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primary antibodies against hdac1, hdac2, hdac3, hdac8  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc primary antibodies against hdac1, hdac2, hdac3, hdac8
    HDAC3 and <t>HDAC8</t> are required for BKPyV LT protein expression. A The expression of class I HDACs was knocked down by siRNA, then cells were infected with BKPyV and LT protein expression was determined by immunofluorescence and flow cytometric analysis 48 h post-infection. Middle panel: Quantification of the LT expression levels in the immunofluorescence assay. Right panel: LT protein expression was determined by intracellular staining and quantified by flow cytometry. B Class I HDACs were inhibited by HDAC inhibitors, cells were infected with BKPyV, and LT protein expression was determined by immunofluorescence and flow cytometric analysis 48 h postinfection. Middle panel: Quantification of the LT expression levels in the immunofluorescence assay. Right panel: LT protein expression was determined by intracellular staining and quantified by flow cytometry. BKPyV infection without siRNA or HDAC inhibitor treatment was considered 100%. (Green, LT protein; Red, Evan’s Blue stain). Data are representative of at least three independent experiments and are shown as the mean ± SD (* P < 0.05; ** P < 0.01; *** P < 0.001). (MFI: Mean fluorescence intensity)
    Primary Antibodies Against Hdac1, Hdac2, Hdac3, Hdac8, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/primary antibodies against hdac1, hdac2, hdac3, hdac8/product/Cell Signaling Technology Inc
    Average 90 stars, based on 1 article reviews
    primary antibodies against hdac1, hdac2, hdac3, hdac8 - by Bioz Stars, 2026-05
    90/100 stars

    Images

    1) Product Images from "Histone deacetylase III interactions with BK polyomavirus large tumor antigen may affect protein stability"

    Article Title: Histone deacetylase III interactions with BK polyomavirus large tumor antigen may affect protein stability

    Journal: Virology Journal

    doi: 10.1186/s12985-023-02128-6

    HDAC3 and HDAC8 are required for BKPyV LT protein expression. A The expression of class I HDACs was knocked down by siRNA, then cells were infected with BKPyV and LT protein expression was determined by immunofluorescence and flow cytometric analysis 48 h post-infection. Middle panel: Quantification of the LT expression levels in the immunofluorescence assay. Right panel: LT protein expression was determined by intracellular staining and quantified by flow cytometry. B Class I HDACs were inhibited by HDAC inhibitors, cells were infected with BKPyV, and LT protein expression was determined by immunofluorescence and flow cytometric analysis 48 h postinfection. Middle panel: Quantification of the LT expression levels in the immunofluorescence assay. Right panel: LT protein expression was determined by intracellular staining and quantified by flow cytometry. BKPyV infection without siRNA or HDAC inhibitor treatment was considered 100%. (Green, LT protein; Red, Evan’s Blue stain). Data are representative of at least three independent experiments and are shown as the mean ± SD (* P < 0.05; ** P < 0.01; *** P < 0.001). (MFI: Mean fluorescence intensity)
    Figure Legend Snippet: HDAC3 and HDAC8 are required for BKPyV LT protein expression. A The expression of class I HDACs was knocked down by siRNA, then cells were infected with BKPyV and LT protein expression was determined by immunofluorescence and flow cytometric analysis 48 h post-infection. Middle panel: Quantification of the LT expression levels in the immunofluorescence assay. Right panel: LT protein expression was determined by intracellular staining and quantified by flow cytometry. B Class I HDACs were inhibited by HDAC inhibitors, cells were infected with BKPyV, and LT protein expression was determined by immunofluorescence and flow cytometric analysis 48 h postinfection. Middle panel: Quantification of the LT expression levels in the immunofluorescence assay. Right panel: LT protein expression was determined by intracellular staining and quantified by flow cytometry. BKPyV infection without siRNA or HDAC inhibitor treatment was considered 100%. (Green, LT protein; Red, Evan’s Blue stain). Data are representative of at least three independent experiments and are shown as the mean ± SD (* P < 0.05; ** P < 0.01; *** P < 0.001). (MFI: Mean fluorescence intensity)

    Techniques Used: Expressing, Infection, Immunofluorescence, Staining, Flow Cytometry, Fluorescence



