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CUT&RUN: A New Way to Analyze Epigenetic Marks and Mechanisms


C​leavage ​U​nder ​T​argets ​&​ ​R​elease ​U​sing ​N​uclease (CUT&RUN) is a new technology that can be used to explore protein-DNA-interactions. Current techniques used to map protein-DNA interactions have certain limitations. Cell Signaling Technology​ ​ (CST) offers a ​CUT&RUN​ assay that overcomes many of the challenges faced with other whole-genome mapping techniques. To learn more, visit the CUT&RUN webpage.

Watch this webinar recording to:

  • Discover the difference between CUT&RUN and ChIP
  • Learn how CUT&RUN is compatible with low cell numbers and reduces background when analyzing protein-DNA interactions
  • Hear first-hand how Paul Marie from the LBMC, France, has incorporated CUT&RUN into his research around NF-κB pathway activation

Featured speaker

Francesco Pinto, PhD

Field Application Scientist

Cell Signaling Technology

Like the chromatin immunoprecipitation (ChIP) assay, Cleavage Under Targets & Release Using Nuclease (CUT&RUN) is a powerful and versatile technique used for probing protein-DNA interactions within the natural chromatin context of the cell. The CUT&RUN assay can be combined with downstream qPCR or NG-seq to analyze histone modifications and binding of transcription factors, DNA replication factors, or DNA repair proteins at specific target genes or across the entire genome. CUT&RUN provides a rapid, robust, and true low cell number assay for detection of protein-DNA interactions in the cell. Today, I will discuss how CUT&RUN can be performed in as little as one to two days using 100,000 cells per assay.

Featured speaker

Paul Marie

PhD Student


Paul Marie is a final-year PhD student in the Regulation of Genome Architecture and Dynamics of Splicing (ReGArDS) group in the Laboratory of Biology and Modeling of the Cell (LBMC) at ENS-Lyon. His work focuses on the NF-κB pathway activation – notably by the viral oncogene Tax of HTLV-1 – and its impact on genome architecture, transcriptional regulation, and alternative splicing. In a recent publication, he identified a new function of NF-kB in alternative splicing regulation that relies on an intragenic recruitment of the splicing regulator DDX17 by the NF-kB factor RelA. He now aims to assess the functional impact of such mechanism on histone regulation and chromatin architecture. Using Chromosome Conformation Capture assays, his preliminary result indicates that Tax affects the genome architecture. His current goal is to further characterize, in a genome-wide manner, the impact of RelA intragenic recruitment on the epigenetic pattern established by Tax. To this end, he has developed qChIP and CUT&RUN approaches targeting transcription factor RelA and several histone marks using the CUT&RUN Assay Kit from Cell Signaling Technology.