Deepali Bhandari, Ph.D. Assistant Professor, Biochemistry Department of Chemistry and Biochemistry, MLSC-233 California State University Long Beach 1250 Bellflower Blvd., Long Beach, CA-90840
Biosketch B.S./M.S. Microbiology, Panjab University Chandigarh, India Ph.D. Molecular Biology, Loyola University Chicago Postdoctoral fellowship, HHMI, University of California San Diego
Research Interests Dr. Deepali Bhandari is an Assistant Professor of Biochemistry at CSULB. A protein biochemist and cell biologist by training, Dr. Bhandari uses mammalian cells as a model system to study fundamental questions in cellular biochemistry. One of the major questions her research is focused on is to understand cells’ ability to withstand Endoplasmic Reticulum (ER) stress. The ER is a site of many important cellular functions including protein folding, post-translational modifications and maintaining calcium homeostasis in virtually every mammalian cell. Perturbations in these functions generate ER stress and lead to activation of a signaling program known as the “Unfolded protein response (UPR)”. By triggering UPR, cells initially try to restore normal function, however, if the damage is beyond repair and homeostasis is not achieved within a reasonable time frame, the UPR ultimately commits cells to apoptosis. How cells make this life-or-death decision remains an exciting and unanswered question. She is interested in identifying signaling proteins/mechanisms that play a decisive role in determining whether cells survive or succumb to ER stress. Apart from normal physiological conditions such as in secretory cells, ER stress is also experienced during many pathological conditions such as diabetes, neurodegeneration, cardiovascular diseases and cancer. Cancer cells exhibit high levels of ER stress due to their high rates of glucose metabolism and hypoxic conditions resulting in accumulation of under-glycosylated misfolded proteins in the ER. Interestingly, cancer cells are able to alleviate high levels of ER stress and their adaptive ability to survive through ER stress has been correlated to their invasiveness/malignancy and chemo-resistance. Thus, to be able to design effective strategies for cancer treatment, it is crucial to delineate the signaling mechanisms that endow cancer cells with a cyto-protective phenotype. Her long-term goal is to determine if the switch from survival to apoptotic signaling by UPR can be manipulated to achieve pharmacological intervention not only in cancer but also other diseases whose etiology involves ER stress.
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