김효정 교수
Hyun Jung Kim
서울대학교 · 의학
연구실 소개
김효정 교수의 연구실은 대사질환과 난세포성 대사 이상에서의 염증 반응, 특히 IL-6가 인슐린 저항성에 미치는 영향을 동물 모델을 활용해 규명하고 있습니다. 또한 식물에서의 세포분열과 낙엽 조절을 담당하는 사이토키닌 신호전달 경로의 분자 기전을 밝히며, 특히 F-box 단백질이 신호 종료를 어떻게 조절하는지에 초점을 맞추고 있습니다. 최근에는 코로나19 패an드레임 시기의 정보 과부하 문제와 뇌간 기능 장애에서의 전정기능 회복 양상에 대한 임상적 연구도 수행하고 있습니다. 이러한 연구들은 분자생물학, 대사학, 신경과학, 식물분자생물학의 융합적 접근을 통해 이루어지고 있습니다.
연구 현황
연구 성과 추이
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주요 논문
15The circulating level of the inflammatory cytokine interleukin (IL)-6 is elevated in various insulin-resistant states including type 2 diabetes, obesity, cancer, and HIV-associated lipodystrophy. To determine the role of IL-6 in the development of insulin resistance, we examined the effects of IL-6 treatment on whole-body insulin action and glucose metabolism in vivo during hyperinsulinemic-euglycemic clamps in awake mice. Pretreatment of IL-6 blunted insulin's ability to suppress hepatic glucos
Cytokinins are plant hormones with profound roles in growth and development, including control of leaf longevity. Although the cytokinin signal is known to be perceived by histidine kinase receptors, the underlying molecular mechanism and specificity of the receptors leading to delayed leaf senescence have not yet been elucidated. Here, we found that AHK3, one of the three cytokinin receptors in Arabidopsis, plays a major role in controlling cytokinin-mediated leaf longevity through a specific p
In view of more rapid resolution of static vestibular imbalance after VN, evaluation of the dynamic vestibular imbalances may provide more useful information for underlying vestibulopathy, especially in the compensated phase. The different temporal profiles ofdynamic vestibular recovery may reflect different chronological characteristics of vestibular compensation according to stimulus frequency. Direction reversal of HSN and VIN during follow-up suggests that lateralization of VNbased on the di
The global outbreak of coronavirus disease (COVID-19) in 2020 has significantly affected the information environment as well as the daily life of individuals across the world, with information about COVID-19 dominating all media channels. The information provided at the time of a health crisis like COVID-19 is critical in helping people learn about the disease and the recommendations to prevent infection. However, studies have shown that when people are overwhelmed by too much information (refer
Cytokinins are plant hormones that play critical roles in growth and development. In Arabidopsis, the transcriptional response to cytokinin is regulated by action of type-B Arabidopsis response regulators (ARRs). Although central elements in the cytokinin signal transduction pathway have been identified, mechanisms controlling output remain to be elucidated. Here we demonstrate that a family of F-box proteins, called the kiss me deadly (KMD) family, targets type-B ARR proteins for degradation. K
Nonalcoholic fatty liver disease (NAFLD), the hepatic manifestation of the metabolic syndrome, has emerged as one of the most common causes of chronic liver disease in developed countries over the last decade. NAFLD comprises a spectrum of pathological hepatic changes, including steatosis, steatohepatitis, advanced fibrosis, and cirrhosis. Autophagy, a homeostatic process for protein and organelle turnover, is decreased in the liver during the development of NAFLD. Previously, we have shown that
Hepatic ischemia/reperfusion (I/R) injury can arise as a complication of liver surgery and transplantation. Sirtuin 1 (SIRT1), an NAD+-dependent deacetylase, modulates inflammation and apoptosis in response to oxidative stress. SIRT1, which is regulated by p53 and microRNA-34a (miR-34a), can modulate non-alcoholic fatty liver disease, fibrosis and cirrhosis. Since carbon monoxide (CO) inhalation can protect against hepatic I/R, we hypothesized that CO could ameliorate hepatic I/R injury by regul
In the skeletal muscle, a 200-km run activates the expression of ubiquitin ligases muscle-specific RING finger 1 and muscle atrophy F-box as well as various cellular stresses, among which are ER stress, oxidative stress, and inflammation. Meanwhile, compensatory mechanisms seem also triggered: the unfolded protein response is up-regulated, and the chymotrypsin-like activity of the proteasome is repressed.
Carbon monoxide (CO) can confer protection against cellular stress, whereas the potential involvement of autophagy and lysosomal biogenesis remains incompletely understood. We demonstrate here that the activation of protein kinase R (PKR)-like endoplasmic reticulum (ER) kinase (PERK) with CO increased the nuclear translocation of transcription factor EB (TFEB). PERK activation by CO increased intracellular Ca<sup>2+</sup> concentration and the phosphatase activity of calcineurin against TFEB. Mo
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