Systems Biology

Dr. Sibel Demir-Deviren is currently a Clinical Professor specialized in non-surgical treatments of spinal disorders in the Departments of Orthopaedic Surgery and Neurological Surgery at the University of California, San Francisco and a Physiatrist at the UCSF Spine Center. Upon graduation from Hacettepe University, Ankara, Turkey (1993) with a degree in Medicine, she went on to complete her residency at the Ankara Education and Research Hospital in the field of Physical Medicine and Rehabilitation. Continuing her postgraduate work in this area, Dr.

My research investigates the roles of the extracellular Ca2+, gama-aminobutyric acid (GABA), insulin-like growth factor-1 (IGF1), parathyroid hormone (PTH), FGF23, and vitamin D, and their respective receptors (CaSR, GABBR1, IGF1R, PTH1R, Klotho, and VDR) in (1) controlling mineral homeostasis; (2) mediating skeletal development and facture healing; (3) regulating neuroendocrine functions; and (4) neuroprotection.

Our lab studies basic mechanisms by which signaling between cells coordinates morphogenesis. Understanding this control has significance beyond its fundamental importance in development since birth defects are the leading cause of death for infants during the first year of life.

Originally from Liverpool, England, Andrew graduated with a PhD in Molecular Biology and Biophysics from King’s College London. He did two postdoctoral fellowships, the first with Simon Hughes at King’s College London and the second with Tom Rando at Stanford University. Andrew started his own lab at the Center for Regenerative Medicine, MGH, Harvard University in 2008. In 2015 he moved to UCSF to begin the next phase of his lab's journey.

The long-term goal of my research is to understand the role of tissue secretory senescent cells in aging, autoimmunity and metabolic diseases. Our recent discovery shows that pancreatic beta cells acquire a secretome during T1D in mice and human and exhibit many non-cell autonomous properties. Senescent beta cells can remodel the islet environment in a paracrine manner by promoting bystander senescence and immune surveillance. We have identified key immune cells that can selectively eliminated senescent beta cells to halted progression of beta cell destruction prevent T1D in mouse models.