Dr. Hubmacher is an Assistant Professor in the Leni & Peter W. May Department of Orthopaedics at the Icahn School of Medicine at Mount Sinai in New York City. He received his graduate degree from the Technical University Karlsruhe (Germany) and his PhD in Biochemistry from the University in Luebeck (Germany).
Dr. Hubmacher got introduced to the fascinating world of extracellular matrix and connective tissue biology during his postdoctoral training with Dr. Dieter Reinhardt at McGill University in Montreal (Canada), where he focused on fundamental aspects of fibrillin microfibril formation. Dr. Hubmacher continued his training as a project staff in the laboratory of Dr. Suneel Apte at the Cleveland Clinic Lerner Research Institute in Cleveland (Ohio), where he started to use mouse genetics to interrogate the relationship between ADAMTS proteases, ADAMTS-like proteins and fibrillins.
Dr. Hubmacher’s current research focuses on the role of the extracellular matrix in the formation and function of musculoskeletal tissues, such as tendon and skeletal muscle. Specifically, he studies the mechanisms of how a group of secreted extracellular matrix proteins, ADAMTS proteases and ADAMTS-like proteins, in conjunction with fibrillin microfibrils, govern the formation of musculoskeletal tissues. A functional interaction between these proteins is strongly suggested by the fact that mutations in specific ADAMTS proteases and ADAMTS-like proteins or mutations in fibrillin-1 (FBN1) can cause the same human genetic disorders, such as geleophysic dysplasia or Weill-Marchesani syndrome. These musculoskeletal disorders are characterized by severe short stature, short hands and feet, stiff joints, and a pseudomuscular built. To elucidate the biological role of ADAMTS proteases and ADAMTS-like proteins, Dr. Hubmacher’s laboratory has generated mouse models of these disorders and uses cell-based assays and biochemical and biophysical approaches to dissect hierarchical protein-protein interactions in the extracellular matrix and to determine responses of tissue-resident cells to faulty extracellular matrices deposited in disease conditions. The ultimate goal of these studies is to harness the knowledge of these mechanisms to guide tissue repair processes after injury and to contribute towards the identification of novel tissue engineering approaches.
