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P histone h3 ser10

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P-Histone H3 (Ser10) is a primary antibody that specifically recognizes histone H3 phosphorylated at serine 10. Histone H3 phosphorylation at serine 10 is a well-characterized epigenetic modification associated with various cellular processes, including chromosome condensation and transcriptional regulation.

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Lab products found in correlation

β actin, by Cell Signaling Technology (2 mentions) Bx60 microscope, by Olympus (2 mentions) Cleaved parp, by Cell Signaling Technology (2 mentions) P akt, by Cell Signaling Technology (1 mentions) Anti mouse igg hrp, by Cell Signaling Technology (1 mentions) Fetal bovine serum (fbs), by Thermo Fisher Scientific (1 mentions) Sodium dodecyl sulfate (sds), by Merck Group (1 mentions) Dimethyl sulfoxide (dmso), by Merck Group (1 mentions) Sodium chloride (nacl), by Merck Group (1 mentions) Cell culture media, by Thermo Fisher Scientific (1 mentions) Tris base, by Merck Group (1 mentions) Anti rabbit igg hrp, by Cell Signaling Technology (1 mentions) Ubiquitin, by Cell Signaling Technology (1 mentions) Donkey anti rabbit igg h l alexa fluor 488 ab150073, by Abcam (1 mentions) Colchicine, by Merck Group (1 mentions) Sorbitol, by Merck Group (1 mentions) Hydroxyurea, by Merck Group (1 mentions) Leptomycin b, by Merck Group (1 mentions) Rpa32, by Abcam (1 mentions) Nup153, by Abcam (1 mentions)

Spelling variants of this product

Histone H3 (504 citations) P-Histone H3 (25 citations) Anti-p-Histone H3-ser10 (7 citations)

8 protocols using p histone h3 ser10

1

Comprehensive Antibody Characterization Protocol

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Chemical reagents, such as DMSO, NaCl, SDS, and Tris base for buffer preparation were obtained from Sigma-Aldrich (St. Louis, MO). The FBS, cell culture media, and antibiotics were purchased from Invitrogen (Grand Island, NY). Antibodies against Skp2 (#2652, IB:1:2000, IHC: 1:100), HK1 (#2024, IB: 1:2000), HK2 (#2867, IB: 1:2000, IHC:1:200), p-Akt (#4060, IB: 1:1000), Akt (#4691, IB: 1:2000), p-S6 (#4858, IB: 1:4000), p-Histone H3 (Ser10) (#53348, IF: 1:200), ubiquitin (#3936, IB: 1:1000), β-actin (#4970, IB: 1:5000), p27 (#3686, IB: 1:1000), anti-rabbit IgG HRP (#7074), and anti-mouse IgG HRP (#7076) were obtained from Cell Signaling Technology, Inc. (Beverly, MA). HK2 (LS‑C404653) antibody for IHC staining was obtained from LifeSpan BioSciences, Inc. Antibodies against Ki67 (ab16667, IHC: 1: 250) and donkey anti-rabbit IgG H&L (Alexa Fluor® 488) (ab150073, IF: 1:800) were purchased from Abcam (Cambridge, UK).
Zhou L., Yu X., Li M., Gong G., Liu W., Li T., Zuo H., Li W., Gao F, & Liu H. (2019). Cdh1-mediated Skp2 degradation by dioscin reprogrammes aerobic glycolysis and inhibits colorectal cancer cells growth. EBioMedicine, 51, 102570.
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2

