anti ctbp1  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti ctbp1
    Anti Ctbp1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    anti ctbp1  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti ctbp1
    Anti Ctbp1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    rabbit anti human ctbp1  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc rabbit anti human ctbp1
    Expression levels of <t> CTBP1 </t> and the clinicopathological characteristics of patients with HCC.
    Rabbit Anti Human Ctbp1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "C-Terminus of E1A Binding Protein 1 Stimulates Malignant Phenotype in Human Hepatocellular Carcinoma"

    Article Title: C-Terminus of E1A Binding Protein 1 Stimulates Malignant Phenotype in Human Hepatocellular Carcinoma

    Journal: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research

    doi: 10.12659/MSM.920114

    Expression levels of  CTBP1  and the clinicopathological characteristics of patients with HCC.
    Figure Legend Snippet: Expression levels of CTBP1 and the clinicopathological characteristics of patients with HCC.

    Techniques Used: Expressing

    CTBP1 was highly expressed in HCC tissues. ( A ) High CTBP1 expression in HCC tissues was observed via IHC. ( B ) The protein of CTBP1 was highly expressed in HCC tissues. ** P<0.01 vs. hepatic tissues. ( C ) Positive CTBP1 expression predicted a shorter survival time. HCC – hepatocellular carcinoma; CTBP – C-terminus of the E1A binding proteins.
    Figure Legend Snippet: CTBP1 was highly expressed in HCC tissues. ( A ) High CTBP1 expression in HCC tissues was observed via IHC. ( B ) The protein of CTBP1 was highly expressed in HCC tissues. ** P<0.01 vs. hepatic tissues. ( C ) Positive CTBP1 expression predicted a shorter survival time. HCC – hepatocellular carcinoma; CTBP – C-terminus of the E1A binding proteins.

    Techniques Used: Expressing, Binding Assay

    CTBP1 promoted the malignancy of hepatic astrocytes. ( A ) Modifications in activation of the PI3K/Akt pathway. ( B ) Growth curve of the LX-2 cells as determined via the CCK-8. ( C ) Colony formation activity in 2D monolayer cultures. ( D ) The in vitro invasive activity of LX-2 cells was detected by the Transwell chamber method. ( E ) The in vitro migratory activity of LX-2 cells was investigated using the cell scratch assay. ** P<0.01 vs. the vector group. CTBP – C-terminus of the E1A binding proteins.
    Figure Legend Snippet: CTBP1 promoted the malignancy of hepatic astrocytes. ( A ) Modifications in activation of the PI3K/Akt pathway. ( B ) Growth curve of the LX-2 cells as determined via the CCK-8. ( C ) Colony formation activity in 2D monolayer cultures. ( D ) The in vitro invasive activity of LX-2 cells was detected by the Transwell chamber method. ( E ) The in vitro migratory activity of LX-2 cells was investigated using the cell scratch assay. ** P<0.01 vs. the vector group. CTBP – C-terminus of the E1A binding proteins.

    Techniques Used: Activation Assay, CCK-8 Assay, Activity Assay, In Vitro, Wound Healing Assay, Plasmid Preparation, Binding Assay

    CTBP1 silencing reduced the migratory activity of HCC cells. ( A ) The consequences of CTBP1 loss on the PI3K/Akt signaling in Hep3B cells. ( B ) The growth rate of Hep3B cells was assessed via CCK-8 assay. ( C ) The colony formation activity of Hep3B cells was evaluated using 2D culture. ( D ) The in vitro invasive activity of Hep3B cells. ( E ) The in vitro migratory activity of Hep3B cells. ** P<0.01, vs. the scramble group.
    Figure Legend Snippet: CTBP1 silencing reduced the migratory activity of HCC cells. ( A ) The consequences of CTBP1 loss on the PI3K/Akt signaling in Hep3B cells. ( B ) The growth rate of Hep3B cells was assessed via CCK-8 assay. ( C ) The colony formation activity of Hep3B cells was evaluated using 2D culture. ( D ) The in vitro invasive activity of Hep3B cells. ( E ) The in vitro migratory activity of Hep3B cells. ** P<0.01, vs. the scramble group.