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    HDAC3 and <t>HDAC8</t> are required for BKPyV LT protein expression. A The expression of class I HDACs was knocked down by siRNA, then cells were infected with BKPyV and LT protein expression was determined by immunofluorescence and flow cytometric analysis 48 h post-infection. Middle panel: Quantification of the LT expression levels in the immunofluorescence assay. Right panel: LT protein expression was determined by intracellular staining and quantified by flow cytometry. B Class I HDACs were inhibited by HDAC inhibitors, cells were infected with BKPyV, and LT protein expression was determined by immunofluorescence and flow cytometric analysis 48 h postinfection. Middle panel: Quantification of the LT expression levels in the immunofluorescence assay. Right panel: LT protein expression was determined by intracellular staining and quantified by flow cytometry. BKPyV infection without siRNA or HDAC inhibitor treatment was considered 100%. (Green, LT protein; Red, Evan’s Blue stain). Data are representative of at least three independent experiments and are shown as the mean ± SD (* P < 0.05; ** P < 0.01; *** P < 0.001). (MFI: Mean fluorescence intensity)
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    KEY RESOURCES TABLE
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    Image Search Results


    HDAC3 and HDAC8 are required for BKPyV LT protein expression. A The expression of class I HDACs was knocked down by siRNA, then cells were infected with BKPyV and LT protein expression was determined by immunofluorescence and flow cytometric analysis 48 h post-infection. Middle panel: Quantification of the LT expression levels in the immunofluorescence assay. Right panel: LT protein expression was determined by intracellular staining and quantified by flow cytometry. B Class I HDACs were inhibited by HDAC inhibitors, cells were infected with BKPyV, and LT protein expression was determined by immunofluorescence and flow cytometric analysis 48 h postinfection. Middle panel: Quantification of the LT expression levels in the immunofluorescence assay. Right panel: LT protein expression was determined by intracellular staining and quantified by flow cytometry. BKPyV infection without siRNA or HDAC inhibitor treatment was considered 100%. (Green, LT protein; Red, Evan’s Blue stain). Data are representative of at least three independent experiments and are shown as the mean ± SD (* P < 0.05; ** P < 0.01; *** P < 0.001). (MFI: Mean fluorescence intensity)

    Journal: Virology Journal

    Article Title: Histone deacetylase III interactions with BK polyomavirus large tumor antigen may affect protein stability

    doi: 10.1186/s12985-023-02128-6

    Figure Lengend Snippet: HDAC3 and HDAC8 are required for BKPyV LT protein expression. A The expression of class I HDACs was knocked down by siRNA, then cells were infected with BKPyV and LT protein expression was determined by immunofluorescence and flow cytometric analysis 48 h post-infection. Middle panel: Quantification of the LT expression levels in the immunofluorescence assay. Right panel: LT protein expression was determined by intracellular staining and quantified by flow cytometry. B Class I HDACs were inhibited by HDAC inhibitors, cells were infected with BKPyV, and LT protein expression was determined by immunofluorescence and flow cytometric analysis 48 h postinfection. Middle panel: Quantification of the LT expression levels in the immunofluorescence assay. Right panel: LT protein expression was determined by intracellular staining and quantified by flow cytometry. BKPyV infection without siRNA or HDAC inhibitor treatment was considered 100%. (Green, LT protein; Red, Evan’s Blue stain). Data are representative of at least three independent experiments and are shown as the mean ± SD (* P < 0.05; ** P < 0.01; *** P < 0.001). (MFI: Mean fluorescence intensity)

    Article Snippet: Primary antibodies against HDAC1, HDAC2, HDAC3, and HDAC8 were purchased from Cell Signaling Technology Inc. (Danvers, Massachusetts, USA).

    Techniques: Expressing, Infection, Immunofluorescence, Staining, Flow Cytometry, Fluorescence

    Literature review identified the transcriptional addiction genes.

    Journal: Aging (Albany NY)

    Article Title: Profiling and integrated analysis of transcriptional addiction gene expression and prognostic value in hepatocellular carcinoma

    doi: 10.18632/aging.204676

    Figure Lengend Snippet: Literature review identified the transcriptional addiction genes.

