Joon Kim

Korea University, Sŏul, Seoul, South Korea

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Publications (78)258.87 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Some ribosomal proteins are important regulators of development and DNA repair. However, few studies have been conducted on ribosomal protein S3 (rpS3) in the ischemic hippocampus. In the present study, we investigated ischemia-induced changes in rpS3 immunoreactivity, rpS3 mRNA, and protein levels in the hippocampal CA1 region of Mongolian gerbil after 5 min of transient forebrain ischemia. RpS3 immunoreactivity and its protein level were found to be significantly elevated at 6 hr after ischemia/reperfusion and then continuously decreased with time. RT-PCR analysis also showed that rpS3 mRNA levels were significantly elevated in CA1 at 6 hr after transient ischemia. In addition, during the course of this study, we developed a delivery vector (Pep-1) and its rpS3 fusion protein (Pep-1-rpS3) to elucidate the role of rpS3 in ischemia-induced damage. Pep-1-rpS3 administration to ischemic animals significantly and dose dependently increased neuronal survival in the stratum pyramidale of CA1. Moreover, Pep-1-rpS3 treatment reduced terminal deoxynucleotidyl dUTP nick-end labeling-positive CA1 pyramidal cell numbers in the stratum pyramidale. To elucidate how Pep-1-rpS3 ameliorates ischemic damage, changes in 4-hydroxy-2-nonnenal (HNE; an indicator of lipid peroxidation) immunoreactivity and protein levels were investigated. HNE levels and immunoreactivities in Pep-1-rpS3-treated ischemic animals were lower than in corresponding Pep-1-treated ischemic animals. These results indicate that rpS3 has a neuroprotective effect in the brain exposed to ischemia.
    Journal of Neuroscience Research 07/2008; 86(8):1823-35. · 2.97 Impact Factor
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    ABSTRACT: To make stable and biocompatible non-viral gene carriers for therapeutic gene therapy, we developed a cationic lipid-based emulsion (CLE) prepared by an oil-in-water (O/W) emulsion method, wherein squalene oil was used as an oil core and the cationic lipid, 1,2-dioleoyl-sn-glycero-3-trimethylammonium-propane (DOTAP), was employed as an emulsifier. To evaluate in vivo characteristics such as toxicity and time-dependent gene expression, a bioluminescence reporter gene in pCMV-luc plasmid DNA was simply mixed with CLE in aqueous condition, resulting in a CLE/DNA complex. The CLE/DNA complex was optimized to form a compact and stable nano-sized particle by adding different amounts of plasmid DNA, and an optimal cationic lipid-to-DNA (C/D) weight ratio of 4 was identified. Freshly prepared CLE/DNA complex, with a C/D of 4, showed a high transfection efficiency and minimal cytotoxicity in vitro, compared to controls of a liposome (DOTAP)/DNA complex and a branched poly(ethyleneimine) (Mw=25 kDa) (bPEI)/DNA complex, respectively. The in vivo characteristics of the CLE/DNA complex were evaluated after intravenous injection into Balb/c mice. Time-dependent gene expression data in vivo were obtained using a non-invasive, whole animal bioluminescence imaging system. These data showed that the CLE/DNA complex offered prolonged high-level gene expression for 1 week, particularly in the liver and spleen. On the other hand, the controls of DOTAP/DNA complex and bPEI/DNA complex showed a relatively lower gene expression, because of the unstable and toxic properties of the control carriers. Our in vivo gene expression data demonstrate the potential of the CLE/DNA complex as a non-viral gene carrier for in vivo gene delivery.
    Journal of Controlled Release 06/2008; 128(1):89-97. · 7.63 Impact Factor
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    ABSTRACT: The stargazer (stg) mutant mouse, having mutation in stargazin, the calcium channel gamma2 subunit, exhibited several neurological disorders including spontaneous absence seizure, cerebellar ataxia, and head tossing. To understand the molecular pathogenic mechanism of the absence seizure resulted from the loss of stargazin function, the thalamic proteomes between control mouse and stg mouse were compared. We identified 12 proteins expressed differentially (> 1.6-fold) by fluorescence two-dimensional difference gel electrophoresis and tandem mass spectrometry. Six of them are involved in basic metabolism including energy metabolism, three in stress response, two in axonal growth regulation, and one in the endoplasmic reticulum processing. All except mortalin showed decreased level of expression in stg mouse. Two stress-related proteins, mouse stress induced phosphoprotein 1 and peroxiredoxin 6 exhibited reduced levels of expression in stg mouse, while the level of another stress protein, mortalin was increased. Analysis of oxidative protein carbonylation in thalamic proteome of stg mouse showed higher level of carbonylated proteins in stg mouse than in control mouse. Interestingly, down-regulation of stress protein mouse stress induced phosphoprotein 1, metabolic enzyme isovaleryl-CoA dehydrogenase, and the two in neuronal axon growth, collapsin response mediator protein 2 and fascin homolog 1 coincides with the results of our previous study on gamma-butyrolactone-induced transient absence seizure. Our results suggest that the pathogenesis mechanism underlying absence seizure may involve the molecular events contributed by these proteins.
