Snippet: Restoring CTCF expression in CD4 + T cells from aGVHD cases improves Treg/Th17 cell imbalance by increasing p53 expression. (A , B) ChIP-qPCR analysis of the enrichment of p300 binding (A) and H3K9/K14 (B) acetylation levels in the p53 promoter region in CD4 + T cells from three separate aGVHD cases after CTCF overexpression. Values are relative to those obtained with input DNA prepared from untreated chromatin. Data are mean ± SD from three independent experiments. (C , D) Real-time PCR analysis of p53, Foxp3, IL-10 (C) , RORγt, and IL-17A (D) expression levels in CD4 + T cells from three separate aGVHD cases after CTCF overexpression. Data are mean ± SD from three independent experiments. ∗ P

    Techniques Used: Expressing, Chromatin Immunoprecipitation, Real-time Polymerase Chain Reaction, Binding Assay, Over Expression

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    Avidin-Biotin Assay:

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    Chromatin Immunoprecipitation:

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    Negative Control:

    Article Title: RUNX1-mediated alphaherpesvirus-host trans-species chromatin interaction promotes viral transcription
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    Immunoprecipitation:

    Article Title: RUNX1-mediated alphaherpesvirus-host trans-species chromatin interaction promotes viral transcription
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    Magnetic Beads:

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    Article Snippet: .. Briefly, 2 × 107 cells were harvested and lysed by RIP lysis buffer, then incubated with magnetic beads conjugated with antibody against IgG (Cell Signaling Technology, Beverly, MA, USA) or FUBP1 (Thermo Fisher Scientific, USA). ..

    Western Blot:

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    Lysis:

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    Cell Signaling Technology Inc anti ctcf rabbit monoclonal antibody
    Transcriptional profiling of genes altered with <t>CTCF</t> knockdown. a Heat map of differentially expressed (DE) transcripts following 5 days of CTCF <t>shRNA</t> induction (Dox) versus uninduced vehicle control (vehicle). CTCF knockdown in HPECE6/E7 leads to 1308 significantly altered gene transcripts (FDR
    Anti Ctcf Rabbit Monoclonal Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti ctcf rabbit monoclonal antibody/product/Cell Signaling Technology Inc
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    99
    Cell Signaling Technology Inc rabbit anti ctcf
    Foxg1Cre -mediated deletion of <t>Ctcf</t> results in a massive increase in apoptosis. A , Table of genotypes obtained during the embryonic and postnatal periods. Ratios at each time point were analyzed using a χ 2 test. Het, Ctcf flox/WT ;Foxg1-cre +/− . B , Dark-field images of control and Ctcf Foxg1-cre embryos at E13.5. (Please note limbs were taken for genotyping). C , H E staining of E13.5 sagittal cryosections demonstrates complete loss of cortex (Ctx), hippocampal hem (H), basal ganglia (BG), lens (L), and anterior retina (AR), but not the posterior retina (PR), in Ctcf Foxg1-cre embryos. D , Dark-field images of control and Ctcf Foxg1-cre embryos at E11.5. The dashed circle outlines the telencephalon, which is visibly reduced in size in the Ctcf Foxg1-cre embryos compared to littermate controls. E , Immunodetection of CTCF (red) in E11.5 sagittal cryosections confirms specific loss of CTCF expression in the forebrain neuroepithelium of Ctcf Foxg1-cre embryos. F , Pregnant females were subjected to a 1 h BrdU pulse before being killed. Immunodetection of BrdU in E11.5 control and Ctcf Foxg1-cre cortical neuroepithelium is shown. G , BrdU + cells were counted and expressed as a percentage of the total number of DAPI + cells ( n = 3). H , Immunodetection of activated <t>caspase-3</t> (red) in control and Ctcf Foxg1-cre cortical neuroepithelium at E11.5. I , AC3 + cells were counted and expressed as a percentage of the total number of DAPI + cells ( n = 3). J , TUNEL (green) detection in E11.5 control and Ctcf Foxg1-cre cortical neuroepithelium. Error bars represent the SEM. Original magnification: C , 25×; E , 50×; F , H , J , 200×. Scale bars: C , top, 1 mm; bottom, 400 μm; E , 200 μm; F , H , 50 μm; J , 100 μm.
    Rabbit Anti Ctcf, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Transcriptional profiling of genes altered with CTCF knockdown. a Heat map of differentially expressed (DE) transcripts following 5 days of CTCF shRNA induction (Dox) versus uninduced vehicle control (vehicle). CTCF knockdown in HPECE6/E7 leads to 1308 significantly altered gene transcripts (FDR