    Article Snippet: We incubated the tissue microarrays with the primary antibody against HDAC2 (Servicebio, GB11371, Wuhan), followed by the secondary antibody (Servicebio, GB23303, Wuhan) and 3,3’-diaminobenzidine (DAB) IHC kit (DAKO, K5007, Denmark).

    Techniques:

    Each genetic parameter of the risk signature.

    Journal: Aging (Albany NY)

    Article Title: Profiling and integrated analysis of transcriptional addiction gene expression and prognostic value in hepatocellular carcinoma

    doi: 10.18632/aging.204676

    Figure Lengend Snippet: Each genetic parameter of the risk signature.

    Article Snippet: We incubated the tissue microarrays with the primary antibody against HDAC2 (Servicebio, GB11371, Wuhan), followed by the secondary antibody (Servicebio, GB23303, Wuhan) and 3,3’-diaminobenzidine (DAB) IHC kit (DAKO, K5007, Denmark).

    Techniques:

    Expression levels of HDAC2 in different tissues. ( A ) HDAC2 expression in normal and tumor tissues in the TCGA-LIHC cohort. ( B ) HDAC2 expression in normal and tumor tissues in the ICGC-JP cohort. ( C ) The protein level of HDAC2 in normal and tumor tissues in HPA database. ( D ) The protein levels of HDAC2 in tumor tissue, paracancerous tissue, and distal tissue in the tissue microarray.

    Journal: Aging (Albany NY)

    Article Title: Profiling and integrated analysis of transcriptional addiction gene expression and prognostic value in hepatocellular carcinoma

    doi: 10.18632/aging.204676

    Figure Lengend Snippet: Expression levels of HDAC2 in different tissues. ( A ) HDAC2 expression in normal and tumor tissues in the TCGA-LIHC cohort. ( B ) HDAC2 expression in normal and tumor tissues in the ICGC-JP cohort. ( C ) The protein level of HDAC2 in normal and tumor tissues in HPA database. ( D ) The protein levels of HDAC2 in tumor tissue, paracancerous tissue, and distal tissue in the tissue microarray.

    Article Snippet: We incubated the tissue microarrays with the primary antibody against HDAC2 (Servicebio, GB11371, Wuhan), followed by the secondary antibody (Servicebio, GB23303, Wuhan) and 3,3’-diaminobenzidine (DAB) IHC kit (DAKO, K5007, Denmark).

    Techniques: Expressing, Microarray

    Relationship between HDAC2 expression and patient survival. ( A ) Kaplan-Meier survival analysis of patients with different HDAC2 expressions in TCGA-LIHC cohort. ( B ) Kaplan-Meier survival analysis of patients with different HDAC2 expressions in ICGC-JP cohort. ( C ) Scored for each sample of the tissue microarray. ( D , E ) Kaplan-Meier survival analysis of patients with different tissue scores in the tissue microarrays.

    Journal: Aging (Albany NY)

    Article Title: Profiling and integrated analysis of transcriptional addiction gene expression and prognostic value in hepatocellular carcinoma

    doi: 10.18632/aging.204676

    Figure Lengend Snippet: Relationship between HDAC2 expression and patient survival. ( A ) Kaplan-Meier survival analysis of patients with different HDAC2 expressions in TCGA-LIHC cohort. ( B ) Kaplan-Meier survival analysis of patients with different HDAC2 expressions in ICGC-JP cohort. ( C ) Scored for each sample of the tissue microarray. ( D , E ) Kaplan-Meier survival analysis of patients with different tissue scores in the tissue microarrays.

    Article Snippet: We incubated the tissue microarrays with the primary antibody against HDAC2 (Servicebio, GB11371, Wuhan), followed by the secondary antibody (Servicebio, GB23303, Wuhan) and 3,3’-diaminobenzidine (DAB) IHC kit (DAKO, K5007, Denmark).

    Techniques: Expressing, Microarray

    Correlation of HDAC2 score with HCC pathological characteristics in the tissue microarray set. ( A ) HDAC2 score in tumor recurrence and non-recurrence groups. ( B ) HDAC2 score in tumor metastatic and non-metastatic groups. ( C ) HDAC2 score in different tumor size groups. ( D ) HDAC2 score in different tumor stage groups. ( E , F ) Univariate and multivariate regression analyses for HDAC2 score as an independent prognostic factor.