    Techniques Used: Activity Assay, CCK-8 Assay, In Vitro

    anti ctbp1  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti ctbp1
    Anti Ctbp1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    anti ctbp1  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti ctbp1
    The formation of the <t>CtIP-CtBP1/2-HDAC1-AP1</t> complex in vivo and in vitro (A) CtIP immunoprecipitated CtBP1, CtBP2, HDAC1, JUN, and FOS. Three independent tumor tissues with equal weights (0.1 g) were mixed and then homogenized. The CtIP-purified complex in the homogenate was probed with antibodies indicated in the figure. (B and C) Co-IP results. Different combinations of vectors were co-transfected into Saos2 cells, and IP assays were performed using anti-Flag and anti-Myc agarose beads. The input and output proteins were probed with anti-Flag and anti-Myc, respectively. (B) CtIP directly interacted with CtBP1/2 in vitro . (C) CtBP1 directly interacted with CtIP, CtBP2, and HDAC1 in vitro . All data in this figure were independently repeated in triplicates and one representative blot is shown.
    Anti Ctbp1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "The CtIP-CtBP1/2-HDAC1-AP1 transcriptional complex is required for the transrepression of DNA damage modulators in the pathogenesis of osteosarcoma"

    Article Title: The CtIP-CtBP1/2-HDAC1-AP1 transcriptional complex is required for the transrepression of DNA damage modulators in the pathogenesis of osteosarcoma

    Journal: Translational Oncology

    doi: 10.1016/j.tranon.2022.101429

    The formation of the CtIP-CtBP1/2-HDAC1-AP1 complex in vivo and in vitro (A) CtIP immunoprecipitated CtBP1, CtBP2, HDAC1, JUN, and FOS. Three independent tumor tissues with equal weights (0.1 g) were mixed and then homogenized. The CtIP-purified complex in the homogenate was probed with antibodies indicated in the figure. (B and C) Co-IP results. Different combinations of vectors were co-transfected into Saos2 cells, and IP assays were performed using anti-Flag and anti-Myc agarose beads. The input and output proteins were probed with anti-Flag and anti-Myc, respectively. (B) CtIP directly interacted with CtBP1/2 in vitro . (C) CtBP1 directly interacted with CtIP, CtBP2, and HDAC1 in vitro . All data in this figure were independently repeated in triplicates and one representative blot is shown.
    Figure Legend Snippet: The formation of the CtIP-CtBP1/2-HDAC1-AP1 complex in vivo and in vitro (A) CtIP immunoprecipitated CtBP1, CtBP2, HDAC1, JUN, and FOS. Three independent tumor tissues with equal weights (0.1 g) were mixed and then homogenized. The CtIP-purified complex in the homogenate was probed with antibodies indicated in the figure. (B and C) Co-IP results. Different combinations of vectors were co-transfected into Saos2 cells, and IP assays were performed using anti-Flag and anti-Myc agarose beads. The input and output proteins were probed with anti-Flag and anti-Myc, respectively. (B) CtIP directly interacted with CtBP1/2 in vitro . (C) CtBP1 directly interacted with CtIP, CtBP2, and HDAC1 in vitro . All data in this figure were independently repeated in triplicates and one representative blot is shown.

    Techniques Used: In Vivo, In Vitro, Immunoprecipitation, Purification, Co-Immunoprecipitation Assay, Transfection

