Matthew Blake Greenblatt   Assistant Professor of Pathology and Laboratory Medicine

  • +1 212 746 2040


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research overview

  • Approximately half of all women and a fifth of all men will experience a skeletal fracture due to low bone mass.  These fractures kill as many women each year as breast cancer. Improving clinical outcomes in this area will ultimately require finding new therapeutic agents that promote the activity of osteoblasts, the cells that build bone, which in turn will require improving our understanding of the molecular pathways involved in this process.  To this end, we are focused on using a combination of genetics, cellular biochemistry and genome-wide screening to discover new molecular pathways that regulate the activity of osteoblasts.  In particular, we are interested in how tuning the activity of the genes involved in the ability of osteoblasts to perceive signals from their environment can control the formation of bone, focusing  on an ancient and fundamentally important family of signaling molecules, the mitogen activated protein kinases (MAPKs).  Currently, we are exploring how dysregulation of MAPK signaling contributes to skeletal disease and how MAPK pathways can be targeted to benefit bone health.

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