    Journal: Aging (Albany NY)

    Article Title: Profiling and integrated analysis of transcriptional addiction gene expression and prognostic value in hepatocellular carcinoma

    doi: 10.18632/aging.204676

    Figure Lengend Snippet: Correlation of HDAC2 score with HCC pathological characteristics in the tissue microarray set. ( A ) HDAC2 score in tumor recurrence and non-recurrence groups. ( B ) HDAC2 score in tumor metastatic and non-metastatic groups. ( C ) HDAC2 score in different tumor size groups. ( D ) HDAC2 score in different tumor stage groups. ( E , F ) Univariate and multivariate regression analyses for HDAC2 score as an independent prognostic factor.

    Article Snippet: We incubated the tissue microarrays with the primary antibody against HDAC2 (Servicebio, GB11371, Wuhan), followed by the secondary antibody (Servicebio, GB23303, Wuhan) and 3,3’-diaminobenzidine (DAB) IHC kit (DAKO, K5007, Denmark).

    Techniques: Microarray

    Overexpression of HDAC2 Inhibits Senescence in C2C12 Cells. ( A ) β-Galactosidase staining measurement of cellular senescence after 24 hours of 0.3% CSE between the different groups, 100×. ( B ) The protein expression level of P53, P21, SMP30 in cells with or without 0.3% CSE. ( C ) The mRNA level of P53, P21 in cells with or without 0.3% CSE. ( D ) The protein expression level of NF-κBp65 and IKK in cells with or without 0.3% CSE. Values are expressed as means±SD. Experiments were repeated 3 times with similar results. * p <0.05 vs control NC group (LV-NC), # p <0.05 vs CSE+LV-NC group.

    Journal: International Journal of Chronic Obstructive Pulmonary Disease

    Article Title: Histone Deacetylase 2 Suppresses Skeletal Muscle Atrophy and Senescence via NF-κB Signaling Pathway in Cigarette Smoke-Induced Mice with Emphysema

    doi: 10.2147/COPD.S314640

    Figure Lengend Snippet: Overexpression of HDAC2 Inhibits Senescence in C2C12 Cells. ( A ) β-Galactosidase staining measurement of cellular senescence after 24 hours of 0.3% CSE between the different groups, 100×. ( B ) The protein expression level of P53, P21, SMP30 in cells with or without 0.3% CSE. ( C ) The mRNA level of P53, P21 in cells with or without 0.3% CSE. ( D ) The protein expression level of NF-κBp65 and IKK in cells with or without 0.3% CSE. Values are expressed as means±SD. Experiments were repeated 3 times with similar results. * p <0.05 vs control NC group (LV-NC), # p <0.05 vs CSE+LV-NC group.

    Article Snippet: The membranes were then incubated with primary antibodies against HDAC2, P53, P21, IKK, and NF-κBp65 (1:1000, Cell Signaling Technology, USA) and MURF1, MAFbx, and SMP30 (1:1000, Abcam, UK) overnight at 4°C, followed by incubation with fluorescent secondary antibodies (1:1000, Cell Signaling Technology, USA).

    Techniques: Over Expression, Staining, Expressing, Control

    Effects of NF-κB pathway on HDAC2-regulated atrophy and senescence in C2C2 cells. ( A ) Western blot assays for NF-κBp65 expression after overexpression of HDAC2 and PDTC in CSE. ( B ) Immunofluorescence detection of myotube diameter, 100×. ( C ) Western blot assays for MURF1, MAFbx, P53, and P21. Values are expressed as means±SD. Experiments were repeated 3 times with similar results. * p <0.05 vs CSE group, # p <0.05 vs CSE+LV-HDAC2 group, $ p <0.05 vs CSE+PDTC group.