    Depletion of CtIP and CtBPs decreased cell viability, colony formation, cell invasion, and tumor growth (A) MTT assay results for CtIP-CtBP1/2-HDAC1-AP1 components in the knockdown cells. * P < 0.01 and ** P < 0.01. (B) Tumor xenograft results for CtIP-CtBP1/2-HDAC1-AP1 components in the knockdown cells (for each cell line, 10 mice were injected). * P < 0.01 and ** P < 0.01. Tumor volumes were measured at 5-day intervals. *** P < 0.001. (C) Colony numbers after cell culture (knockdown cells of individual CtIP-CtBP1/2-HDAC1-AP1 components) for 14 days. ns: no significance. ** P < 0.01 and *** P < 0.001. (D) Invaded cell numbers in Boyden chamber assays. ns: no significance. ** P < 0.01 and *** P < 0.001. All data in this figure are presented as the mean ± SD of three independent experiments.
    Figure Legend Snippet: Depletion of CtIP and CtBPs decreased cell viability, colony formation, cell invasion, and tumor growth (A) MTT assay results for CtIP-CtBP1/2-HDAC1-AP1 components in the knockdown cells. * P < 0.01 and ** P < 0.01. (B) Tumor xenograft results for CtIP-CtBP1/2-HDAC1-AP1 components in the knockdown cells (for each cell line, 10 mice were injected). * P < 0.01 and ** P < 0.01. Tumor volumes were measured at 5-day intervals. *** P < 0.001. (C) Colony numbers after cell culture (knockdown cells of individual CtIP-CtBP1/2-HDAC1-AP1 components) for 14 days. ns: no significance. ** P < 0.01 and *** P < 0.001. (D) Invaded cell numbers in Boyden chamber assays. ns: no significance. ** P < 0.01 and *** P < 0.001. All data in this figure are presented as the mean ± SD of three independent experiments.

    Techniques Used: MTT Assay, Injection, Cell Culture

    Identification of CtIP-CtBP1/2-HDAC1-AP1 downstream targets by microarray analysis and conserved AP1 consensus sequence (A) Microarray results. RNA samples from Control-KD, CtIP-KD1, and CtBP1-KD1 cells (in Saos2 background), as well as Control-OE, CtIP-OE, and CtBP1-OE cells (in hFOB1.19 background) were subjected to microarray analysis. Genes that were consistently dysregulated in CtIP-KD1 and CtBP1-KD1 but conversely expressed in CtIP-OE and CtBP1-OE cells are presented. Data are presented as the mean ± SD of three independent experiments. (B) Prediction of AP1 binding sites on the promoters of potential target genes of CtIP-CtBP1/2-HDAC1-AP1. The promoters (2000 bp length in the upstream of ATG) of the genes shown in the figure were used to identify the AP1 binding sites (TGAG/CTCA).
    Figure Legend Snippet: Identification of CtIP-CtBP1/2-HDAC1-AP1 downstream targets by microarray analysis and conserved AP1 consensus sequence (A) Microarray results. RNA samples from Control-KD, CtIP-KD1, and CtBP1-KD1 cells (in Saos2 background), as well as Control-OE, CtIP-OE, and CtBP1-OE cells (in hFOB1.19 background) were subjected to microarray analysis. Genes that were consistently dysregulated in CtIP-KD1 and CtBP1-KD1 but conversely expressed in CtIP-OE and CtBP1-OE cells are presented. Data are presented as the mean ± SD of three independent experiments. (B) Prediction of AP1 binding sites on the promoters of potential target genes of CtIP-CtBP1/2-HDAC1-AP1. The promoters (2000 bp length in the upstream of ATG) of the genes shown in the figure were used to identify the AP1 binding sites (TGAG/CTCA).

    Techniques Used: Microarray, Sequencing, Binding Assay

    A schematic diagram of the assembly of the CtIP-CtBP1/2-HDAC1-AP1 complex and its role in osteosarcoma tumorigenesis Overexpressed CtIP couples with CtBP1/2 heterodimer, HDAC1, and AP1 subunits to assemble a transcriptional complex. This complex binds to the promoters of MLH1, MSH3, BRCA1 , and CDKN1A to repress their expression. The downregulation of these genes impairs the DNA repair process and increases genome stability, causing tumorigenesis.
    Figure Legend Snippet: A schematic diagram of the assembly of the CtIP-CtBP1/2-HDAC1-AP1 complex and its role in osteosarcoma tumorigenesis Overexpressed CtIP couples with CtBP1/2 heterodimer, HDAC1, and AP1 subunits to assemble a transcriptional complex. This complex binds to the promoters of MLH1, MSH3, BRCA1 , and CDKN1A to repress their expression. The downregulation of these genes impairs the DNA repair process and increases genome stability, causing tumorigenesis.

