Dong Min Shin
연세대학교 의과대학 · 생화학·유전·분자생물학
Dong Min Shin 교수의 연구실은 마이코박터이움 투버클로시스의 병원성 메커니즘과 면역조절을 중심으로, 특히 매크로파지 내에서의 세균 생존 전략과 자가분해작용(자기포식), 염증 반응, 세포 사멸 조절을 ROS 및 칼슘 신호전달 경로를 통해 규명하고 있습니다. 또한 골절손실 관련 질환의 치료 전략으로서 NFATc1 활성화 경로와 칼슘 신호전달 분자의 기능적 역할, 특히 허모어 단백질이 Ca²⁺ 파동의 주파수 조절에 기여하는 메커니즘을 연구하고 있습니다. 이는 감염병 및 뼈 대사질환의 새로운 치료 타겟을 모색하는 데 기여하고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
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