    Journal: International Journal of Chronic Obstructive Pulmonary Disease

    Article Title: Histone Deacetylase 2 Suppresses Skeletal Muscle Atrophy and Senescence via NF-κB Signaling Pathway in Cigarette Smoke-Induced Mice with Emphysema

    doi: 10.2147/COPD.S314640

    Figure Lengend Snippet: Effects of NF-κB pathway on HDAC2-regulated atrophy and senescence in C2C2 cells. ( A ) Western blot assays for NF-κBp65 expression after overexpression of HDAC2 and PDTC in CSE. ( B ) Immunofluorescence detection of myotube diameter, 100×. ( C ) Western blot assays for MURF1, MAFbx, P53, and P21. Values are expressed as means±SD. Experiments were repeated 3 times with similar results. * p <0.05 vs CSE group, # p <0.05 vs CSE+LV-HDAC2 group, $ p <0.05 vs CSE+PDTC group.

    Article Snippet: The membranes were then incubated with primary antibodies against HDAC2, P53, P21, IKK, and NF-κBp65 (1:1000, Cell Signaling Technology, USA) and MURF1, MAFbx, and SMP30 (1:1000, Abcam, UK) overnight at 4°C, followed by incubation with fluorescent secondary antibodies (1:1000, Cell Signaling Technology, USA).

    Techniques: Western Blot, Expressing, Over Expression, Immunofluorescence

    HDAC2 is frequently downregulated in human metastatic colorectal tissues. a Relative expression of HDAC1, HDAC2, HDAC3, and HDAC8 in CRC tissues. Data were collected from Oncomine, including 330 cases of primary site and 43 cases of metastasis. b Kaplan-Meier analyses of the correlations between HDAC1, HDAC2, HDAC3, and HDAC8 expression levels and overall survival in 362 patients with CRC. Data were collected from TCGA. We labeled TCGA samples as “high” or “low” according to whether the expression of HDAC1, HDAC2, HDAC3 and HDAC8 was higher or lower than the corresponding median value among all samples. c , d Expression of HDAC2 in 22 paired CRC samples. e Representative immunohistochemical staining of a tissue array containing CRC samples with anti-HDAC2 antibody. Magnification: 40× (upper) and 200× (lower). f, g Expression correlations between HDAC2 and E-cadherin in CRC samples. Data were collected from TCGA, including 471 COAD samples and 167 READ samples. h Expression of E-cadherin and HDAC2 in CRC cell lines detected by Western Blot. ** P < 0 .01; * P < 0.05. The data are representatives and are presented as mean ± standard error of the mean of 3 assays

    Journal: Journal of Experimental & Clinical Cancer Research : CR

    Article Title: HDAC2 inhibits EMT-mediated cancer metastasis by downregulating the long noncoding RNA H19 in colorectal cancer

    doi: 10.1186/s13046-020-01783-9

    Figure Lengend Snippet: HDAC2 is frequently downregulated in human metastatic colorectal tissues. a Relative expression of HDAC1, HDAC2, HDAC3, and HDAC8 in CRC tissues. Data were collected from Oncomine, including 330 cases of primary site and 43 cases of metastasis. b Kaplan-Meier analyses of the correlations between HDAC1, HDAC2, HDAC3, and HDAC8 expression levels and overall survival in 362 patients with CRC. Data were collected from TCGA. We labeled TCGA samples as “high” or “low” according to whether the expression of HDAC1, HDAC2, HDAC3 and HDAC8 was higher or lower than the corresponding median value among all samples. c , d Expression of HDAC2 in 22 paired CRC samples. e Representative immunohistochemical staining of a tissue array containing CRC samples with anti-HDAC2 antibody. Magnification: 40× (upper) and 200× (lower). f, g Expression correlations between HDAC2 and E-cadherin in CRC samples. Data were collected from TCGA, including 471 COAD samples and 167 READ samples. h Expression of E-cadherin and HDAC2 in CRC cell lines detected by Western Blot. ** P < 0 .01; * P < 0.05. The data are representatives and are presented as mean ± standard error of the mean of 3 assays

    Article Snippet: Specific primary antibodies against HDAC2 (Cell Signaling Technology) were used for IHC with a 2-step protocol.

