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Genomic analysis reveals HDAC1 regulates clinically relevant transcriptional programs in Pancreatic cancer

ABSTRACT: We performed ChIP-seq analysis on H3K27ac in MIA PaCa-2 cells with HDAC1 overexpression using the antibody Abcam H3K27ac (Abcam, ab4729), a non-targeting scrableled sgRNA control, and two replicates for each.

ORGANISM(S): Homo sapiens

PROVIDER: GSE209895 | GEO | 2023/05/31

REPOSITORIES: GEO

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H3K4me1 and H3K27ac ChIP-seq in Ring1a KO and Ring1a/b dKO mouse ES cells

Project description:H3K4me1 (ab8895 Abcam) and H3K27ac (ab4729 Abcam) antibodies were used for ChIP-seq in Ring1a-/- mouse ES cells and after 48h tamoxifen treatment in conditional knock-out of Ring1b in the Ring1a -/- background.

2015-08-01 | E-MTAB-3156 | biostudies-arrayexpress

Genome-wide maps of chromatin state in iBMDM (immortalized bone-marrow-derived macrophages) cells without or with virus infection.

Project description:iBMDM cells were infected with VSV (Vesicular Stomatitis Virus) or HSV-1 (Herpes Simplex Virus 1) for 8 hours, followed by CHIP-seq analysis with H3K27AC antibody (Abcam, ab4729). We find that chromatin state changed with virus infection, some enhacer and superenhancer were induced to promote anti-viral gene expression. Conclusions: virus infection induce enhancer and superenhancer activation.

2022-06-29 | GSE133784 | GEO

ChIP-chip of siGFP- or siHOTTIP-treated foreskin fibroblasts with anti-H3K4me3, anti-H3K27me3, anti-H3K4me2, anti-histone, anti-MLL1, and anti-WDR5 antibodies on HOX tiling array

Project description:Coordinate loss of MLL1 and WDR5 occupancy caused by HOTTIP knockdown were observed in distal HOXA genes. These regions correspondingly lost H3K4me3 and H3K4me2, without changes in pan-histone or H3K27me3. human foreskin fibroblasts (CRL2091), anti-H3K4me3 (Abcam ab8580, lot#1016899), anti-H3K4me2 (Abcam ab32356, lot#947550), anti-H3K27me3 (Abcam ab4729, lot#1021724), anti-histone H3 (Abcam ab1791, lot#1025144), anti-MLL1 (gift of R. Roeder, Rockefeller University), and anti-WDR5 (gift of W. Herr, UNIL)

2011-03-21 | GSE26540 | GEO

Histone modification profiling (using the iChIP protocol) for two markers of regulatory activity (H3K4me3, H3K27ac) from a panel of genetically diverse crosses of Drosophila melanogaster during embryogenesis

Project description:Profiling of histone modifications with the iChIP protocol (PMID25103404) using antibodies against two markers of regulatory activity: H3K27ac (abcam, ab4729) and H3K4me3 (Millipore, 07-473). All paternal fly lines were taken from the Drosophila Genetic Reference Panel crossed to a common mother (PMID31308546). Data were collected at three time points (2-4h, 6-8h, 10-12h at 25C) with two biological replicates per collection.

2020-12-04 | E-MTAB-8880 | biostudies-arrayexpress

CUT&Tag analysis of H3K4me3, H3K27Ac,H2A119Ub and H3K27me3 in treated KPC1199 murine PDAC cell line

Project description:To gain mechanistic insight into how Epigenetic factors reprogramming tumor immune microenvironment in response to IFNγ stimulation. we performed CUT&Tag sequencing in murine PDAC cells.For comparison of the transcription profile between IFNγ-PD-L1all and IFNγ+PD-L1all cells, we treated KPC1199 cells with vehicle control or 10 ng/mL recombinant mouse IFNγ for 20 hours and harvested them. For comparison of PD-L1hi with PD-L1all, cells were either sorted with the top 15% PD-L1+ or total of IFNγ+PD-L1all PDAC cells, and freshly collected as soon as possible. Hyperactive pA-Tn5 Transposase for CUT&Tag kit from Vazyme (TD901), and antibodies against H3K4me3 from Abcam (ab213224), H3K27Ac from Abcam (ab4729),H2A119Ub from Cell Signaling (8240T) and H3K27me3 from Abcam (ab6002) were employed. Trueprep index kit v2 and v3 for illumina were used to establish DNA library.

2024-08-20 | GSE222133 | GEO

siRNA knockdown of C1GALT1 in MIA PaCa-2 cells

Project description:To determine the C1GALT1 regulated gene expression profile in MIA PaCa-2 cells.

2017-12-04 | GSE90668 | GEO

RNA expression analysis after Mia PaCa 2 cell treatment with demethylating agent 5-Aza-2’-deoxycitidine (5-Aza)

Project description:Transcriptional profiling of Mia PaCa 2 cells treated with 5-Aza for 96 h. Relative abundance to untreated control cells was used to estimate the effect of DNA demethylation on the expression of the RNAs. Two-condition experiment, 5-Aza-treated vs. untretated Mia PaCa 2 cells. Biological replicates: 2. Technical replicates: 2.

2015-06-30 | E-GEOD-62959 | biostudies-arrayexpress

RNA Sequencing Facilitates Quantitative Analysis of LINC00901 overexpression and Control MIA PaCa-2 Cell Transcriptomes

Project description:RNA Sequencing Facilitates Quantitative Analysis of LINC00901 overexpression and Control MIA PaCa-2 Cell Transcriptomes

2022-05-01 | GSE169660 | GEO

Human PDAC Cells: scramble Control vs. RINT shRNA downregulated

Project description:Time resolved transcriptional profiling of scramble and RINT1 down-regulated MIA PaCa-2 PDAC cells

2024-01-01 | GSE165629 | GEO

HDAC1/2 is indispensable for mouse and bovine ZGA via regulating distribution of H3K27ac and H3K4me3 [ChIP-seq]

Project description:Zygotic genome activation (ZGA) is an impressed biological event following fertilization during early embryo development. Precise reprogramming of epigenetic modifications (e.g. histone H3 lysine 27 acetylation, H3K27ac) have been found contribute to safeguard ZGA in zebrafish and Drosophila, but the dynamic of H3K27ac and the underlying regulation mechanism in mammal embryos are still enigmatic yet. As the main erasers for histone acetylation, histone deacetylase 1 and 2 (HDAC1 and HDAC2) are reported essential for mouse oogenesis and embryo lineage development, while it is unclear if they are functional for ZGA. Here, we observed significant global decrease of H3K27ac during ZGA in both mouse and bovine embryos, and accumulation of HDAC1/2 is responsible for the decline of H3K27ac. Repression of HDAC1/2 by dominant negative mutation led to arrested development at late 2-cell stage in mouse embryos, accompanied by downregulation of genes supposed to be expressed during ZGA. ChIP-seq revealed abnormal distribution of H3K27ac, and DUX participates in H3K27ac aberrant hyper-acetylation in embryos overexpressed mutant HDAC1/2. Moreover, suppression of HDAC1/2 also restrains H3K4me3 removal at gene body regions via impeding expression of KDM5s during mouse ZGA, and compensatory exogenous Kdm5b mRNA can fix the exceeding H3K4me3 and failed ZGA. Intriguingly, function of HDAC1/2 seems to be conservative between mouse and bovine embryos. Together, this study reveals that HDAC1/2 is indispensable for mouse and bovine ZGA via regulating distribution of H3K27ac and H3K4me3.

2022-05-21 | GSE182554 | GEO

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