News from the Broad

The Broad Institute is committed to open sharing not only of its scientific data and tools, but also information and news about our progress towards achieving our mission. Below are just a few highlights from the Broad scientific community.
  • Consortium uncovers therapeutic leads for Huntington’s Disease

    August 3rd, 2015

    The rare, inherited neurodegenerative disorder Huntington's Disease (HD) has no known cure. But research from the Genetic Modifiers of Huntington’s Disease (GeM-HD) Consortium published last week in Cell reveals promising genetic targets for therapeutic development. Identified by genome-wide association, variants of these genes modify the age of neurologic onset of HD, supporting the notion that HD pathogenesis can be influenced prior to the appearance of clinical disease.

  • Out of the lamplight

    July 30th, 2015
    New research from Broad's cell circuits program is the first to apply genome-wide CRISPR screening to primary cells and reveals new and known regulators of an important immune response circuit.
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  • Commentary outlines plan for crowdsourced Chemical Probes Portal

    July 27th, 2015

    Chemical probes — small molecules that interact with a protein’s function — can be powerful tools to reveal the roles of targeted proteins in health and disease, but probes are sometimes of low quality, and high-quality ones can be misused. In a Nature Chemical Biology commentary, a multi-institutional team, including Broad Institute’s Stuart Schreiber, Nathanael Gray, and Joanne Kotz, describe plans for a new community-driven wiki-like site, called the Chemical Probes Portal, that crowdsources medicinal chemistry and pharmacology expertise to catalog the best chemical probes for a given protein target. The resource aims to support research in basic biology and the pursuit of new therapeutics.

  • American History 201

    July 21st, 2015
    Genetic studies link indigenous peoples in the Amazon and Australasia
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  • Researchers use new methods to localize genetic risk of type 1 diabetes

    July 17th, 2015

    Variation in human leukocyte antigen (HLA) genes accounts for one-half of the genetic risk in type 1 diabetes (T1D), but scientists have found it challenging to pinpoint the specific variants that account for this risk. This week, a team led by Soumya Raychaudhuri and Xinli Hu of Broad Institute and Brigham and Women’s Hospital published a study that used new genotype imputation methods to identify independent amino acid positions, as well as interactions within the HLA region, that account for T1D risk. Taking this approach, they found that three key amino acid positions in HLA-DQ and HLA-DR molecules drive the vast majority of T1D risk. To learn more, read their paper online in Nature Genetics.