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アクティブ・モティフの受託サービスを利用したお客様のご意見は
こちら＞＞customer testimonials
お見積り依頼
各種サービスへのご質問、お見積りは
こちら ＞＞ Epigenetic Services Information Request.
日本語での対応はこちら＞＞ japantech@activemotif.com
受託サービスを利用した文献
- How We Can Help
- なぜアクティブ・モティフのエピジェネティクス受託サービスを選択するのか？
- Academic Customers
- Pharma Customers
- Pharma Publications
Genome-wide analysis using Next-Gen sequencing has significantly broadened the ability of scientists to understand epigenetic events. However, reproducibly generating high-quality, interpretable data from chromatin immunoprecipitation (ChIP) experiments can be challenging as it requires prior knowledge of working antibodies, optimized protocols for various cell types and knowledge of cell type-specific binding sites. Add in the technical and bioinformatics challenges associated with generating whole-genome data sets, and ChIP-Seq may literally be beyond your reach. That’s why our Epigenetic Services team provides a wide variety of ChIP services. This makes it possible for you to utilize our expertise and research tools without having to be an expert in the techniques yourself.
アクティブ・モティフ社が提供するエピジェネティクス受託サービスのゴールは，最先端研究をより広い生命科学コミュニティで利用していただくことです。 10年以上の間，弊社はエピジェネティクス受託サービスをアカデミックな研究所，官公庁，バイオテクノロジーおよび製薬会社での研究を促進するために，高水準の技術を提供してきました。
経験 – 唯一のトータルChIPサービスプロバイダー
- 10 年以上 ChIP受託サービスを提供
- 10,000以上のChIP試料を処理した実績
- 4,000以上のChIP-on-chip タイリングアレイを処理
- 3,000以上のChIP-Seq の実績
専門知識 – 各ステップの最適化に時間を浪費する必要はありません
- 250種以上の推奨抗体
- 10種および25以上の組織タイプに最適化されたクロマチン調製プロトコール
- 各アッセイのためのカスタムプライマー設計とテスト
- 効率的な品質確認ステップによる確実な高品質ChIP-Seqデータ
連携交流 – 試料とデータの制御
- 弊社米国研究スタッフと直接のコミュニケーションが可能
- 実験デザインおよび適切なコントロールの推奨
- 次の実験ステップへの提案および助言
バイオインフォマティクス支援 – 重要な生物学的質問に対応
- アッセイデータを十分に解析して納品
- ピークコーリングを含むChIP-Seqデータ解析
- Data ビジュアルフォーマットおよびExcel出力によるデータ納品
- 遺伝子リスト生成
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Some of our customers in the Pharmaceutical industry include ... |
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Pharmaceutical customer publications referencing our Epigenetic Services
Epizyme
- EZH2 inhibition by tazemetostat results in altered dependency on B-cell activation signaling in DLBCL. Brach et al. 2017. Mol Cancer Ther. doi: 10.1158/1535-7163.MCT-16-0840.
- Selective Inhibition of EZH2 by EPZ-6438 Leads to Potent Antitumor Activity in EZH2-Mutant Non-Hodgkin Lymphoma. Knutson, K. et al. 2017. Mol Cancer Ther. DOI: 10.1158/1535-7163.MCT-13-0773.
Genentech
- Therapeutic targeting of the CBP/p300 bromodomain blocks the growth of castration-resistant prostate cancer. Lingyan, Jin et al. 2017. Cancer Res. doi: 10.1158/0008-5472.CAN-17-0314.
- Repression of stress-induced LINE-1 expression protects cancer cell subpopulations from lethal drug exposure. Gulfem, Dilek Guler et al. 2017. Cancer Cell. DOI: https://doi.org/10.1016/j.ccell.2017.07.002.
- Transcription factor Etv5 is essential for the maintenance of alveolar type II cells. Zhang, Z. et al. 2017. Proc Natl Acad Sci. 114 (15) 3903-3908. doi.org/10.1073/pnas.1621177114.
- An alternative approach to ChIP-Seq normalization enables detection of genome- wide changes in histone H3 lysine 27 trimethylation upon EZH2 inhibition. Egan, B. et al. 2016. PLoS One. doi.org/10.1371/journal.pone.0166438.
- CCAT1 is an enhancer-templated RNA that predicts BET sensitivity in colorectal cancer. McCleland, M.L. et al. 2016. J Clin Invest. doi: 10.1158/0008-5472.CAN-17-0314.
- Loss of NAPRT1 expression by tumor-specific promoter methylation provides a novel predictive biomarker for NAMPT inhibitors. Shames, D.S. et al. 2013. Clin Cancer Res. DOI: 10.1158/1078-0432.CCR-13-1186.
- Specification of type 2 innate lymphocytes by the transcriptional determinant Gfi1. Spooner, C.J et al. 2013. Nat Immunol. doi:10.1038/ni.2743.
- Loss of the tumor suppressor BAP1 causes myeloid transformation. Gulfem, Dilek Guler et al. 2012. Science. 337: 1541. DOI: 10.1126/science.1221711.
GSK
- EZH2 inhibition as a therapeutic strategy for lymphoma with EZH2-activating mutations. McCabe, M. et al. 2012. Nature. 492, pages 108–112. doi:10.1038/nature11606.
BMS
- Sensitivity of small cell lung cancer to BET inhibition is mediated by regulation of ASCL1 gene expression. Lenhard, R. et al. 2015. Mol Cancer Ther. 14: 2167. DOI: 10.1158/1535-7163.MCT-15-0037.
Pfizer
- IRAK4 kinase activity controls Toll-like receptor–induced inflammation through the transcription factor IRF5 in primary human monocytes. Cushing, L. et al (2017) J Biol Chem. doi:10.1074/jbc. M117.796912.
- Reciprocal regulation of amino acid import and epigenetic state through Lat1 and EZH2. Dann, S.G. et al. 2017. EMBO. DOI 10.15252/embj.201488166.
Mirati
- The class I/IV HDAC inhibitor mocetinostat increases tumor antigen presentation, decreases immune suppressive cell types and augments checkpoint inhibitor therapy. Briere, D. et al. 2017. Cancer Immunology, Immunotherapy. DOI: 10.1007/s00262-017-2091-y.