    Techniques Used: Expressing

    anti ctbp1  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti ctbp1
    a , b KURAMOCHI cells were infected with indicated shRNAs. Cell death receptor expression was examined by western blotting ( a ), DR4 and DR5 mRNA levels were examined by qPCR ( b ), ** p < 0.01 as compared with shCtrl group. Arrow in FAS blot points to unmodified FAS, and higher molecular weight forms are consistent with known glycosylation . c – e KURAMOCHI cells were treated with indicated siRNAs along with shRNAs. Cleaved caspase 8, and the knockdown efficiency of DR4 and <t>CtBP1/2</t> was determined by immunoblotting ( c ); caspase 8 activity was examined by enzymatic assay ( d ), ** p < 0.01 as compared with shCtrl group; and viable cells were counted by Trypan blue assay at indicated time points ( e ). *** p < 0.001 as compared with shCtrl group.
    Anti Ctbp1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "CtBP determines ovarian cancer cell fate through repression of death receptors"

    Article Title: CtBP determines ovarian cancer cell fate through repression of death receptors

    Journal: Cell Death & Disease

    doi: 10.1038/s41419-020-2455-7

    a , b KURAMOCHI cells were infected with indicated shRNAs. Cell death receptor expression was examined by western blotting ( a ), DR4 and DR5 mRNA levels were examined by qPCR ( b ), ** p < 0.01 as compared with shCtrl group. Arrow in FAS blot points to unmodified FAS, and higher molecular weight forms are consistent with known glycosylation . c – e KURAMOCHI cells were treated with indicated siRNAs along with shRNAs. Cleaved caspase 8, and the knockdown efficiency of DR4 and CtBP1/2 was determined by immunoblotting ( c ); caspase 8 activity was examined by enzymatic assay ( d ), ** p < 0.01 as compared with shCtrl group; and viable cells were counted by Trypan blue assay at indicated time points ( e ). *** p < 0.001 as compared with shCtrl group.
    Figure Legend Snippet: a , b KURAMOCHI cells were infected with indicated shRNAs. Cell death receptor expression was examined by western blotting ( a ), DR4 and DR5 mRNA levels were examined by qPCR ( b ), ** p < 0.01 as compared with shCtrl group. Arrow in FAS blot points to unmodified FAS, and higher molecular weight forms are consistent with known glycosylation . c – e KURAMOCHI cells were treated with indicated siRNAs along with shRNAs. Cleaved caspase 8, and the knockdown efficiency of DR4 and CtBP1/2 was determined by immunoblotting ( c ); caspase 8 activity was examined by enzymatic assay ( d ), ** p < 0.01 as compared with shCtrl group; and viable cells were counted by Trypan blue assay at indicated time points ( e ). *** p < 0.001 as compared with shCtrl group.

    Techniques Used: Infection, Expressing, Western Blot, Molecular Weight, Activity Assay, Enzymatic Assay

    a Cartoon showing the DR4 promoter. Black bars labeled 1–6 represent the location of PCR amplicons used in ChIP experiments. b Cartoon showing the DR5 promoter. Black bars labeled 1–6 represent the location of PCR amplicons used in ChIP experiments. c CtBP1/2 occupancy at the DR4 promoter in OVCA429 cells. ChIP was performed with OVCA429 chromatin, and PCR amplicons from ( a ) were used for ChIP, ** p < 0.01 as compared with normal IgG group. d CtBP1/2 occupancy at the DR5 promoter in OVCA429 cells. ChIP was performed with OVCA429 chromatin, and PCR amplicons from ( b ) were used for ChIP, ** p < 0.01 as compared with normal IgG group.
    Figure Legend Snippet: a Cartoon showing the DR4 promoter. Black bars labeled 1–6 represent the location of PCR amplicons used in ChIP experiments. b Cartoon showing the DR5 promoter. Black bars labeled 1–6 represent the location of PCR amplicons used in ChIP experiments. c CtBP1/2 occupancy at the DR4 promoter in OVCA429 cells. ChIP was performed with OVCA429 chromatin, and PCR amplicons from ( a ) were used for ChIP, ** p < 0.01 as compared with normal IgG group. d CtBP1/2 occupancy at the DR5 promoter in OVCA429 cells. ChIP was performed with OVCA429 chromatin, and PCR amplicons from ( b ) were used for ChIP, ** p < 0.01 as compared with normal IgG group.