    Journal of Neurochemistry 03/2008; 104(5):1260-70. · 3.97 Impact Factor
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    ABSTRACT: The biological effects of low-dose radiation have been investigated and debated for more than a century, but its cellular effects and regulatory mechanisms remain poorly understood. This study shows the human cellular responses to low-dose radiation in CCD-18 Lu cells, which are derived from normal human lung fibroblasts. We examined a colony-forming assay for cell survival by ionizing radiation. Live cell counting and cell cycle analysis were measured for cell proliferation and cell cycle progression following low-dose irradiation. We examined Raf and Akt phosphorylation to determine the proliferation mechanism resulting from low-dose radiation. We also observed that p53 and p21 were related to cell cycle response. We found that 0.05 Gy of ionizing radiation enhanced cell proliferation and did not change the progression of the cell cycle. In addition, 0.05 Gy of ionizing radiation transiently activated Raf and Akt, but did not change phospho-p53, p53 and p21 in CCD-18 Lu cells. However, 2 Gy of ionizing radiation induced cell cycle arrest, phosphorylation of p53, and expression of p53 and p21. The phosphorylation of Raf and Akt proteins induced by 0.05 Gy of ionizing radiation was abolished by pre-treatment with an EGFR inhibitor, AG1478, or a PI3k inhibitor, LY294002. Cell proliferation stimulated by 0.05 Gy of ionizing radiation was blocked by the suppression of Raf and Akt phosphorylation with these inhibitors. These results suggest that 0.05 Gy of ionizing radiation stimulates cell proliferation through the transient activation of Raf and Akt in CCD-18 Lu cells.
    Molecules and Cells 01/2008; 24(3):424-30. · 2.21 Impact Factor
  • Journal- Korean Physical Society 01/2008; 52(4). · 0.51 Impact Factor
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    ABSTRACT: We have developed a robotic system for an automated parallel cell cultivation process that enables screening of induction parameters for the soluble expression of recombinant protein. The system is designed for parallelized and simultaneous cultivation of up to 24 different types of cells or a single type of cell at 24 different conditions. Twenty-four culture vessels of about 200 ml are arranged in four columns x six rows. The system is equipped with four independent thermostated waterbaths, each of which accommodates six culture vessels. A two-channel liquid handler is attached in order to distribute medium from the reservoir to the culture vessels, to transfer seed or other reagents, and to take an aliquot from the growing cells. Cells in each vessel are agitated and aerated by sparging filtered air. We tested the system by growing Escherichia coli BL21(DE3) cells harboring a plasmid for a model protein, and used it in optimizing protein expression conditions by varying the induction temperature and the inducer concentration. The results revealed the usefulness of our custom-made cell cultivation robot in screening optimal conditions for the expression of soluble proteins.
    Journal of Microbiology and Biotechnology 12/2007; 17(11):1868-74. · 1.40 Impact Factor
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    ABSTRACT: GCN4 is a typical eukaryotic transcriptional activator that is implicated in the expression of many genes involved in amino acids and purine biosyntheses under stress conditions. It is degraded by 26S proteasomes following ubiquitination. However, the immediate receptor for ubiquitinated Gcn4p has not yet been identified. We investigated whether ubiquitinated Gcn4p binds directly to Rpn10p as the ubiquitinated substrate receptor of the 26S proteasome. We found that the level of Gcn4p increased in cells deleted for Rpn10p but not in cells deleted for RAD23 and DSK2, the other ubiquitinated substrate receptors and, unlike Rpn10p, neither of these proteins recognized ubiquitinated Gcn4p. These results suggest that Rpn10p is the receptor that binds the polyubiquitin chain during ubiquitin-dependent proteolysis of Gcn4p.
