Je Kyung Seong
서울대학교 수의과학대학 발생유전학교실 · 의학
Je Kyung Seong 교수의 연구실은 만성 염증성 질환, 특히 비염성 폴립과 대사질환에서의 단백질 및 지질 대사 변화를 중심으로 연구를 진행하고 있습니다. 특히 MUC8 등 점액 관련 유전자 발현 조절, 산화 스트레스에 의한 세포 적응 메커니즘, 고지방 식이에 의한 지방세포 내 플라스말로지네이트 대사 변화와 관련된 신호전달 경로를 규명하고 있습니다. 이는 천식, 비염, 비만 관련 대사질환의 발병 기전 규명과 새로운 치료 타겟 탐색에 기여하고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
Polyps are believed to be the source of mucus hypersecretion in chronic inflammation of the sinus. However, it is not clear which mucins are responsible for the hypersecretion of mucus by nasal polyps. We describe the over-expression of MUC8 mRNA in nasal polyps and the upregulation of MUC8 mRNA expression and downregulation of MUC5AC mRNA expression by inflammatory mediators. We found that the level of MUC8 mRNA, but not the level of MUC5AC mRNA, increased in nasal polyps. We also found that th
When cells are first exposed to low levels of oxidative stress, they develop a resistance to a subsequent challenge of the same stress, even at higher levels. Although some protein(s) induced by oxidative stress likely mediated this adaptive response, the nature of these proteins is unknown. In this study, the total proteins extracted from human U937 leukemia cells exposed to 50 micromM H(2)O(2) for 24 h to induce an optimal protective response were analyzed by two-dimensional polyacrylamide gel
We report here a proteomic analysis of differentially expressed liver proteins of both C57BL/6J (B6, atherosclerosis-susceptible strain) and C3H/HeJ mice (C3H, atherosclerosis-resistant strain), which were fed either control or a high-fat enriched atherogenic diet for eight weeks. We observed differential patterns of plasma lipids between the two strains when both were fed atherogenic diets. That is, although low density lipoprotein cholesterol level was highly elevated in both, the levels of to
Dysregulation of adipose tissue plasmalogen metabolism is associated with obesity-related metabolic diseases. We report that feeding mice a high-fat diet reduces adipose tissue lysoplasmalogen levels and increases transmembrane protein 86 A (TMEM86A), a putative lysoplasmalogenase. Untargeted lipidomic analysis demonstrates that adipocyte-specific TMEM86A-knockout (AKO) increases lysoplasmalogen content in adipose tissue, including plasmenyl lysophosphatidylethanolamine 18:0 (LPE P-18:0). Surpri
