Calcium (Ca) is a second messenger used by all cells to regulate numerous cellular processes ranging from cell proliferation to cell death. Fluctuations in calcium signaling are involved in many human pathologies. The two sources of calcium used for signaling between cells come from the extracellular environment and internal stores. The Endoplasmic reticulum/Sarcoplasmic Reticulum (ER/SR) are the intracellular storage compartments for Ca.  The ER/SR have two types of receptors responsible for regulating calcium release. They include inositol 1,4,5-trisphosphate receptors  (InsP3R)  and ryanodine receptors (RYR).  The primary agonists acting on these receptors are inositol 1,4,5-trisphosphate (InsP3)and Ca.  Many cell-surface receptors that increase InsP3 induce the simultaneous intracellular production of  sphingolipids and sphingolipid metabolites including sphingosine, and sphingosine-1-phosphate which are a family of intracellular second messengers  fundamental in a multitude of biological responses. Recent studies have provided evidence for the role of sphingolipid metabolites in calcium mobilization from internal stores, but their mechanism of action is unclear and the intracellular Ca channel(s) they activate still unidentified. Furthermore, their functional interactions with InsP3 have not been characterized. Using single-cell microfluorimetry and videoanalysis, I  am currently investigating the mechanisms by which sphingosine and sphingosine-1-phosphate act to modulate calcium release. I am also working with prostate cancer cells co-cultured with human osteoblasts and examining calcium mobilization in the cancer cells to determine the effects of co-cultured conditions on their metastatic potential. The primary goal of my research is to identify the mechanisms and intracellular channels through which sphingosine and sphingosine-1P mobilize intracellular Ca and characterize their role in cellular signaling. Ultimately I hope to identify the cellular and molecular mechanisms involved in the metastatic potential of cancer cells.