February 09, 1996 - February 09, 2029

  • Date:09TuesdayJanuary 2018

    From human genetics to a new mechanism underlying type 2 diabetes.

    More information
    Time
    10:00 - 10:30
    Location
    Nella and Leon Benoziyo Building for Biological Sciences
    LecturerDr. Eitan Hoch
    Broad Institute of MIT and Harvard, Cambridge, MA
    Organizer
    Department of Biomolecular Sciences
    Contact
    AbstractShow full text abstract about Solute Carriers (SLCs) account for approximately 2% of known...»
    Solute Carriers (SLCs) account for approximately 2% of known human coding genes, and play diverse roles in human physiology. Despite ~100 SLCs being implicated in human disease, they also remain one of the most under-studied groups of genes in human biology.
    Genetic variants in one such uncharacterized SLC, namely SLC16A11, were recently identified as one of the largest genetic risk signals for type 2 diabetes (T2D).
    I will describe the functional follow-up to the genetic discovery of SLC16A11, which led to the identification of two distinct molecular mechanisms that link SLC16A11 dysfunction to disease.
    This work suggests that SLC16A11 is a promising therapeutic target for T2D.

    Solute Carriers (SLCs) account for approximately 2% of known human coding genes, and play diverse roles in human physiology. Despite ~100 SLCs being implicated in human disease, they also remain one of the most under-studied groups of genes in human biology.
    Genetic variants in one such uncharacterized SLC, namely SLC16A11, were recently identified as one of the largest genetic risk signals for type 2 diabetes (T2D).
    I will describe the functional follow-up to the genetic discovery of SLC16A11, which led to the identification of two distinct molecular mechanisms that link SLC16A11 dysfunction to disease.
    This work suggests that SLC16A11 is a promising therapeutic target for T2D.

    Solute Carriers (SLCs) account for approximately 2% of known human coding genes, and play diverse roles in human physiology. Despite ~100 SLCs being implicated in human disease, they also remain one of the most under-studied groups of genes in human biology.
    Genetic variants in one such uncharacterized SLC, namely SLC16A11, were recently identified as one of the largest genetic risk signals for type 2 diabetes (T2D).
    I will describe the functional follow-up to the genetic discovery of SLC16A11, which led to the identification of two distinct molecular mechanisms that link SLC16A11 dysfunction to disease.
    This work suggests that SLC16A11 is a promising therapeutic target for T2D.
    Lecture