    Journal: Clinical Epigenetics

    Article Title: CTCF loss mediates unique DNA hypermethylation landscapes in human cancers

    doi: 10.1186/s13148-020-00869-7

    Figure Lengend Snippet: Transcriptional profiling of genes altered with CTCF knockdown. a Heat map of differentially expressed (DE) transcripts following 5 days of CTCF shRNA induction (Dox) versus uninduced vehicle control (vehicle). CTCF knockdown in HPECE6/E7 leads to 1308 significantly altered gene transcripts (FDR

    Article Snippet: CTCF shRNA and controls were analyzed by western blotting using anti-CTCF rabbit monoclonal antibody (Cell Signaling #3418) to verify knockdown.

    Techniques: shRNA

    Knockdown of CTCF protein results in DNA hypermethylation preferentially at CTCF sites. a Workflow of methylated DNA immunoprecipitation followed by copy number array application (MeDIP-chip) for detecting methylation alterations. NspI restriction fragments were bound to anti-5-methylcytosine antibody, eluted, and hybridized to a Affymetrix Cytoscan HD probe. An unenriched total input fraction was processed for comparison. b Short hairpin mediated CTCF knockdown in two separate shRNA targeting CTCF verified by western blotting after 3 and 5 days of shRNA induction including shRNA non-silencing control (shNSC). Data shown are one representative of 3 independent experiments using immortalized HPECs. Percentage knockdown compared to shCTCF -Dox control, quantified by ImageJ. c Volcano plot of detected methylation changes in CTCF knockdown HPECE6/E7 after 5 days of dox exposure (cut-point, methylation Abs. Log2FC > 1.5, P

    Journal: Clinical Epigenetics

    Article Title: CTCF loss mediates unique DNA hypermethylation landscapes in human cancers

    doi: 10.1186/s13148-020-00869-7

    Figure Lengend Snippet: Knockdown of CTCF protein results in DNA hypermethylation preferentially at CTCF sites. a Workflow of methylated DNA immunoprecipitation followed by copy number array application (MeDIP-chip) for detecting methylation alterations. NspI restriction fragments were bound to anti-5-methylcytosine antibody, eluted, and hybridized to a Affymetrix Cytoscan HD probe. An unenriched total input fraction was processed for comparison. b Short hairpin mediated CTCF knockdown in two separate shRNA targeting CTCF verified by western blotting after 3 and 5 days of shRNA induction including shRNA non-silencing control (shNSC). Data shown are one representative of 3 independent experiments using immortalized HPECs. Percentage knockdown compared to shCTCF -Dox control, quantified by ImageJ. c Volcano plot of detected methylation changes in CTCF knockdown HPECE6/E7 after 5 days of dox exposure (cut-point, methylation Abs. Log2FC > 1.5, P

    Article Snippet: CTCF shRNA and controls were analyzed by western blotting using anti-CTCF rabbit monoclonal antibody (Cell Signaling #3418) to verify knockdown.

    Techniques: Methylation, Immunoprecipitation, Methylated DNA Immunoprecipitation, Chromatin Immunoprecipitation, shRNA, Western Blot