Comprehensive DNA Damage Response Assay

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ATR, p-CHK1 (S345), RPA70, and p-histone H3 (Ser10) antibodies were obtained from Cell Signaling; ATRIP, NUP153, and RPA32 were obtained from Abcam; TPR, γH2AX (S139), and lamin A Abs were obtained from Sigma and Millipore; and Chk1 was obtained from Leica. EdU (click-IT), RPA70-, TopBP1-, and RAD17-small hairpin RNAs (shRNAs) were obtained from Invitrogen and Origene Technologies, respectively. ATR-specific inhibitor and ATR shRNA were from Dr. Oscar Capetillo (Centro Nacional de Oncologia [CNIO]) (Toledo et al., 2011 (link)); the GFP-ATR plasmid was from Dr. Randal Tibbetts (Tibbetts et al., 2000 (link)); RFP-Lamin was from Prof. Howard J. Worman (Columbia University) (Ostlund et al., 2006 (link)); and RFP-Nucleophosmin was a gift by Dr. Michelle Hill (University of Queensland). GFP-H2B and m-cherry-H2B were from IFOM. Colchicine, α-tubulin Ab, Leptomycin B, Hydroxy Urea, sorbitol, Aphidicholine, and R3306 CDK1-specific inhibitor were obtained from Sigma.
Kumar A., Mazzanti M., Mistrik M., Kosar M., Beznoussenko G.V., Mironov A.A., Garrè M., Parazzoli D., Shivashankar G.V., Scita G., Bartek J, & Foiani M. (2014). ATR Mediates a Checkpoint at the Nuclear Envelope in Response to Mechanical Stress. Cell, 158(3), 633-646.
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3

Quantitative Analysis of Angiogenesis, Proliferation, and Apoptosis

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IHC was performed according to a previously described protocol [64 (link)]. The slides were stained with antibodies against CD31 (Cell Signaling Technology, Beverly, MA, USA, #77699), p-histone H3 Ser10 (Cell Signaling Technology, Beverly, MA, USA, #9701), and cleaved PARP (Cell Signaling Technology, Beverly, MA, USA, #5625) to assess the microvessel density, cell proliferation, and apoptosis, respectively. At least 10 fields were randomly captured at a magnification of 100× on each IHC-stained slide using an Olympus BX60 microscope (Olympus, Tokyo, Japan). To quantify the mean of the microvessel density, the p-histone H3 Ser10, and the cleaved PARP cells, all the positively stained cells in the captured images were counted and expressed as a percentage value compared with the total number of cells in that region.
Ng W.H., Soo K.C, & Huynh H. (2024). Vinorelbine Improves the Efficacy of Sorafenib against Hepatocellular Carcinoma: A Promising Therapeutic Approach. International Journal of Molecular Sciences, 25(3), 1563.
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4

Quantifying Tumor Microenvironment Markers

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IHC was performed according to a previously described protocol [62 (link)]. The slides were stained with antibodies against CD31 (Cell Signaling Technology, #77699); p-histone H3 Ser10 (Cell Signaling Technology, #9701); and cleaved PARP (Cell Signaling Technology, #5625) to assess the microvessel density, cell proliferation, and apoptosis, respectively. At least 10 fields were randomly captured at a magnification of 100× on each IHC-stained slide using an Olympus BX60 microscope (Olympus, Tokyo, Japan). To quantify the mean of the microvessel density, the p-histone H3 Ser10, and the cleaved PARP cells, all the positively stained cells in the captured images were counted and expressed as a percentage value compared with the total number of cells in that region.
Huynh H., Ng W.H, & Soo K.C. (2023). Everolimus Acts in Synergy with Vinorelbine to Suppress the Growth of Hepatocellular Carcinoma. International Journal of Molecular Sciences, 25(1), 17.
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5

Nuclear Fractionation and Immunoblotting

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The cultured cells were lysed and kidney tissues homogenized in radioimmunoprecipitation assay buffer containing protease inhibitors. Nuclear fractions were prepared with the NE-PER kit (Thermo Scientific, Rockford, Illinois, USA) according to the manufacturer's instruction. Protein samples were processed for immunoblot analysis as previously described [40 (link)]. The antibodies against Nrf2 and lipocalin-2 were purchased from Abcam, those against GSK3β, p-GSK3β (S9), β-Tubulin and p-Histone H3 (Ser10) were purchased from Cell Signaling Technology, and those against HO-1, nitrotyrosine and histone H3 were acquired from Santa Cruz Biotechnology.
Lu M., Wang P., Qiao Y., Jiang C., Ge Y., Flickinger B., Malhotra D.K., Dworkin L.D., Liu Z, & Gong R. (2019). GSK3β-mediated Keap1-independent regulation of Nrf2 antioxidant response: A molecular rheostat of acute kidney injury to chronic kidney disease transition. Redox Biology, 26, 101275.
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6