    Techniques: Expressing, Labeling, Immunohistochemical staining, Staining, Western Blot

    Reduced HDAC2 induces EMT in CRC. a Altered mRNA expression in DLD1 HDAC2 KO cells. b , c Pathway analysis of changed genes in DLD1 HDAC2 KO cells (compared with DLD1 WT cells). d Merged mRNAs for EMT-related genes and those identified in our microarray. e , f Migration ability of DLD1 HDAC2 KO cells detected by transwell. g , k , l EMT markers were analyzed by immunoblotting and IF with the indicated antibodies in DLD1 HDAC2 WT and KO cells. h , i Migration ability of SW480 HDAC2 RNAi cells detected by transwell. j EMT markers were analyzed by immunoblotting with the indicated antibodies in SW480 HDAC2 RNAi cells. ** P < 0 .01; * P < 0.05. The data are representatives and are presented as mean ± standard error of the mean of 3 assays

    Journal: Journal of Experimental & Clinical Cancer Research : CR

    Article Title: HDAC2 inhibits EMT-mediated cancer metastasis by downregulating the long noncoding RNA H19 in colorectal cancer

    doi: 10.1186/s13046-020-01783-9

    Figure Lengend Snippet: Reduced HDAC2 induces EMT in CRC. a Altered mRNA expression in DLD1 HDAC2 KO cells. b , c Pathway analysis of changed genes in DLD1 HDAC2 KO cells (compared with DLD1 WT cells). d Merged mRNAs for EMT-related genes and those identified in our microarray. e , f Migration ability of DLD1 HDAC2 KO cells detected by transwell. g , k , l EMT markers were analyzed by immunoblotting and IF with the indicated antibodies in DLD1 HDAC2 WT and KO cells. h , i Migration ability of SW480 HDAC2 RNAi cells detected by transwell. j EMT markers were analyzed by immunoblotting with the indicated antibodies in SW480 HDAC2 RNAi cells. ** P < 0 .01; * P < 0.05. The data are representatives and are presented as mean ± standard error of the mean of 3 assays

    Article Snippet: Specific primary antibodies against HDAC2 (Cell Signaling Technology) were used for IHC with a 2-step protocol.

    Techniques: Expressing, Microarray, Migration, Western Blot

    Reduced HDAC2 induces EMT in CRC by upregulating H19. a Altered non-coding RNAs expression in DLD1 HDAC2 KO cells. b Expression of H19 in DLD1 HDAC2 KO cells. c Expression of H19 in CRC cells. d Expression of H19 in SW480 HDAC2 RNAi cells. e , f , g Migration ability of DLD1 HDAC2 KO H19 RNAi cells detected by transwell. h Detection of EMT markers by Western Blot in DLD1 HDAC2 KO H19 RNAi cells. i , j Migration ability of SW620 H19 RNAi cells detected by transwell. h Detection of EMT markers by Western Blot in SW620 H19 RNAi cells. ** P < 0 .01; * P < 0.05. The data are representatives and are presented as mean ± standard error of the mean of 3 assays

    Journal: Journal of Experimental & Clinical Cancer Research : CR

    Article Title: HDAC2 inhibits EMT-mediated cancer metastasis by downregulating the long noncoding RNA H19 in colorectal cancer

    doi: 10.1186/s13046-020-01783-9

    Figure Lengend Snippet: Reduced HDAC2 induces EMT in CRC by upregulating H19. a Altered non-coding RNAs expression in DLD1 HDAC2 KO cells. b Expression of H19 in DLD1 HDAC2 KO cells. c Expression of H19 in CRC cells. d Expression of H19 in SW480 HDAC2 RNAi cells. e , f , g Migration ability of DLD1 HDAC2 KO H19 RNAi cells detected by transwell. h Detection of EMT markers by Western Blot in DLD1 HDAC2 KO H19 RNAi cells. i , j Migration ability of SW620 H19 RNAi cells detected by transwell. h Detection of EMT markers by Western Blot in SW620 H19 RNAi cells. ** P < 0 .01; * P < 0.05. The data are representatives and are presented as mean ± standard error of the mean of 3 assays

    Article Snippet: Specific primary antibodies against HDAC2 (Cell Signaling Technology) were used for IHC with a 2-step protocol.

