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一站式表观遗传学服务，您只需要提供样本，我们交付给您完整的数据分析！我们提供ChIP-Seq、CUT&Tag、DNA甲基化测序、ATAC-Seq、基因表达、染色质结构mapping、IP-mass spec以及单细胞服务。
表观遗传学
用较少的起始样本获得高质量的组蛋白标记CUT&Tag结果。只需要提供细胞或组织样本，即可在数周内收到完整分析的数据。
Native mapping of transcription factors and histone marks with lower input than traditional ChIP.
Experience ultra-fast, high-throughput ChIP with up to 96 reactions, requiring as little as 300K-1M cells per sample.
Standalone
Custom bioinformatic analysis using data from our kits and services.
Universal and unbiased identification of CRISPR-Cas9 off-target activity.
Single-Cell
Mapping open chromatin, gene expression, or both, at the single-cell level.
Single-Cell ATAC-Seq (scATAC-Seq)
Single-Cell RNA-Seq (scRNA-Seq)
Single-Nucleus RNA-Seq (snRNA-Seq)
Single-Cell Multiome
质谱
客户评价
通过访问我们的客户评价页面，了解我们服务的客户的想法。
请求报价
要获取报价，请填写我们的表观遗传学服务咨询表。
表观遗传学技术服务发表文献列表
Sample Submission Portal
Our online sample submission portal allows you to easily upload your service project samples and track your project status. Follow the sample submission instructions in the portal to ensure that all your samples arrive at Active Motif in the best possible condition and properly associated with your project.
使用NGS进行全基因组分析，大大扩展了科学家了解表观遗传事件的能力。但是，从染色质免疫沉淀（ChIP）实验中可再现地生成高质量，可解释的数据具有挑战性，因为它需要工作抗体的先验知识，各种细胞类型的优化方案以及特定细胞类型特异性结合位点的知识。加上与生成全基因组数据集相关的技术和生物信息学挑战，ChIP-Seq可能确实超出了您的能力范围。这就是我们的表观遗传学服务团队提供各种ChIP服务的原因。这使您可以利用我们的专业知识和研究工具，而不必自己成为技术专家。
Active Motif 表观遗传学服务的目标是使更广泛的生命科学研究者能够进行前沿研究。十多年来，我们一直为最先进的技术提供服务，这些服务已帮助加速了学术实验室，政府机构，生物技术和制药公司科学家的研究。
经验–我们是唯一的一站式ChIP服务提供商
- 超过10年提供ChIP服务的经验
- 处理了超过15000个ChIP样本
- 处理了超过10000个ChIP-Seq反应
专业–不需要花数周的时间来优化每个步骤
- 针对350个靶标的抗体建议
- 针对超过15个物种及25类组织的染色质制备优化方法
- 为每个实验定制引物并测试
- 使用QC步骤来有效确保最终ChIP-Seq数据的高质量
合作互助–控制您的样本和数据
- 直接联系我们实验室的科学家
- 有关实验设计和适合对照的建议
- 包含问题排查
- 后续步骤的建议/帮助
生物信息学支持-回答重要的生物学问题
- 所有交付的数据均经过全面分析
- 以多种可视化格式和自定义Excel输出的数据
- 快速生成基因列表
- 我们所有服务的示例数据均可下载
我们众多的科研客户包括
我们众多的制药企业客户包括
引用我们表观遗传服务的制药企业客户发表文章
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.