    Molecules and Cells 11/2007; 24(2):194-9. · 2.21 Impact Factor
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    ABSTRACT: The native form of serpins (serine protease inhibitors) is a metastable conformation, which converts into a more stable form upon complex formation with a target protease. It has been suggested that movement of helix-F (hF) and the following loop connecting to strand 3 of beta-sheet A (thFs3A) is critical for such conformational change. Despite many speculations inferred from analysis of the serpin structure itself, direct experimental evidence for the mobilization of hF/thFs3A during the inhibition process is lacking. To probe the mechanistic role of hF and thFs3A during protease inhibition, a disulfide bond was engineered in alpha(1)-antitrypsin, which would lock the displacement of thFs3A from beta-sheet A. We measured the inhibitory activity of each disulfide-locked mutant and its heat stability against loop-sheet polymerization. Presence of a disulfide between thFs3A and s5A but not between thFs3A and s3A caused loss of the inhibitory activity, suggesting that displacement of hF/thFs3A from strand 5A but not from strand 3A is required during the inhibition process. While showing little influence on the inhibitory activity, the disulfide between thFs3A and s3A retarded loop-sheet polymerization significantly. This successful protein engineering of alpha(1)-antitrypsin is expected to be of value in clinical applications. Based on our current studies, we propose that the reactive-site loop of a serpin glides through between s5A and thFs3A for the full insertion into beta-sheet A while a substantial portion of the interactions between hF and s3A is kept intact.
    Protein Science 10/2007; 16(9):1842-50. · 2.74 Impact Factor
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    ABSTRACT: This study shows the human cellular responses and the mechanism of low-dose ionizing radiation in CCD 18 Lu cells, which are derived from normal human lung fibroblasts. Cell proliferation and viability assay were measured for the cells following gamma-irradiation using trypan blue, BrdU incorporation, and Wst-1 assay. We also examined genotoxicity using a micronuclei formation assay. The activation of the MAPKs pathway was determined by Western blot analysis, and the siRNA system was used to inhibit the expression of ERK1/2 and p38. We found that 0.05 Gy of ionizing radiation stimulated cell proliferation and did not change Micronuclei frequencies. In addition, 0.05 Gy of ionizing radiation activated ERK1/2 and p38, but did not activate JNK1/2 in cells. A specific ERK1/2 inhibitor, U0126, decreased the phosphorylation of ERK1/2 proteins induced by 0.05 Gy of ionizing radiation, and a similar suppressive effect was observed with a p38 inhibitor, PD169316. Suppression of ERK1/2 and p38 phosphorylation with these inhibitors decreased cell proliferation, which was stimulated by 0.05 Gy of ionizing radiation. Furthermore, downregulation of ERK1/2 and p38 expression using siRNA blocked the cell proliferation that had been increased by 0.05 Gy of ionizing radiation. These results suggest that 0.05 Gy of ionizing radiation enhances cell proliferation through the activation of ERK1/2 and p38 in normal human lung fibroblasts.
    Journal of Radiation Research 10/2007; 48(5):407-15. · 1.45 Impact Factor
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    ABSTRACT: Absence seizure has been of interest because the symptom is related to sensory processing. However, the mechanism that causes the disease is not understood yet. To better understand the molecular mechanism related to the disease progress at protein level, we performed proteomic studies using the thalamus of mice for which absence seizure was induced by gamma-butyrolactone (GBL). Differential proteome expression between GBL-treated mice and control mice was examined by fluorescence 2D difference gel electrophoresis (DIGE) at three different time points (5, 10, and 30 min) after GBL-administration. We identified 16 proteins differentially expressed by >1.4-fold at any of the three time points. All proteins besides the serine protease inhibitor EIA were down-regulated in absence seizure-induced mice. The down-regulated proteins can be classified into five groups by their biological functions: cytoskeleton rearrangement, neuroprotection, neurotransmitter secretion, calcium binding, and metabolism. The maximum level of change was reached by 10 min after GBL-treatment, with the expression level returning back to the original at 30 min when mice were awakened from absence seizure thereby demonstrating the proteomic response is reversible. Our results suggest that absence seizures are associated with restricted functional sets of proteins, whose down-regulation may interfere with general function of neuronal cells.