    Foxg1Cre -mediated deletion of Ctcf results in a massive increase in apoptosis. A , Table of genotypes obtained during the embryonic and postnatal periods. Ratios at each time point were analyzed using a χ 2 test. Het, Ctcf flox/WT ;Foxg1-cre +/− . B , Dark-field images of control and Ctcf Foxg1-cre embryos at E13.5. (Please note limbs were taken for genotyping). C , H E staining of E13.5 sagittal cryosections demonstrates complete loss of cortex (Ctx), hippocampal hem (H), basal ganglia (BG), lens (L), and anterior retina (AR), but not the posterior retina (PR), in Ctcf Foxg1-cre embryos. D , Dark-field images of control and Ctcf Foxg1-cre embryos at E11.5. The dashed circle outlines the telencephalon, which is visibly reduced in size in the Ctcf Foxg1-cre embryos compared to littermate controls. E , Immunodetection of CTCF (red) in E11.5 sagittal cryosections confirms specific loss of CTCF expression in the forebrain neuroepithelium of Ctcf Foxg1-cre embryos. F , Pregnant females were subjected to a 1 h BrdU pulse before being killed. Immunodetection of BrdU in E11.5 control and Ctcf Foxg1-cre cortical neuroepithelium is shown. G , BrdU + cells were counted and expressed as a percentage of the total number of DAPI + cells ( n = 3). H , Immunodetection of activated caspase-3 (red) in control and Ctcf Foxg1-cre cortical neuroepithelium at E11.5. I , AC3 + cells were counted and expressed as a percentage of the total number of DAPI + cells ( n = 3). J , TUNEL (green) detection in E11.5 control and Ctcf Foxg1-cre cortical neuroepithelium. Error bars represent the SEM. Original magnification: C , 25×; E , 50×; F , H , J , 200×. Scale bars: C , top, 1 mm; bottom, 400 μm; E , 200 μm; F , H , 50 μm; J , 100 μm.

    Journal: The Journal of Neuroscience

    Article Title: Dual Effect of CTCF Loss on Neuroprogenitor Differentiation and Survival

    doi: 10.1523/JNEUROSCI.3769-13.2014

    Figure Lengend Snippet: Foxg1Cre -mediated deletion of Ctcf results in a massive increase in apoptosis. A , Table of genotypes obtained during the embryonic and postnatal periods. Ratios at each time point were analyzed using a χ 2 test. Het, Ctcf flox/WT ;Foxg1-cre +/− . B , Dark-field images of control and Ctcf Foxg1-cre embryos at E13.5. (Please note limbs were taken for genotyping). C , H E staining of E13.5 sagittal cryosections demonstrates complete loss of cortex (Ctx), hippocampal hem (H), basal ganglia (BG), lens (L), and anterior retina (AR), but not the posterior retina (PR), in Ctcf Foxg1-cre embryos. D , Dark-field images of control and Ctcf Foxg1-cre embryos at E11.5. The dashed circle outlines the telencephalon, which is visibly reduced in size in the Ctcf Foxg1-cre embryos compared to littermate controls. E , Immunodetection of CTCF (red) in E11.5 sagittal cryosections confirms specific loss of CTCF expression in the forebrain neuroepithelium of Ctcf Foxg1-cre embryos. F , Pregnant females were subjected to a 1 h BrdU pulse before being killed. Immunodetection of BrdU in E11.5 control and Ctcf Foxg1-cre cortical neuroepithelium is shown. G , BrdU + cells were counted and expressed as a percentage of the total number of DAPI + cells ( n = 3). H , Immunodetection of activated caspase-3 (red) in control and Ctcf Foxg1-cre cortical neuroepithelium at E11.5. I , AC3 + cells were counted and expressed as a percentage of the total number of DAPI + cells ( n = 3). J , TUNEL (green) detection in E11.5 control and Ctcf Foxg1-cre cortical neuroepithelium. Error bars represent the SEM. Original magnification: C , 25×; E , 50×; F , H , J , 200×. Scale bars: C , top, 1 mm; bottom, 400 μm; E , 200 μm; F , H , 50 μm; J , 100 μm.

    Article Snippet: Primary antibodies used were as follows: rabbit anti-CTCF (1:400; Cell Signaling Technology), rabbit anti-cleaved caspase 3 (AC3; Asp175; 1:400; Cell Signaling Technology), mouse anti-BrdU (1:50; BD Biosciences), rabbit anti-PUMA (1:200; Cell Signaling Technology), rabbit anti-TBR2 (1:200; Abcam), goat anti-SOX2 (1:400; Santa Cruz Biotechnology), goat anti-PAX6 (1:200; Santa Cruz Biotechnology), rabbit anti-SOX2 (1:100; Millipore Bioscience Research Reagents), rabbit anti-Ki67 (1:200; Abcam), rabbit anti-TBR1 (1:200; Abcam), mouse anti-SATB2 (1:200; Abcam), and rabbit anti-CTIP2 (1:200; Abcam).

