전양숙 교수
Yang-Sook Jeon
서울대학교 · 생화학·유전·분자생물학
연구실 소개
전양숙 교수의 연구실은 히스톤 에피유전적 조절, 산소 농도에 따른 세포 반응, 그리고 신경퇴행성질환의 분자 기전을 중심으로 연구를 진행하고 있습니다. 특히 히스톤 디메틸화 효소인 PHF2와 Jumonji 도메인을 가진 히스톤 디메틸라제의 기능을 규명하며 지방세포 분화와 알츠하이머병 등 신경퇴행성 질환에서의 유전자 조절 메커니즘을 탐구하고 있습니다. 또한, 저산소 상태에서의 전사 인자 HIF-1α의 조절 메커니즘과 항암 및 폐질환 모델에서의 산소 조절 반응을 연구함으로써 세포의 대사 적응과 질병 발생 기전을 밝히는 데 초점을 맞추고 있습니다.
연구 현황
연구 성과 추이
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주요 논문
15Hypoxia-inducible factor-1 alpha (HIF-1α) is a transcription factor essential for cancer cell survival. The reprogramming of lipid metabolism has emerged as a hallmark of cancer, yet the relevance of HIF-1α to this process remains elusive. In this study, we profile HIF-1α-interacting proteins using proteomics analysis and identify fatty acid-binding protein 5 (FABP5) as a critical HIF-1α-binding partner. In hepatocellular carcinoma (HCC) tissues, both FABP5 and HIF-1α are upregulated, and their
Atrial natriuretic peptide (ANP) is a cardiac peptide, the transcription of which is up-regulated in the ischaemic ventricle. However, the molecular mechanism of ANP induction is unclear. This study demonstrated that ANP mRNA expression in rat ventricular myocardium is induced in an early phase of ischaemia, preceded by hypoxia-inducible factor-1 (HIF-1) alpha expression. The ANP gene was also induced by hypoxia or HIF-1 inducers such as CoCl2 and desferrioxamine in H9c2 and neonatal cardiomyocy
Hypoxia-inducible factor α proteins (HIF-αs) are regulated oxygen dependently and transactivate numerous genes essential for cellular adaptation to hypoxia. NEDD8, a member of the ubiquitin-like family, covalently binds to its substrate proteins, and thus, regulates their stabilities and functions. In the present study, we examined the possibility that the HIF signaling is regulated by the neddylation. HIF-1α expression and activity were inhibited by knocking down APPBP1 E1 enzyme for NEDD8 conj
Cadmium is a substantial industrial and environmental pollutant which seriously impairs erythropoiesis. Cd has been demonstrated to aggravate anemia by suppressing erythropoietin gene expression in anemic patients. As hypoxic induction of erythropoietin mRNA depends on a transcription factor, hypoxia‐inducible factor 1 (HIF‐1), we hypothesized that Cd suppresses the hypoxic activation of HIF‐1. In hypoxic Hep3B cells, all mRNAs of various genes, which are known to be upregulated by HIF‐1 activat
Chilling injury in pepper (Capsicum annuum L.) fruit during cold storage and market distribution results in quality loss. In the present study, seed browning, a major chilling injury symptom, was observed in pepper fruit stored at 2 °C, but not at 13 °C. To alleviate this symptom, we applied vapour treatments of 50 μM methyl jasmonate (MeJA) or 250 μM methyl salicylate (MeSA), or a combination of both, and investigated the effect of treatments on seed browning in pepper fruit during cold storage
Histone modifications on major transcription factor target genes are one of the major regulatory mechanisms controlling adipogenesis. Plant homeodomain finger 2 (PHF2) is a Jumonji domain-containing protein and is known to demethylate the histone H3K9, a repressive gene marker. To better understand the function of PHF2 in adipocyte differentiation, we constructed stable PHF2 knock-down cells by using the mouse pre-adipocyte cell line 3T3-L1. When induced with adipogenic media, PHF2 knock-down ce
Although obesity is a newly considered risk factor for cancer, the mechanisms by which adipocyte-derived metabolites accelerate cancer malignancy have yet to be elucidated. To identify the connection among heterogeneous cell types, conventional methods including Transwell assays or conditioned media (CM) have been used; however, these methods do not fully reflect niche effects in the tumor microenvironment (TME). Here, we established an oxygen permeable polydimethylsiloxane (PDMS)-based three-di
These results suggest that HIF-1alpha functions as an intrinsic defense molecule that enables prostate cells to survive in a zinc-rich environment.
This study provides novel associations of genetic factors to Aβ accumulation and AD-related neurodegeneration to influence AD susceptibility.
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