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The Conboy Laboratory

Engineering Longevity

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Discoveries & Projects

  • Understanding Fundamental Properties of Adult Stem Cells
    The reprogramming of terminally differentiated muscle cells to their proliferating progenitors holds not only theoretical value but is also therapeutically relevant. Our focus is on developing technology for enhancing regeneration of muscle and other tissue in vivo. […]
  • Understanding Fundamental Properties of Embryonic Stem Cells 
    One of our projects is focused on such key stem cell property as asymmetric division and specifically, on the non-random template segregation (NRTS) of chromosomes (which is a topic of high controversy). […]
  • Mammalian In Vivo Bio-Orthogonal Proteomics
    In an effort to identify the proteins that are capable of attenuating and reversing tissue aging, we developed a method where the proteome of only one parabiont is selectively labeled utilizing bio-orthogonal non-canonical amino acid tagging (BONCAT) for subsequent identification in the tissues of the parabiotic partner. […]
  • Heterochronic Parabiosis and Beyond
    The spearheaded by us heterochronic parabiosis studies have established the fundamental paradigm that the age-related decline of progenitor cell activity can be modulated by systemic factors that change with age. […]
  • Making Gene Editing A Therapeutic Reality
    CRISPR/Cas9 based therapeutics have the potential to revolutionize the treatment of genetic diseases. One particularly exciting class of Cas9 therapeutics are therapies that can correct gene mutations via homology directed repair (HDR). […]
  • Defined Pharmacology for Tissue Repair
    This work has lead to new bio-tech Juvena and in the Conboy lab we focus on development of novel pharmaceuticals for simultaneous “rejuvenation” of muscle, brain, bone, liver, etc. mammalian tissues. […]
  • Establishing New Aging & Rejuvenation Paradigms
    Much of our work has been focused on establishing new paradigms in multi-tissue stem cell aging, rejuvenation and regulation by conserved morphogenic signaling pathways. […]

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