H3k27ac 8173

Manufactured by Cell Signaling Technology

Sourced in United States

H3K27ac (8173S) is an antibody product offered by Cell Signaling Technology. It is designed to detect acetylation of lysine 27 on histone H3 protein. This modification is associated with active gene transcription.

Automatically generated - may contain errors

Lab products found in correlation

Novaseq 6000, by Illumina (3 mentions) H3k27me3 9733s, by Cell Signaling Technology (2 mentions) H3k4me3 ab1012, by Abcam (2 mentions) Alizarin red s, by Merck Group (2 mentions) H3k4me1, by Merck Group (1 mentions) Cleaved notch1 val1744, by Cell Signaling Technology (1 mentions) Bcip nbt liquid substrate system, by Merck Group (1 mentions) Complete protease cocktail, by Roche (1 mentions) Antibodies against gapdh, by Merck Group (1 mentions) Doxycycline, by Selleck Chemicals (1 mentions) Cd44 15675 1 ap, by Proteintech (1 mentions) Aldh1a1 sirna, by Santa Cruz Biotechnology (1 mentions) Bay11 7082, by Merck Group (1 mentions) Bcip nbt liquid substrate, by Merck Group (1 mentions) Anti akt 4685, by Cell Signaling Technology (1 mentions) Ly294002 l9908, by Merck Group (1 mentions)

Spelling variants of this product

H3K27ac (74 citations)

7 protocols using h3k27ac 8173

ChIP-seq Analysis for Histone Modifications

Cited 5 times

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ChIP-seq was performed using ChIPmentation (19 (link)) with the following antibodies: H3K27me3 (9733S),
and H3K27ac (8173S) from Cell Signaling Technology, and H3K4me1 (ab1012) from
Abcam. Sequencing was performed on a NovaSeq 6000 (Illumina, San Diego, CA) to
obtain ~50 million 2×150 bp reads. Data were analyzed via adapter
trimming with trimgalore and alignment to GRCh38 using bwamem (20 ). Normalized coverage for visualization and
analysis used the deeptools “bamCoverage” tool (21 (link)), and peaks were called with MACS2 (22 (link)). Statistical comparisons with DESeq2
(23 (link)) used raw fragment counts at peak
summits, and visualizations were prepared with Gviz (24 ). Superenhancer analysis was conducted using ROSE
software (25 (link),26 (link)) with default parameters.

Wilson E.R., Helton N.M., Heath S.E., Fulton R.S., Payton J.E., Welch J.S., Walter M.J., Westervelt P., DiPersio J.F., Link D.C., Miller C.A., Ley T.J, & Spencer D.H. (2021). Focal disruption of DNA methylation dynamics at enhancers in IDH-mutant AML cells. Leukemia, 36(4), 935-945.

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ChIP-seq analysis of epigenomic marks

Cited 3 times

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ChIP-seq was performed using ChIPmentation [13 (link)] with the following antibodies: CTCF (2899S), H3K27me3 (9733S), and H3K27ac (8173S) from Cell Signaling Technology and H3K4me3 (ab1012) from Abcam. Sequencing was performed on a NovaSeq 6000 (Illumina, San Diego, CA) to obtain ~50 million 150 bp paired-end reads. Data were analyzed via adapter trimming with trimgalore and alignment to GRCh38 using bwa mem [14 ]. Normalized coverage for visualization and analysis used the deeptools “bamCoverage” tool [15 (link)], and peaks were called with macs2 [16 (link)] for CTCF and epic2 [17 (link)] for histone marks. Statistical comparisons with DESeq2 [18 (link)] used raw fragment counts at peak summits, and visualizations were prepared with Gviz [19 (link)].

Ghasemi R., Struthers H., Wilson E.R, & Spencer D.H. (2020). Contribution of CTCF binding to transcriptional activity at the HOXA locus in NPM1-mutant AML cells. Leukemia, 35(2), 404-416.

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ChIPmentation: Comprehensive Epigenomic Profiling

Cited 3 times

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ChIP-seq was performed using ChIPmentation (12 (link)) with the following antibodies: CTCF (2899S), H3K27me3 (9733S), and H3K27ac (8173S) from Cell Signaling Technology and H3K4me3 (ab1012) from Abcam. Sequencing was performed on a NovaSeq 6000 (Illumina, San Diego, CA) to obtain ~50 million 150 bp paired-end reads. Data were analyzed via adapter trimming with trimgalore and alignment to GRCh38 using bwa mem (13 ). Normalized coverage for visualization and analysis used the deeptools ‘bamCoverage’ tool (14 (link)), and peaks were called with macs2 (15 (link)) for CTCF and epic2 (16 (link)) for histone marks. Statistical comparisons with DESeq2 (17 (link)) used raw fragment counts at peak summits and visualizations were prepared with Gviz (18 ).

Ghasemi R., Struthers H., Wilson E.R, & Spencer D.H. (2020). Contribution of CTCF binding to transcriptional activity at the HOXA locus in NPM1-mutant AML cells. Leukemia, 35(2), 404-416.