    Journal of Neurochemistry 09/2007; 102(3):646-56. · 3.97 Impact Factor
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    ABSTRACT: A yeast transcriptional activator, Gcn4p, induces the expression of genes that are involved in amino acid and purine biosynthetic pathways under amino acid starvation. Gcn4p has an acidic activation domain in the central region and a bZIP domain in the C-terminus that is divided into the DNA-binding motif and dimerization leucine zipper motif. In order to identify amino acids in the DNA-binding motif of Gcn4p which are involved in transcriptional activation, we constructed mutant libraries in the DNA-binding motif through an innovative application of random mutagenesis. Mutant library made by oligonucleotides which were mutated randomly using the Poisson distribution showed that the actual mutation frequency was in good agreement with expected values. This method could save the time and effort to create a mutant library with a predictable mutation frequency. Based on the studies using the mutant libraries constructed by the new method, the specific residues of the DNA-binding domain in Gcn4p appear to be involved in the transcriptional activities on a conserved binding site.
    Journal of Microbiological Methods 07/2007; 69(3):442-50. · 2.16 Impact Factor
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    ABSTRACT: A yeast transcriptional activator, Gcn4p, induces the expression of genes that are involved in amino acid and purine biosynthetic pathways under amino acid starvation. Gcn4p has an acidic activation domain in the central region and a bZIP domain in the C-terminus that is divided into the DNA-binding motif and dimerization leucine zipper motif. In order to identify amino acids in the DNA-binding motif of Gcn4p which are involved in transcriptional activation, we constructed mutant libraries in the DNA-binding motif through an innovative application of random mutagenesis. Mutant library made by oligonucleotides which were mutated randomly using the Poisson distribution showed that the actual mutation frequency was in good agreement with expected values. This method could save the time and effort to create a mutant library with a predictable mutation frequency. Based on the studies using the mutant libraries constructed by the new method, the specific residues of the DNA-binding domain in Gcn4p appear to be involved in the transcriptional activities on a conserved binding site.
    Journal of Microbiological Methods 07/2007; 69(3):442-50. · 2.16 Impact Factor
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    ABSTRACT: The 26S proteasome, composed of the 20S core and 19S regulatory complexes, is important for the turnover of polyubiquitinated proteins. Each subunit of the complex plays a special role in proteolytic function, including substrate recruitment, deubiquitination, and structural contribution. To assess the function of some non-essential subunits in the 26S proteasome, we isolated the 26S proteasome from deletion strains of RPN13 and RPN14 using TAP affinity purification. The stability of Gcn4p and the accumulation of ubiquitinated Gcn4p were significantly increased, but the affinity in the recognition of proteasome was decreased. In addition, the subcomplexes of the isolated 26S proteasomes from deletion mutants were less stable than that of the wild type. Taken together, our findings indicate that Rpn13p and Rpn14p are involved in the efficient recognition of 26S proteasome for the proteolysis of ubiquitinated Gcn4p.
    FEBS Letters 06/2007; 581(13):2567-73. · 3.58 Impact Factor
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    ABSTRACT: PEN-2 is a component of the gamma-secretase complex, which is involved in the cleavage of the beta-amyloid precursor protein. The aim of this study was to determine the mechanism by which PEN-2 overexpression regulates gamma-secretase expression and the production of Abeta-42. In order to determine this, a hybrid gene harboring human PEN-2 was constructed, and used in the transfection of SK-N-MC human neuroepitheliomal cells. This cell line was also co-transfected with a combination of human mutant presenilin 2 (hPS2m) and APPsw. Our results indicated that (i) human PEN-2 overexpression induced an increase in gamma-secretase activity and its proteins, including PS1-CTF, APH-1, and nicastrin, thus production of Abeta-42, (ii) co-transfection of human PEN-2 with both hPS2m and APPsw exerted no more profound effects on the induction of gamma-secretase proteins and its activity than did transfection with hPEN-2 alone. Thus, PEN-2 overexpression may facilitate assembly into the more active gamma-secretase complex, and may also induce an increase in activity, thus affecting Abeta-42 production.