    Techniques: Expressing, Migration, Western Blot

    HDAC2 inhibits the expression of H19 by interacting with the transcription factor SP1 and catalyzing H3K27 deacetylation. a ChIP analysis of HDAC2 enrichment in the promoter of H19 gene in DLD1 WT or HDAC2 KO cells. b Detection of acetylated histone H2AK5, H2BK16 and H3K27 in DLD1 WT or HDAC2 KO cells. c ChIP analysis of acetylated histone H2AK5, H2BK16 and H3K27 enrichment in the promoter of H19 gene in DLD1 WT or HDAC2 KO cells. d A schematic of the H19 promoter-luciferase construct is depicted with the locations of the SP1 binding sites and the sequences of the point mutations. e , f Dual luciferase assay of 293 cells cotransfected with the H19 promoter reporter constructs (wild-type or mutants at three SP1 binding sites) and the shHDAC2 or HDAC2 plasmids. g Interaction between HDAC2 and SP1 displayed by Co-IP. h , i Expression of H19 in SP1 RNAi CRC cells. ** P < 0 .01; * P < 0.05. The data are representatives and are presented as mean ± standard error of the mean of 3 assays

    Journal: Journal of Experimental & Clinical Cancer Research : CR

    Article Title: HDAC2 inhibits EMT-mediated cancer metastasis by downregulating the long noncoding RNA H19 in colorectal cancer

    doi: 10.1186/s13046-020-01783-9

    Figure Lengend Snippet: HDAC2 inhibits the expression of H19 by interacting with the transcription factor SP1 and catalyzing H3K27 deacetylation. a ChIP analysis of HDAC2 enrichment in the promoter of H19 gene in DLD1 WT or HDAC2 KO cells. b Detection of acetylated histone H2AK5, H2BK16 and H3K27 in DLD1 WT or HDAC2 KO cells. c ChIP analysis of acetylated histone H2AK5, H2BK16 and H3K27 enrichment in the promoter of H19 gene in DLD1 WT or HDAC2 KO cells. d A schematic of the H19 promoter-luciferase construct is depicted with the locations of the SP1 binding sites and the sequences of the point mutations. e , f Dual luciferase assay of 293 cells cotransfected with the H19 promoter reporter constructs (wild-type or mutants at three SP1 binding sites) and the shHDAC2 or HDAC2 plasmids. g Interaction between HDAC2 and SP1 displayed by Co-IP. h , i Expression of H19 in SP1 RNAi CRC cells. ** P < 0 .01; * P < 0.05. The data are representatives and are presented as mean ± standard error of the mean of 3 assays

    Article Snippet: Specific primary antibodies against HDAC2 (Cell Signaling Technology) were used for IHC with a 2-step protocol.

    Techniques: Expressing, Luciferase, Construct, Binding Assay, Co-Immunoprecipitation Assay

    H19 promotes EMT by sponging miR-22 and upregulating MMP14. a Expression of MMPs in DLD1 HDAC2 KO cells. b , c Detection of MMP14 by Western blot. d , e Migration ability of DLD1 HDAC2 KO MMP14 RNAi cells detected by transwell. f Detection of EMT markers by Western blot in DLD1 HDAC2 KO MMP14 RNAi cells. g , h The correction between H19 and MMP14 expression in colorectal cancer samples. Data were collected from TCGA, including 471 cases of COAD and 167 cases of READ. i Expression of MMP14 in CRC cells. j Schematic diagrams of the mutual interactions between miRNA- 22-3P and H19. k Schematic diagrams of the mutual interactions between miRNA-22-3P and 3’UTR of MMP14. l , m The interactions between miRNA- 22-3P and H19 detected by anti-Ago2 RIP in DLD1 HDAC2 KO cells. n Expression of H19 in DLD1 HDAC2 KO cells transfected with miRNA- 22-3P mimincs. o , p Migration of DLD1 HDAC2 KO cells transfected with miRNA- 22-3P mimincs detected by transwell. q Detection of EMT markers and MMP14 by Western blot in DLD1 HDAC2 KO cells transfected with miRNA- 22-3P mimincs. ** P < 0 .01; * P < 0.05. The data are representatives and are presented as mean ± standard error of the mean of 3 assays