    Techniques Used: Labeling

    a Western blotting was performed to determine abundance of the indicated proteins in OVCA429 cells after infection with the indicated lentiviral shRNAs. b Fold induction of DR4/5 mRNAs in OVCA429 cells infected with the indicated lentiviral shRNAs was assessed by qPCR. c Western blotting to determine CtBP1/2 abundance in input and IP’s from ChIP experiments with OVCA429 cells when infected with indicated lentiviral shRNAs. d CtBP1/2 occupancy at DR4/5 promoters in OVCA429 cells. ChIP was performed with OVCA429 chromatin from cells in which CtBP1 or CtBP2 were knocked down with the indicated lentiviral shRNA’s. Indicated PCR amplicons were used for ChIP. e ChIP-reChIP assay showing CtBP1/2 occupancy at the indicated regions of the DR4/5 promotors. ChIP-reChIP was performed with OVCA429 chromatin and the first antibodies on the left hand side of the graphs, and second antibodies on the right hand side of each graph, ** p < 0.01 as compared with normal IgG group.
    Figure Legend Snippet: a Western blotting was performed to determine abundance of the indicated proteins in OVCA429 cells after infection with the indicated lentiviral shRNAs. b Fold induction of DR4/5 mRNAs in OVCA429 cells infected with the indicated lentiviral shRNAs was assessed by qPCR. c Western blotting to determine CtBP1/2 abundance in input and IP’s from ChIP experiments with OVCA429 cells when infected with indicated lentiviral shRNAs. d CtBP1/2 occupancy at DR4/5 promoters in OVCA429 cells. ChIP was performed with OVCA429 chromatin from cells in which CtBP1 or CtBP2 were knocked down with the indicated lentiviral shRNA’s. Indicated PCR amplicons were used for ChIP. e ChIP-reChIP assay showing CtBP1/2 occupancy at the indicated regions of the DR4/5 promotors. ChIP-reChIP was performed with OVCA429 chromatin and the first antibodies on the left hand side of the graphs, and second antibodies on the right hand side of each graph, ** p < 0.01 as compared with normal IgG group.

    Techniques Used: Western Blot, Infection

    anti ctbp1  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti ctbp1
    a , b KURAMOCHI cells were infected with indicated shRNAs. Cell death receptor expression was examined by western blotting ( a ), DR4 and DR5 mRNA levels were examined by qPCR ( b ), ** p < 0.01 as compared with shCtrl group. Arrow in FAS blot points to unmodified FAS, and higher molecular weight forms are consistent with known glycosylation . c – e KURAMOCHI cells were treated with indicated siRNAs along with shRNAs. Cleaved caspase 8, and the knockdown efficiency of DR4 and <t>CtBP1/2</t> was determined by immunoblotting ( c ); caspase 8 activity was examined by enzymatic assay ( d ), ** p < 0.01 as compared with shCtrl group; and viable cells were counted by Trypan blue assay at indicated time points ( e ). *** p < 0.001 as compared with shCtrl group.
    Anti Ctbp1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti ctbp1/product/Cell Signaling Technology Inc
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti ctbp1 - by Bioz Stars, 2023-02
    94/100 stars

    Images

    1) Product Images from "CtBP determines ovarian cancer cell fate through repression of death receptors"

    Article Title: CtBP determines ovarian cancer cell fate through repression of death receptors