    Techniques: Staining, Immunodetection, Expressing, TUNEL Assay

    NestinCre -mediated deletion of CTCF results in activation of caspase-mediated apoptosis. A , Table of genotype ratios obtained during the embryonic period. Ratios at each time point were analyzed by a χ 2 test. B , Immunodetection of CTCF in E12.5 control and Ctcf Nes-cre coronal forebrain sections. C , Immunodetection of CTCF in E14 control and Ctcf Nes-cre coronal forebrain sections. D , Quantification of AC3 immunostaining in E12.5, E14, and E15.5 forebrain tissue ( n = 3). AC3 + cells were counted and expressed per unit area (square millimeter). E , Immunodetection of AC3 in E15.5 control and Ctcf Nes-cre basal ganglia. F , Immunodetection of AC3 in control and Ctcf Nes-cre at 4 DIV. Het, Ctcf flox/WT ;Nestin-cre ; Ctx, cortex; BG, basal ganglia; H, hippocampal hem. Error bars represent the SEM. Original magnification: B , C , 50×; D , 100×; E , 200×. Scale bars: B , 220 μm; C , 300 μm; E , 100 μm; F , 25 μm.

    Journal: The Journal of Neuroscience

    Article Title: Dual Effect of CTCF Loss on Neuroprogenitor Differentiation and Survival

    doi: 10.1523/JNEUROSCI.3769-13.2014

    Figure Lengend Snippet: NestinCre -mediated deletion of CTCF results in activation of caspase-mediated apoptosis. A , Table of genotype ratios obtained during the embryonic period. Ratios at each time point were analyzed by a χ 2 test. B , Immunodetection of CTCF in E12.5 control and Ctcf Nes-cre coronal forebrain sections. C , Immunodetection of CTCF in E14 control and Ctcf Nes-cre coronal forebrain sections. D , Quantification of AC3 immunostaining in E12.5, E14, and E15.5 forebrain tissue ( n = 3). AC3 + cells were counted and expressed per unit area (square millimeter). E , Immunodetection of AC3 in E15.5 control and Ctcf Nes-cre basal ganglia. F , Immunodetection of AC3 in control and Ctcf Nes-cre at 4 DIV. Het, Ctcf flox/WT ;Nestin-cre ; Ctx, cortex; BG, basal ganglia; H, hippocampal hem. Error bars represent the SEM. Original magnification: B , C , 50×; D , 100×; E , 200×. Scale bars: B , 220 μm; C , 300 μm; E , 100 μm; F , 25 μm.

    Article Snippet: Primary antibodies used were as follows: rabbit anti-CTCF (1:400; Cell Signaling Technology), rabbit anti-cleaved caspase 3 (AC3; Asp175; 1:400; Cell Signaling Technology), mouse anti-BrdU (1:50; BD Biosciences), rabbit anti-PUMA (1:200; Cell Signaling Technology), rabbit anti-TBR2 (1:200; Abcam), goat anti-SOX2 (1:400; Santa Cruz Biotechnology), goat anti-PAX6 (1:200; Santa Cruz Biotechnology), rabbit anti-SOX2 (1:100; Millipore Bioscience Research Reagents), rabbit anti-Ki67 (1:200; Abcam), rabbit anti-TBR1 (1:200; Abcam), mouse anti-SATB2 (1:200; Abcam), and rabbit anti-CTIP2 (1:200; Abcam).

    Techniques: Activation Assay, Immunodetection, Immunostaining

    Role of TP53 and CTCF in regulation of DLL4 gene expression A. Ideogram representing primers used in this ChIP assay for DLL4 proximal promoter region (upper panel) and regulation of DLL4 gene expression in LFS and MCF7 cells by ChIP assay. HS27 cells were used as control (lower panel). B. Ideogram representing primers used in this ChIP assay for DLL4 distal promoter region (upper panel) and regulation of DLL4 gene expression in LFS and MCF7 cells by ChIP assay in DLL4 proximal promoter region. HS27 cells were used as control (lower panel). C. TP53 and CTCF protein levels in LFS, MCF7 and IMR32 cancer cell lines. D. Determining the interaction between TP53 and CTCF by co-immunoprecipitation.