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Western Blot and ChIP-seq Antibodies

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Western blots were performed using the following antibodies: Actin and CTCF from Millipore Sigma (clone C4; 07–729) and cleaved NOTCH1 (Val1744) from Cell Signaling Technology (4147). ChIP-seq were performed using the following antibodies: CTCF from Millipore Sigma (07-729), H3K27Ac (8173S), and H3K27me3 (9733S) from Cell Signaling Technology, and H3K4me1 (07-473) from Millipore.

Fang C., Wang Z., Han C., Safgren S.L., Helmin K.A., Adelman E.R., Serafin V., Basso G., Eagen K.P., Gaspar-Maia A., Figueroa M.E., Singer B.D., Ratan A., Ntziachristos P, & Zang C. (2020). Cancer-specific CTCF binding facilitates oncogenic transcriptional dysregulation. Genome Biology, 21, 247.

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Osteogenic Differentiation Pathway Regulation

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Anti‐Histone 3 (#17168‐1‐AP) antibody was purchased from Proteintech Group Inc, anti‐p300 (#ab10485) antibody was from Abcam, and anti‐JNK (#9252) and anti‐phospho‐JNK (#4668), anti‐c‐Jun (#9165), anti‐phospho‐c‐Jun (#3270), anti‐RUNX2 (#12556) and H3K27ac (#8173) antibodies were obtained from Cell Signaling Technology. The osteogenic differentiation medium (#SCM121), chemical reagent Bay 11‐7082 (#B5556), Alizarin Red S (#A5533) and BCIP/NBT liquid substrate system (#B1911) were all purchased from Sigma.

Fu L., Peng S., Wu W., Ouyang Y., Tan D, & Fu X. (2019). LncRNA HOTAIRM1 promotes osteogenesis by controlling JNK/AP‐1 signalling‐mediated RUNX2 expression. Journal of Cellular and Molecular Medicine, 23(11), 7517-7524.

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Stemness Targeting Compounds Evaluation

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Antibodies against KLF4 (sc‐166238), DACH1 (sc‐398706), ABCB5 (sc‐517210), and SOX2 (sc‐365823) were purchased from Santa Cruz Biotechnology (CA, USA). Antibodies against ALDH1A1 (36671S), pan AKT (4685S), AKT pT308 (13038S), EGFR (4267S), EGFR pY1068 (3777S), Ki‐67 (9449S), RARα (62294), and H3K27ac (8173) were purchased from Cell Signaling Technology (MA, USA). Antibodies against CD133 (18470‐1‐AP) and CD44 (15675‐1‐AP) were purchased from Proteintech (Wuhan, China). Antibodies against GAPDH were purchased from Sigma–Aldrich (Shanghai, China). The antibody against ERK1/2 pT202/Y304 (AF1015) was purchased from Affinity Biosciences (Jiangsu, China). The antibody against MERTK (AF1015) was purchased from Thermo Fisher Scientific (MA, USA). DACH1 siRNA (sc‐77089), ABCB5 siRNA (sc‐89856), MERTK siRNA (sc‐37127), KLF4 siRNA (sc‐35480), SOX2 siRNA (sc‐38408), EGF siRNA (sc‐39416), and ALDH1A1 siRNA (sc‐41442) were purchased from Santa Cruz Biotechnology (CA, USA). K₂Cr₂O₇ (207802), 2‐hydroxyethyl agarose (A9045), NAC (A7250), DCFH‐DA (287810), A37 (531726000), Tyrphostin AG 1478 (T4182), RA (R2625), and 3dGRO Basal Medium (S3077A) were purchased from Sigma–Aldrich (MA, USA). Complete Protease Cocktail was purchased from Roche. Doxycycline was purchased from Selleckchem (MA, USA).

Ge X., Li M., Song G., Zhang Z., Yin J., Ge Z., Shi Z., Liu L., Jiang B., Qian X, & Shen H. (2022). Chromium (VI)‐induced ALDH1A1/EGF axis promotes lung cancer progression. Clinical and Translational Medicine, 12(12), e1136.

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Investigating Osteogenic Differentiation Regulators

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Anti‐IκBα (#10268‐1‐AP), anti‐HDAC2 (#12922‐3‐AP) and anti‐HDAC3 (#10255‐1‐AP) antibodies were purchased from Proteintech Group Inc, and anti‐AKT (#4685) and anti‐phospho‐AKT (#4060), anti‐GAPDH (#5174), anti‐RUNX2 (#12556) and H3K27ac (#8173) antibodies were obtained from Cell Signaling Technology (Beverly, MA, USA). The chemical reagents Bay 11‐7082 (#B5556), LY294002 (L9908), Alizarin Red S (#A5533), BCIP/NBT liquid substrate (#B1911) and the commercial osteogenic medium (#SCM121) were all from Sigma.

Zhang Y., Cao X., Li P., Fan Y., Zhang L., Ma X., Sun R., Liu Y, & Li W. (2019). LncRNA NKILA integrates RXFP1/AKT and NF‐κB signalling to regulate osteogenesis of mesenchymal stem cells. Journal of Cellular and Molecular Medicine, 24(1), 521-529.

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