    Journal: Cell Death & Disease

    doi: 10.1038/s41419-020-2455-7

    a , b KURAMOCHI cells were infected with indicated shRNAs. Cell death receptor expression was examined by western blotting ( a ), DR4 and DR5 mRNA levels were examined by qPCR ( b ), ** p < 0.01 as compared with shCtrl group. Arrow in FAS blot points to unmodified FAS, and higher molecular weight forms are consistent with known glycosylation . c – e KURAMOCHI cells were treated with indicated siRNAs along with shRNAs. Cleaved caspase 8, and the knockdown efficiency of DR4 and CtBP1/2 was determined by immunoblotting ( c ); caspase 8 activity was examined by enzymatic assay ( d ), ** p < 0.01 as compared with shCtrl group; and viable cells were counted by Trypan blue assay at indicated time points ( e ). *** p < 0.001 as compared with shCtrl group.
    Figure Legend Snippet: a , b KURAMOCHI cells were infected with indicated shRNAs. Cell death receptor expression was examined by western blotting ( a ), DR4 and DR5 mRNA levels were examined by qPCR ( b ), ** p < 0.01 as compared with shCtrl group. Arrow in FAS blot points to unmodified FAS, and higher molecular weight forms are consistent with known glycosylation . c – e KURAMOCHI cells were treated with indicated siRNAs along with shRNAs. Cleaved caspase 8, and the knockdown efficiency of DR4 and CtBP1/2 was determined by immunoblotting ( c ); caspase 8 activity was examined by enzymatic assay ( d ), ** p < 0.01 as compared with shCtrl group; and viable cells were counted by Trypan blue assay at indicated time points ( e ). *** p < 0.001 as compared with shCtrl group.

    Techniques Used: Infection, Expressing, Western Blot, Molecular Weight, Activity Assay, Enzymatic Assay

    a Cartoon showing the DR4 promoter. Black bars labeled 1–6 represent the location of PCR amplicons used in ChIP experiments. b Cartoon showing the DR5 promoter. Black bars labeled 1–6 represent the location of PCR amplicons used in ChIP experiments. c CtBP1/2 occupancy at the DR4 promoter in OVCA429 cells. ChIP was performed with OVCA429 chromatin, and PCR amplicons from ( a ) were used for ChIP, ** p < 0.01 as compared with normal IgG group. d CtBP1/2 occupancy at the DR5 promoter in OVCA429 cells. ChIP was performed with OVCA429 chromatin, and PCR amplicons from ( b ) were used for ChIP, ** p < 0.01 as compared with normal IgG group.
    Figure Legend Snippet: a Cartoon showing the DR4 promoter. Black bars labeled 1–6 represent the location of PCR amplicons used in ChIP experiments. b Cartoon showing the DR5 promoter. Black bars labeled 1–6 represent the location of PCR amplicons used in ChIP experiments. c CtBP1/2 occupancy at the DR4 promoter in OVCA429 cells. ChIP was performed with OVCA429 chromatin, and PCR amplicons from ( a ) were used for ChIP, ** p < 0.01 as compared with normal IgG group. d CtBP1/2 occupancy at the DR5 promoter in OVCA429 cells. ChIP was performed with OVCA429 chromatin, and PCR amplicons from ( b ) were used for ChIP, ** p < 0.01 as compared with normal IgG group.

    Techniques Used: Labeling

    a Western blotting was performed to determine abundance of the indicated proteins in OVCA429 cells after infection with the indicated lentiviral shRNAs. b Fold induction of DR4/5 mRNAs in OVCA429 cells infected with the indicated lentiviral shRNAs was assessed by qPCR. c Western blotting to determine CtBP1/2 abundance in input and IP’s from ChIP experiments with OVCA429 cells when infected with indicated lentiviral shRNAs. d CtBP1/2 occupancy at DR4/5 promoters in OVCA429 cells. ChIP was performed with OVCA429 chromatin from cells in which CtBP1 or CtBP2 were knocked down with the indicated lentiviral shRNA’s. Indicated PCR amplicons were used for ChIP. e ChIP-reChIP assay showing CtBP1/2 occupancy at the indicated regions of the DR4/5 promotors. ChIP-reChIP was performed with OVCA429 chromatin and the first antibodies on the left hand side of the graphs, and second antibodies on the right hand side of each graph, ** p < 0.01 as compared with normal IgG group.
    Figure Legend Snippet: a Western blotting was performed to determine abundance of the indicated proteins in OVCA429 cells after infection with the indicated lentiviral shRNAs. b Fold induction of DR4/5 mRNAs in OVCA429 cells infected with the indicated lentiviral shRNAs was assessed by qPCR. c Western blotting to determine CtBP1/2 abundance in input and IP’s from ChIP experiments with OVCA429 cells when infected with indicated lentiviral shRNAs. d CtBP1/2 occupancy at DR4/5 promoters in OVCA429 cells. ChIP was performed with OVCA429 chromatin from cells in which CtBP1 or CtBP2 were knocked down with the indicated lentiviral shRNA’s. Indicated PCR amplicons were used for ChIP. e ChIP-reChIP assay showing CtBP1/2 occupancy at the indicated regions of the DR4/5 promotors. ChIP-reChIP was performed with OVCA429 chromatin and the first antibodies on the left hand side of the graphs, and second antibodies on the right hand side of each graph, ** p < 0.01 as compared with normal IgG group.

