Yonsei University · Biochemistry, Genetics and Molecular Biology
Professor Dong Min Shin's research lab focuses on cellular signaling mechanisms, particularly calcium homeostasis and its role in immune response and bone metabolism. The lab investigates how intracellular signaling pathways—especially those involving calcium, reactive oxygen species (ROS), and transcription factors like NFATc1—affect cellular processes such as autophagy, inflammation, and cell death in macrophages and osteoclasts. A key emphasis is placed on understanding host-pathogen interactions, particularly in Mycobacterium tuberculosis infection, and the regulation of Ca2+ signaling by scaffolding proteins like Homer in secretory cells. The lab also explores therapeutic targets in diseases involving dysregulated calcium signaling, such as osteoporosis and cancer.
Figures are computed from collected data and may differ slightly.
The "enhanced intracellular survival" (eis) gene of Mycobacterium tuberculosis (Mtb) is involved in the intracellular survival of M. smegmatis. However, its exact effects on host cell function remain elusive. We herein report that Mtb Eis plays essential roles in modulating macrophage autophagy, inflammatory responses, and cell death via a reactive oxygen species (ROS)-dependent pathway. Macrophages infected with an Mtb eis-deletion mutant H37Rv (Mtb-Δeis) displayed markedly increased accumulati
Aggressive multimodal treatment is highly effective and may cure locally advanced, unresectable malignant thymoma.
The increasing of intracellular calcium concentration is a fundamental process for mediating osteoclastogenesis, which is involved in osteoclastic bone resorption. Cytosolic calcium binds to calmodulin and subsequently activates calcineurin, leading to NFATc1 activation, a master transcription factor required for osteoclast differentiation. Targeting the various activation processes in osteoclastogenesis provides various therapeutic strategies for bone loss. Diverse compounds that modulate calci
Because thymoma is a chemosensitive tumor and frequently recurs in patients with Stage II or greater disease, chemotherapy carries a potential survival benefit and should be incorporated into the multimodality approach to prolong disease-free survival.
Homers are scaffolding proteins that bind G protein-coupled receptors (GPCRs), inositol 1,4,5-triphosphate (IP3) receptors (IP3Rs), ryanodine receptors, and TRP channels. However, their role in Ca2+ signaling in vivo is not known. Characterization of Ca2+ signaling in pancreatic acinar cells from Homer2-/- and Homer3-/- mice showed that Homer 3 has no discernible role in Ca2+ signaling in these cells. In contrast, we found that Homer 2 tunes intensity of Ca2+ signaling by GPCRs to regulate the f
The localization of various Ca(2+) transport and signaling proteins in secretory cells is highly restricted, resulting in polarized agonist-stimulated Ca(2+) waves. In the present work, we examined the possible roles of the Sec6/8 complex or the exocyst in polarized Ca(2+) signaling in pancreatic acinar cells. Immunolocalization by confocal microscopy showed that the Sec6/8 complex is excluded from tight junctions and secretory granules in these cells. The Sec6/8 complex was found in at least tw
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