Multiplex Immunoblotting of Cell Signaling

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Primary Abs against PLK1, PLK2, PLK3, cleaved caspase‐3, p‐Histone H3 (Ser10), PCNA, and β‐actin were acquired from Cell Signaling Technology. Alpha‐tubulin Ab was purchased from Sigma.
Lin S., Yeh C., Huang Y., Chou T, & Wong R.J. (2021). Therapeutic inhibition of polo‐like kinases in anaplastic thyroid cancer. Cancer Science, 112(2), 803-814.
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7

Molecular Mechanism of Vemurafenib Response

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Vemurafenib was purchased from ChemieTek. Sunitinib, imatinib, crenolanib and LDE225 were purchased from Selleck Chemicals LLC. MTT was purchased from Sigma. p-AKT (Ser473)-, AKT-, p-PI3K p85 (γ458)-, p-CRAF(S289/296/301)-, p-MEK 1/2 (S217/221)-, p-ERK 1/2 (Thr202/Tyr204)-, ERK1/2-, PDFGRβ-, p-PDGFRα-, PDGFRα-, PTEN-, VEGFR2-, Cleaved Caspase-3 (Asp175)-, p-Histone H3 (Ser10)-, Gli1- and β-actin-specific monoclonal antibodies (mAbs) were purchased from Cell Signaling Technology. The calnexin-specific mAb TO-5 was developed and characterized as described [55 (link)]. PDGFRα-specific shRNA and GFP-shRNA were provided by the- Vector Core Facility of the University of Pittsburgh Cancer Institute.
Sabbatino F., Wang Y., Wang X., Flaherty K.T., Yu L., Pepin D., Scognamiglio G., Pepe S., Kirkwood J.M., Cooper Z.A., Frederick D.T., Wargo J.A., Ferrone S, & Ferrone C.R. (2014). PDGFRα up-regulation mediated by sonic hedgehog pathway activation leads to BRAF inhibitor resistance in melanoma cells with BRAF mutation. Oncotarget, 5(7), 1926-1941.
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8

Antibody Validation for Cell Cycle Analysis

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All primary monoclonal antibodies (mAb) were purchased from commercial vendors: pS343-Nbs1 (rabbit mAb, Abcam), γH2AX (mouse mAb, Millipore), and Rad51 (rabbit mAb, Epitomics; mouse mAb, Novus Biologicals). Certificates of Analysis were provided for all antibodies. Antibodies were custom-conjugated to fluorescent dyes or haptens: anti-γH2AX-biotin (Millipore), anti-γH2AX to Alexa Fluor 790, anti-pS343-Nbs1 to Digoxigenin (DIG) and anti-Rad51 to Dinitrophenol (DNP) (Molecular Probes, Inc.). New and previously qualified lots of antibodies were compared side-by-side. Validation details can be found in the Supplemental Methods and Supplemental Figs. S1 and S2, and in LoRusso, et al. for pS343-Nbs1 (6 (link)). Cell cycle and apoptosis antibodies used were: p21 Waf1/Cip1 (12D1), cyclin B1 (D5C10), p-histone H3-Ser 10 (rabbit mAb, Cell Signaling Technologies, Danvers, MA), cyclin B1-Alexa-647 (rabbit mAb, [EPR17060] Abcam), geminin (mouse mAb, Abcam), and cleaved caspase-3 rabbit antibody (R&D Systems).
Wilsker D.F., Barrett A.M., Dull A.B., Lawrence S.M., Hollingshead M., Chen A.P., Kummar S., Parchment R.E., Doroshow J.H, & Kinders R.J. (2019). Evaluation of pharmacodynamic responses to cancer therapeutic agents using DNA damage markers. Clinical cancer research : an official journal of the American Association for Cancer Research, 25(10), 3084-3095.
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