    Techniques Used: Western Blot, Infection

    rabbit anti human ctbp1  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc rabbit anti human ctbp1
    Rabbit Anti Human Ctbp1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    rabbit anti human ctbp1  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc rabbit anti human ctbp1
    Rabbit Anti Human Ctbp1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc anti ctbp1
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    Expression levels of  CTBP1  and the clinicopathological characteristics of patients with HCC.

    Journal: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research

    Article Title: C-Terminus of E1A Binding Protein 1 Stimulates Malignant Phenotype in Human Hepatocellular Carcinoma

    doi: 10.12659/MSM.920114

    Figure Lengend Snippet: Expression levels of CTBP1 and the clinicopathological characteristics of patients with HCC.

    Article Snippet: The Western blotting process was performed as previously described [ ] and the PVDF membranes were incubated with the following primary antibodies at 4˚C overnight: rabbit anti-human CTBP1 (cat. no. 8684, Cell Signaling Technology), anti-human CTBP2 (cat. no. 13256, Cell Signaling Technology), anti-human phospho-Akt at Thr308 site (cat. no. 13038, Cell Signaling Technology), anti-human Akt (cat. no. 2920, Cell Signaling Technology), anti-human phospho-phosphatidylinositol-3-kinase p110α (cat. no. 4255, Cell Signaling Technology), and mouse anti-human β-actin (cat. no. ab 8227, Abcam).

    Techniques: Expressing

    CTBP1 was highly expressed in HCC tissues. ( A ) High CTBP1 expression in HCC tissues was observed via IHC. ( B ) The protein of CTBP1 was highly expressed in HCC tissues. ** P<0.01 vs. hepatic tissues. ( C ) Positive CTBP1 expression predicted a shorter survival time. HCC – hepatocellular carcinoma; CTBP – C-terminus of the E1A binding proteins.

    Journal: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research

    Article Title: C-Terminus of E1A Binding Protein 1 Stimulates Malignant Phenotype in Human Hepatocellular Carcinoma

    doi: 10.12659/MSM.920114

    Figure Lengend Snippet: CTBP1 was highly expressed in HCC tissues. ( A ) High CTBP1 expression in HCC tissues was observed via IHC. ( B ) The protein of CTBP1 was highly expressed in HCC tissues. ** P<0.01 vs. hepatic tissues. ( C ) Positive CTBP1 expression predicted a shorter survival time. HCC – hepatocellular carcinoma; CTBP – C-terminus of the E1A binding proteins.

    Article Snippet: The Western blotting process was performed as previously described [ ] and the PVDF membranes were incubated with the following primary antibodies at 4˚C overnight: rabbit anti-human CTBP1 (cat. no. 8684, Cell Signaling Technology), anti-human CTBP2 (cat. no. 13256, Cell Signaling Technology), anti-human phospho-Akt at Thr308 site (cat. no. 13038, Cell Signaling Technology), anti-human Akt (cat. no. 2920, Cell Signaling Technology), anti-human phospho-phosphatidylinositol-3-kinase p110α (cat. no. 4255, Cell Signaling Technology), and mouse anti-human β-actin (cat. no. ab 8227, Abcam).

