Our Research
Our lab explores how endoplasmic reticulum (ER) membranes work and influence activities inside cells, including signaling, communication between organelles, protein production, gene expression, and calcium control. The ER drives important cellular functions like managing calcium signals, folding proteins, and supporting energy metabolism. We investigate how the ER senses cellular signals, handles stress, and determines the balance between cell survival and death, which has major implications for diseases. Our findings highlight the significant role of ER stress signals and solute transporters in cancer, heart disease, and nerve disorders. Right now, our research focuses on ER stress, immune responses, and solute transporters in conditions such as cancer, cardiovascular diseases, and nervous system disorders like multiple sclerosis, with the goal of guiding new treatment options.
Current Studies
Here are examples of research projects currently being pursued in our lab:
Modulators of ER Stress
Through siRNA library screens, we identified cellular proteins regulating ER stress responses and the UPR, such as ER chaperones and folding enzymes. We are using this data to manipulate ER stress pathways and discover new regulators. Fructose a ponent inducer of ER stress coping responses. There is an elevated expression of the fructose transporter (SLC2A5) gene in metastatic cancer cells. We study a significance of SLC2A5 in regulating cancer biology.
ER stress signaling and muscle E-C coupling
We use gene knockout and transgenic methods to study ER proteins and their role in embryogenesis and congenital diseases. Our research shows ER stress and ER chaperones are essential for heart development, as changes in its expression cause severe cardiomyopathies and heart block. We are examining how ER stress signaling pathways contribute to cardiac pathology, such as hypertrophy and heart failure, and investigating the effects of ER stress sensors on cardiac function and excitation-contraction coupling.
ER Chaperones in Neuropathies and Regulation of Blood-Brain Barrier
Mice lacking calnexin show specific nerve problems, such as faulty myelin and reduced motor abilities. Calnexin is found in brain endothelial cells, making it a possible target for treatments aimed at reducing neuroinflammation and repairing myelin damage in conditions like multiple sclerosis. This research explores how calnexin and the immunosuppressive CD200-CD200R pathway contribute to nervous system disorders, blood-brain barrier permeability focusing on human nerve diseases, disorders affecting myelin, and the control of blood-brain barrier permeability.
