Abstract of the Talk

Ca2+ ions are universal second messengers that regulates nearly every aspect of cellular life. The important function of voltage-gated Ca2+ channels in muscle contraction and synaptic transmission is very well established. Ca2+ signals are also generated downstream of activation of plasma membrane receptors to hormones, growth factors and neurotransmitters. One of the most ubiquitous and evolutionarily conserved pathway of receptor-evoked Ca2+ entry is the store-operated Ca2+ entry (SOCE) pathway mediated by the Ca2+ release-activated Ca2+ (CRAC) channel. CRAC channel function is mediated by STIM and Orai proteins. Orai proteins, which consist of a family of three members (Orai1/2/3) encoded by distinct genes, form hexameric and highly Ca2+-selective channels at the plasma membrane. Orai channels are activated by stromal-interacting molecules (STIM1 and STIM2), which are Ca2+ sensing proteins located in the endoplasmic reticulum. Mutations or altered expression of STIM and Orai proteins are associated with a number of diseases, including immune, muscle, cardiovascular and airway diseases and cancer. Here, I will discuss our current understanding of STIM/Orai signaling and regulation, and present our data on the physiological functions of STIM/Orai proteins and their contribution to disease.

Bio

Mohamed Trebak was born in Morocco and completed his graduate studies in the department of Pathology at the University of Liège, in Wallonia, Belgium. He then moved to the Wistar Institute of Philadelphia as a postdoctoral fellow and completed a second postdoc at the National Institutes of Health/NIEHS where he trained in calcium signaling in non-excitable cells. In 2007, he joined Albany Medical College, NY as an Assistant Professor and was promoted to Associate Professor in 2010. In 2015, he moved to the Pennsylvania State University Medical Center as a tenured Professor and then to the Vascular Medicine Institute at the University of Pittsburgh in 2021.