Titlebook: HDAC/HAT Function Assessment and Inhibitor Development; Methods and Protocol Oliver H. Krämer Book 2017 Springer Science+Business Media New

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Using Histone Deacetylase Inhibitors to Analyze the Relevance of HDACs for Translationmerous disease states, including cancer, where the upregulation of HDAC family members leads to dysregulation of genes and proteins involved in cell proliferation, cell cycle regulation, and apoptosis. These observations have pushed HDAC inhibitors (HDACi) to the forefront of therapeutic development

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https://doi.org/10.1007/978-3-319-26896-5and the response to chemotherapy. Here we describe how autophagy can be monitored in living cells by flow cytometry using the cationic amphiphilic tracer dye Cyto-ID. Green. The detection of autophagy induction in the human leukemia cell line K562 after the treatment with the HDAC class I inhibitor

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https://doi.org/10.1007/978-3-030-53544-5lation and methylation, regulate their structure and control gene expression. Histone acetyltransferases (HATs) acetylate lysine residues in histones while histone deacetylases (HDACs) remove this modification. HDAC inhibitors (HDACi) can alter gene expression patterns and induce cytotoxicity in can

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https://doi.org/10.1007/978-3-030-68253-8nisms. In diseases such as cancer deregulated cell migration represents a major problem. Therefore, numerous efforts are under way to understand the molecular mechanisms of tumor cell migration and to generate more efficient tumor therapies. Cell migration assays are one of the most commonly used fu

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The Future of Liberal Democracycetylases (HDAC). HAT activity results in the addition of acetyl groups on the lysine residues of histone tails leading to decondensation of the chromatin, and increased gene transcription in general, whereas HDACs remove these acetyl groups, thus leading to an overall suppression of gene transcript

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https://doi.org/10.1007/978-3-8349-9764-7 provides information on the DNA replication progress and its regulation under normal conditions as well as on replication stress induced by environmental genotoxic agents or cancer drugs. The method relies on the detection of incorporated thymidine analogues during DNA synthesis in the S phase of t