Sung‐Gyoo Park
서울대학교 의과대학 · 의학
Sung-Gyoo Park 교수의 연구실은 간염 바이러스, 특히 간염바이러스 B의 복제 메커니즘과 면역조절 세포인 MDSCs의 기능을 중심으로 연구를 진행하고 있습니다. HBV 폴리머라제의 활성화 및 변이에 영향을 미치는 분자적 요인(예: Hsp60, Hsp90)과 면역세포 간의 상호작용을 규명하며 바이러스 감염의 조절 메커니즘을 밝혀내고 있습니다. 또한 암 발생과 관련된 유전자(DKC1)의 조절 기전과 면역세포 간의 상호작용 메커니즘을 연구하여, 새로운 치료 타겟을 모색하고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
Myeloid-derived suppressor cells (MDSCs) regulate T cell immunity, and this population is a new therapeutic target for immune regulation. A previous study showed that transforming growth factor-β (TGF-β) is involved in controlling MDSC differentiation and immunoregulatory function in vivo. However, the direct effect of TGF-β on MDSCs with various cytokines has not previously been tested. Thus, we examined the effect of various cytokine combinations with TGF-β on MDSCs derived from bone marrow ce
Previous studies showed that hepatitis B virus polymerase (HBV Pol) interacts with host factors such as the Hsp90 complex, which is a critical step in viral genome replication. In this report, we propose that another chaperone, Hsp60, interacts with human HBV Pol and that this is a very important step for maturation of human HBV Pol into the active state. In the immunoprecipitation of recombinant human HBV Pol expressed in insect cells with the recombinant baculovirus expression system, the 60-k
The major role of hepatitis B virus polymerase (HBV pol) is polymerization of nucleotides, but it also participates in protein priming and the packaging of its own genome into capsids. Therefore, HBV pol may require many assistance factors for its roles. Previous reports have shown that Hsp60, a molecular chaperone, activates HBV pol both in vitro and ex vivo, such as inside insect cells. Moreover, HBV pol binds to Hsp60 in the HepG2 host cell line. In this report, we show that Hsp60 plays a rol
Dyskerin pseudouridine synthase 1 (DKC1) is a conserved gene encoding the RNA-binding protein dyskerin, which is an essential component of the telomerase holoenzyme. DKC1 up-regulation is frequently observed in many different human cancers including hepatocellular carcinoma (HCC); however, its regulatory mechanisms remain unclear. Thus, we investigated the regulatory mechanism of DKC1 in HCC progression. We found that protein-disulfide isomerase-associated 3 (PDIA3) interacted with the DKC1 regu
Myeloid-derived suppressor cells (MDSCs) play roles in immune regulation during neoplastic and non-neoplastic inflammatory responses. This immune regulatory function is directed mainly toward T cells. However, MDSCs also regulate other cell populations, including B cells, during inflammatory responses. Indeed, B cells are essential for antibody-mediated immune responses. MDSCs regulate B cell immune responses directly via expression of effector molecules and indirectly by controlling other immun
Although efficient vaccines are available, chronic hepatitis B (HBV) infection poses a major health problem worldwide, and prolonged treatment of chronically infected HBV patients with nucleoside analogs often results in drug-resistant HBV variants. Therefore, it is critical to evaluate the contribution of the HBV polymerase to mutations. FLAG-tagged wild-type (FPolE) and mutant (FPolE/D551A) HBV polymerases have been expressed in insect cells and purified. The purified FPolE showed DNA polymera
The roles of Notch1 and Notch2 in T-cell function have been well studied, but the functional roles of Notch in B cells have not been extensively investigated, except for Notch2 involvement in peripheral marginal zone B-cell differentiation. This study examined the roles of Notch1 in murine primary B cells. During B-cell activation by B-cell receptor ligation, Notch1 was up-regulated while Notch2 was not. In addition, Notch1 up-regulation itself did not contribute to the further activation of B c
Cyclin D1 is frequently overexpressed in hepatocellular carcinoma (HCC) exhibiting increased malignant phenotypes. It has also been known that the hepatitis Bx (HBx) protein is strongly associated with HCC development and progression. Although overexpression of both proteins is related to HCC, the relationship between the two has not been well studied. Here we show that HBx up-regulates cyclin D1 and that this process is mediated by the NF-κB2(p52)/BCL-3 complex. Our experiments indicate that HB