권영혜 교수
Young Hye Kwon
서울대학교 · 의학
연구실 소개
권영혜 교수의 연구실은 간세포의 대사 조절과 손상 회복 메커니즘을 중심으로, 특히 글루타티온 합성과 항산화 체계, 세포주기 조절 단백질(p21, p27)의 기능을 탐구하고 있습니다. 메티오닌 및 시스테인의 대사 조절 효과에서부터, 루테올린과 같은 식물성 폴리페놀이 암세포에서의 세포사멸과 자가분해를 유도하는 p53 의존적 메커니즘을 규명하고 있으며, 비알코올성 간비내성지방간질환(NASH) 및 고지혈증 모델에서 천연소재의 간 보호 작용을 기전적으로 분석하고 있습니다. 특히 단백질 안정성과 번역 후 조절 메커니즘을 통해 간세포의 정지 상태 유지와 손상 반응을 규명하고 있습니다.
연구 현황
연구 성과 추이
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
주요 논문
15Rat hepatocytes cultured for 3 days in basal medium expressed low levels of cysteine dioxygenase (CDO) and high levels of gamma-glutamylcysteine synthetase (GCS). When the medium was supplemented with 2 mmol/l methionine or cysteine, CDO activity and CDO protein increased by >10-fold and CDO mRNA increased by 1.5- or 3.2-fold. In contrast, GCS activity decreased to 51 or 29% of basal, GCS heavy subunit (GCS-HS) protein decreased to 89 or 58% of basal, and GCS mRNA decreased to 79 or 37% of basal
Although a dietary phytochemical luteolin has been shown to regulate various anticancer mechanisms, a role of luteolin in autophagy regulation is mostly unidentified. Here, we investigated whether luteolin exhibits its anticancer effects by induction of apoptosis and autophagy in a p53-dependent manner in colon cancer cells. Cell viability was determined using trypan blue exclusion test. The expressions of proteins and mRNAs were measured by immunoblotting and reverse transcription polymerase ch
GEN alleviated NASH as well as hypercholesterolemia and obesity in ApoE(-/-) mice fed an HFD. Restoration of altered cholesterol metabolism and oxidative stress may be involved in the protective effect of GEN against NASH development.
Urediospore germlings of Uromyces appendiculatus sense topographical signals inherent in host stomata over which they develop appressoria. The site of signal recognition by the fungus is invariably within the apical 6 μm of the germling. The organization of the germling apex before and during initiation of appressorium formation was examined by both electron microscopy and laser scanning confocal microscopy. Most notable were changes in the distribution and organization of the microtubules and a
Liver injury and repair were examined in wild type, p21Waf1/Cip1, and p27Kip1-deficient mice following carbon tetrachloride (CCl4) administration. In wild type liver, p21 expression is induced in a biphasic manner following injection of CCl4, with an early peak of p21 expression occurring in pericentral hepatocytes at 6 h, prior to evidence of injury, and a second peak succeeding regenerative proliferation. In contrast, p27 is present throughout the quiescent liver, but its expression decreases
Hepatocytes rarely proliferate in the healthy adult liver. We explored the roles of the cyclin kinase inhibitors p21 and p27 in maintaining hepatocyte quiescence. p27 is expressed throughout the wild-type liver, but the related protein p21 was not detected. However, p21 was detected in livers of p27-deficient mice. Increased p21 protein levels did not result from an increase in p21 mRNA expression, indicating that p21 expression is regulated post-transcriptionally. p21 protein levels increased i
Obesity is considered a risk factor for neurodegeneration. Because fermentation of soybean increases contents of various bioactive compounds with anti-obesity and anti-diabetic activities, we investigated the protective effect of <i>doenjang</i>, a Korean traditional fermented soybean paste, against neuroinflammation and neurodegeneration in the cortex and hippocampus of mice fed a high-fat (HF) diet. C57BL/6J mice were fed a low-fat diet, an HF diet, an HF-containing steamed soybean diet, or an
Several studies have demonstrated a protective effect of estrogen against the risk of developing neurodegenerative diseases; however, the molecular mechanisms involved have not been fully addressed. Isoflavones have been proposed as potential alternatives to estrogen replacement therapy. Therefore, in the present study, we investigated effects of isoflavones on cell death and tau phosphorylation in SH-SY5Y human neuroblastoma cells. Cells were treated with tunicamycin (TM) to induce endoplasmic
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