    Journal: Journal of Experimental & Clinical Cancer Research : CR

    Article Title: HDAC2 inhibits EMT-mediated cancer metastasis by downregulating the long noncoding RNA H19 in colorectal cancer

    doi: 10.1186/s13046-020-01783-9

    Figure Lengend Snippet: H19 promotes EMT by sponging miR-22 and upregulating MMP14. a Expression of MMPs in DLD1 HDAC2 KO cells. b , c Detection of MMP14 by Western blot. d , e Migration ability of DLD1 HDAC2 KO MMP14 RNAi cells detected by transwell. f Detection of EMT markers by Western blot in DLD1 HDAC2 KO MMP14 RNAi cells. g , h The correction between H19 and MMP14 expression in colorectal cancer samples. Data were collected from TCGA, including 471 cases of COAD and 167 cases of READ. i Expression of MMP14 in CRC cells. j Schematic diagrams of the mutual interactions between miRNA- 22-3P and H19. k Schematic diagrams of the mutual interactions between miRNA-22-3P and 3’UTR of MMP14. l , m The interactions between miRNA- 22-3P and H19 detected by anti-Ago2 RIP in DLD1 HDAC2 KO cells. n Expression of H19 in DLD1 HDAC2 KO cells transfected with miRNA- 22-3P mimincs. o , p Migration of DLD1 HDAC2 KO cells transfected with miRNA- 22-3P mimincs detected by transwell. q Detection of EMT markers and MMP14 by Western blot in DLD1 HDAC2 KO cells transfected with miRNA- 22-3P mimincs. ** P < 0 .01; * P < 0.05. The data are representatives and are presented as mean ± standard error of the mean of 3 assays

    Article Snippet: Specific primary antibodies against HDAC2 (Cell Signaling Technology) were used for IHC with a 2-step protocol.

    Techniques: Expressing, Western Blot, Migration, Transfection

    Low HDAC2 expression promotes colorectal cancer metastasis in vivo. a Metastatic tumors were detected and photographed by a bioluminescent in vivo imager, n = 6. b Hematoxylin and eosin-stained images of mouse lung tissues. c Photos of mice lungs gained from WT, KO and KO shH19 group. d The average number of metastatic nodules in the lungs. e The expression of H19 in metastatic lung nodules determined by FISH. f The expression of HDAC2, E-cadherin and MMP14 determined by IHC staining in metastatic nodules in the lungs. g Schematic depicting mechanism of HDAC2 regulating CRC metastasis. ** P < 0 .01; * P < 0.05. The data are presented as mean ± standard error of the mean

    Journal: Journal of Experimental & Clinical Cancer Research : CR

    Article Title: HDAC2 inhibits EMT-mediated cancer metastasis by downregulating the long noncoding RNA H19 in colorectal cancer

    doi: 10.1186/s13046-020-01783-9

    Figure Lengend Snippet: Low HDAC2 expression promotes colorectal cancer metastasis in vivo. a Metastatic tumors were detected and photographed by a bioluminescent in vivo imager, n = 6. b Hematoxylin and eosin-stained images of mouse lung tissues. c Photos of mice lungs gained from WT, KO and KO shH19 group. d The average number of metastatic nodules in the lungs. e The expression of H19 in metastatic lung nodules determined by FISH. f The expression of HDAC2, E-cadherin and MMP14 determined by IHC staining in metastatic nodules in the lungs. g Schematic depicting mechanism of HDAC2 regulating CRC metastasis. ** P < 0 .01; * P < 0.05. The data are presented as mean ± standard error of the mean

    Article Snippet: Specific primary antibodies against HDAC2 (Cell Signaling Technology) were used for IHC with a 2-step protocol.

    Techniques: Expressing, In Vivo, Staining, Immunohistochemistry

    KEY RESOURCES TABLE

    Journal: Cell chemical biology

    Article Title: A Cell-based Target Engagement Assay for the Identification of Cereblon E3 Ubiquitin Ligase Ligands and Their Application in HDAC6 Degraders

    doi: 10.1016/j.chembiol.2020.04.008

    Figure Lengend Snippet: KEY RESOURCES TABLE

    Article Snippet: Primary antibody against HDAC1, HDAC2, HDAC4, HDAC6, IKZF1, IKZF3 and GSPT1 were purchased from Cell Signaling Technology.

    Techniques: Recombinant, Software