Yun‐Sil Lee
이화여자대학교 약학대학 · 생화학·유전·분자생물학
Yun-Sil Lee 교수의 연구실은 암 및 방사선 유도 폐섬유화와 같은 질병에서 핵심적으로 작용하는 단백질, 특히 HSP27과 TGF-β 시스템 관련 단백질의 기능과 신호전달 기전을 중심으로 연구를 진행하고 있습니다. 특히 HSP27이 세포 사멸 억제 및 염증 반응 조절을 통해 암 치료 저항성과 방사선 유도 폐 섬유화에 기여하는 메커니즘을 규명하고 있으며, 이들의 억제를 통한 새로운 치료 전략 개발에 초점을 맞추고 있습니다. 또한, myostatin과 GDF-11의 조절 메커니즘을 통해 근육 성장 및 조직 섬유화의 분자 기전을 탐구하고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
Heat shock protein 27 (HSP27), induced by heat shock, environmental, and pathophysiological stressors, is a multi-functional protein that acts as a protein chaperone and an antioxidant. HSP27 plays a significant role in the inhibition of apoptosis and actin cytoskeletal remodeling. HSP27 is upregulated in many cancers and is associated with a poor prognosis, as well as treatment resistance, whereby cells are protected from therapeutic agents that normally induce apoptosis. This review highlights
Radiation-induced lung injury (RILI), including acute radiation pneumonitis and chronic radiation-induced lung fibrosis, is the most common side effect of radiation therapy. RILI is a complicated process that causes the accumulation, proliferation, and differentiation of fibroblasts and, finally, results in excessive extracellular matrix deposition. Currently, there are no approved treatment options for patients with radiation-induced pulmonary fibrosis (RIPF) partly due to the absence of effect
Myostatin (MSTN) and growth and differentiation factor-11 (GDF-11) are highly related TGF-β family members that have distinct biological functions. MSTN is expressed primarily in skeletal muscle and acts to limit muscle growth. GDF-11 is expressed more widely and plays multiple roles, including regulating axial skeletal patterning during development. Several MSTN and GDF-11 binding proteins have been identified, including GDF-associated serum protein-1 (GASP-1) and GASP-2, which are capable of i
Collectively, IkBα-NFkB signaling activation by Hsp27, which resulted in the facilitation of Twist, IL1β, and IL6 expression, is involved in the EMT process that is tightly connected to the development of IR-induced lung fibrosis. Our findings also suggest that inhibition of Hsp27 has the potential to become a valuable therapeutic strategy for IR-induced lung fibrosis.