    Journal: Oncotarget

    Article Title: The effect of epigenetic silencing and TP53 mutation on the expression of DLL4 in human cancer stem disorder

    doi: 10.18632/oncotarget.11316

    Figure Lengend Snippet: Role of TP53 and CTCF in regulation of DLL4 gene expression A. Ideogram representing primers used in this ChIP assay for DLL4 proximal promoter region (upper panel) and regulation of DLL4 gene expression in LFS and MCF7 cells by ChIP assay. HS27 cells were used as control (lower panel). B. Ideogram representing primers used in this ChIP assay for DLL4 distal promoter region (upper panel) and regulation of DLL4 gene expression in LFS and MCF7 cells by ChIP assay in DLL4 proximal promoter region. HS27 cells were used as control (lower panel). C. TP53 and CTCF protein levels in LFS, MCF7 and IMR32 cancer cell lines. D. Determining the interaction between TP53 and CTCF by co-immunoprecipitation.

    Article Snippet: Rabbit anti-CTCF and TP53 for ChIP is the same as Co-IP.

    Techniques: Expressing, Chromatin Immunoprecipitation, Immunoprecipitation

    Role of DNA methylation, TP53 and CTCF in regulation of DLL4 gene expression A. silenced DLL4 by DNA methylation in MDA231 cell line is reactivated by inhibitor of DNA methylation 5′-aza-dC. I) DLL 4 expression level in MDA231 cell line is compared with HS27 and MCF7 by RT-PCR assay. II) Reactivation of silenced DLL4 gene in MDA231 by the DNA methylation inhibitor, 5-aza-dC. III) Methylation status of the DLL4 promoter in MDA231 cell lines treated with 5-aza-dC and detected by MS-PCR. IV) Phase-contrast photomicrographs showing morphologic changes in MDA231 cells treated with 2, 5μM, 10μM and 25μM of 5-aza-dC for 3 days, compared with untreated control cells maintained for 3 days. B. The effect of DNA methylation on interaction between CTCF and DLL4 promoter by ChIP assay C. Reactivation of DLL4 gene expression in LFS cell line, 3335, by CTCF and TP53 siRNA treatment. D. A schematic representation of presumable mechanism of regulation of DLL4 gene expression.

    Journal: Oncotarget

    Article Title: The effect of epigenetic silencing and TP53 mutation on the expression of DLL4 in human cancer stem disorder

    doi: 10.18632/oncotarget.11316

    Figure Lengend Snippet: Role of DNA methylation, TP53 and CTCF in regulation of DLL4 gene expression A. silenced DLL4 by DNA methylation in MDA231 cell line is reactivated by inhibitor of DNA methylation 5′-aza-dC. I) DLL 4 expression level in MDA231 cell line is compared with HS27 and MCF7 by RT-PCR assay. II) Reactivation of silenced DLL4 gene in MDA231 by the DNA methylation inhibitor, 5-aza-dC. III) Methylation status of the DLL4 promoter in MDA231 cell lines treated with 5-aza-dC and detected by MS-PCR. IV) Phase-contrast photomicrographs showing morphologic changes in MDA231 cells treated with 2, 5μM, 10μM and 25μM of 5-aza-dC for 3 days, compared with untreated control cells maintained for 3 days. B. The effect of DNA methylation on interaction between CTCF and DLL4 promoter by ChIP assay C. Reactivation of DLL4 gene expression in LFS cell line, 3335, by CTCF and TP53 siRNA treatment. D. A schematic representation of presumable mechanism of regulation of DLL4 gene expression.

    Article Snippet: Rabbit anti-CTCF and TP53 for ChIP is the same as Co-IP.

    Techniques: DNA Methylation Assay, Expressing, Reverse Transcription Polymerase Chain Reaction, Methylation, Mass Spectrometry, Polymerase Chain Reaction, Chromatin Immunoprecipitation