    Techniques: Expressing, Binding Assay

    CTBP1 promoted the malignancy of hepatic astrocytes. ( A ) Modifications in activation of the PI3K/Akt pathway. ( B ) Growth curve of the LX-2 cells as determined via the CCK-8. ( C ) Colony formation activity in 2D monolayer cultures. ( D ) The in vitro invasive activity of LX-2 cells was detected by the Transwell chamber method. ( E ) The in vitro migratory activity of LX-2 cells was investigated using the cell scratch assay. ** P<0.01 vs. the vector group. CTBP – C-terminus of the E1A binding proteins.

    Journal: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research

    Article Title: C-Terminus of E1A Binding Protein 1 Stimulates Malignant Phenotype in Human Hepatocellular Carcinoma

    doi: 10.12659/MSM.920114

    Figure Lengend Snippet: CTBP1 promoted the malignancy of hepatic astrocytes. ( A ) Modifications in activation of the PI3K/Akt pathway. ( B ) Growth curve of the LX-2 cells as determined via the CCK-8. ( C ) Colony formation activity in 2D monolayer cultures. ( D ) The in vitro invasive activity of LX-2 cells was detected by the Transwell chamber method. ( E ) The in vitro migratory activity of LX-2 cells was investigated using the cell scratch assay. ** P<0.01 vs. the vector group. CTBP – C-terminus of the E1A binding proteins.

    Article Snippet: The Western blotting process was performed as previously described [ ] and the PVDF membranes were incubated with the following primary antibodies at 4˚C overnight: rabbit anti-human CTBP1 (cat. no. 8684, Cell Signaling Technology), anti-human CTBP2 (cat. no. 13256, Cell Signaling Technology), anti-human phospho-Akt at Thr308 site (cat. no. 13038, Cell Signaling Technology), anti-human Akt (cat. no. 2920, Cell Signaling Technology), anti-human phospho-phosphatidylinositol-3-kinase p110α (cat. no. 4255, Cell Signaling Technology), and mouse anti-human β-actin (cat. no. ab 8227, Abcam).

    Techniques: Activation Assay, CCK-8 Assay, Activity Assay, In Vitro, Wound Healing Assay, Plasmid Preparation, Binding Assay

    CTBP1 silencing reduced the migratory activity of HCC cells. ( A ) The consequences of CTBP1 loss on the PI3K/Akt signaling in Hep3B cells. ( B ) The growth rate of Hep3B cells was assessed via CCK-8 assay. ( C ) The colony formation activity of Hep3B cells was evaluated using 2D culture. ( D ) The in vitro invasive activity of Hep3B cells. ( E ) The in vitro migratory activity of Hep3B cells. ** P<0.01, vs. the scramble group.

    Journal: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research

    Article Title: C-Terminus of E1A Binding Protein 1 Stimulates Malignant Phenotype in Human Hepatocellular Carcinoma

    doi: 10.12659/MSM.920114

    Figure Lengend Snippet: CTBP1 silencing reduced the migratory activity of HCC cells. ( A ) The consequences of CTBP1 loss on the PI3K/Akt signaling in Hep3B cells. ( B ) The growth rate of Hep3B cells was assessed via CCK-8 assay. ( C ) The colony formation activity of Hep3B cells was evaluated using 2D culture. ( D ) The in vitro invasive activity of Hep3B cells. ( E ) The in vitro migratory activity of Hep3B cells. ** P<0.01, vs. the scramble group.

    Article Snippet: The Western blotting process was performed as previously described [ ] and the PVDF membranes were incubated with the following primary antibodies at 4˚C overnight: rabbit anti-human CTBP1 (cat. no. 8684, Cell Signaling Technology), anti-human CTBP2 (cat. no. 13256, Cell Signaling Technology), anti-human phospho-Akt at Thr308 site (cat. no. 13038, Cell Signaling Technology), anti-human Akt (cat. no. 2920, Cell Signaling Technology), anti-human phospho-phosphatidylinositol-3-kinase p110α (cat. no. 4255, Cell Signaling Technology), and mouse anti-human β-actin (cat. no. ab 8227, Abcam).

    Techniques: Activity Assay, CCK-8 Assay, In Vitro