    Neurochemical Research 06/2007; 32(6):1016-23. · 2.13 Impact Factor
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    ABSTRACT: UV irradiation has been reported to induce p21(WAF1/CIP1) protein degradation through a ubiquitin-proteasome pathway, but the underlying biochemical mechanism remains to be elucidated. Here, we show that ser-114 phosphorylation of p21 protein by glycogen synthase kinase 3beta (GSK-3beta) is required for its degradation in response to UV irradiation and that GSK-3beta activation is a downstream event in the ATR signaling pathway triggered by UV. UV transiently increased GSK-3beta activity, and this increase could be blocked by caffeine or by ATR small interfering RNA, indicating ATR-dependent activation of GSK-3beta. ser-114, located within the putative GSK-3beta target sequence, was phosphorylated by GSK-3beta upon UV exposure. The nonphosphorylatable S114A mutant of p21 was protected from UV-induced destabilization. Degradation of p21 protein by UV irradiation was independent of p53 status and prevented by proteasome inhibitors. In contrast to the previous report, the proteasomal degradation of p21 appeared to be ubiquitination independent. These data show that GSK-3beta is activated by UV irradiation through the ATR signaling pathway and phosphorylates p21 at ser-114 for its degradation by the proteasome. To our knowledge, this is the first demonstration of GSK-3beta as the missing link between UV-induced ATR activation and p21 degradation.
    Molecular and Cellular Biology 05/2007; 27(8):3187-98. · 5.04 Impact Factor
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    ABSTRACT: The consequences of ultraviolet (UV) exposure are implicated in skin aging and cell death. The ribosomal protein S3 (rpS3) is one of the major proteins by which cells counteract the deleterious effects of UV and it plays a role in the repair of damaged DNA. In the present study, we investigated the protective effects of PEP-1-rpS3 fusion protein after UV-induced cell injury. A human rpS3 gene was fused with PEP-1 peptide in a bacterial expression vector to produce a genetic in-frame PEP-1-rpS3 fusion protein. The expressed and purified fusion proteins were efficiently transduced into skin cells in a time- and dose-dependent manner. Once inside the cells, transduced PEP-1-rpS3 fusion protein was stable for 48h. We showed that transduced PEP-1-rpS3 fusion protein increased cell viability and dramatically reduced DNA lesions in the UV exposed skin cells. Immunohistochemical analysis revealed that PEP-1-rpS3 fusion protein efficiently penetrated the epidermis as well as the dermis of the subcutaneous layer when sprayed on animal skin. These results suggest that PEP-1-rpS3 fusion protein can be used in protein therapy for various disorders related to UV, including skin aging and cancer.
    FEBS Letters 01/2007; 580(30):6755-62. · 3.58 Impact Factor
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    ABSTRACT: Nuclear magnetic resonance has been employed as a probe for the collective hydrocarbon chain dynamics in the organic–inorganic model biomembranes (CnH2n+1NH3)2SnCl6, undergoing order–disorder and conformational phase transitions. No anomalies were observed in the laboratory-frame spin–lattice relaxation measurements at the order–disorder phase transitions, whereas a discontinuity was manifest at the conformational phase transitions characteristic of a first-order phase transition. On the other hand, our rotating frame spin–lattice relaxation measurements revealed a low-frequency critical collective chain dynamics in the kilohertz regime associated with the order–disorder phase transition.
    Current Applied Physics 01/2007; 7(1):31-33. · 2.03 Impact Factor
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    ABSTRACT: In this work, systematic X-band electron magnetic resonance (EMR) studies for YMnO3/Si ferroelectric gate structures were performed to trace a variation of interface characteristics as different sputtering condition of O2/(Ar+O2) ratio. Our result showed that the EMR signal intensities were increased with increasing O2/(Ar+O2) ratio. In addition, it was suggested from detailed analyses that the observed EMR signals could be originated from Mn nanoclusters existing in both the polycrystalline Y2O3 layer and the amorphous Si-enriched Y–Si interface layer in YMnO3/Si thin film structure. And also, a correlation between the decrease of crystallinity in YMnO3/Si film and the content of Mn nanoclusters within the polycrystalline Y2O3 layer and/or the amorphous Y–Si layer was discussed.
    Current Applied Physics - CURR APPL PHYS. 01/2007; 7(1):10-12.
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    Sang Hwa Kim, Joon Kim
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    ABSTRACT: RpS3 is a component of the 40S ribosomal subunit of eukaryotes and also plays a role as a base damage endonuclease. Nm23-H1 encodes nucleoside diphosphate kinase A and acts as a suppressor of metastasis in certain human tumors. RpS3 interacted with nm23-H1, and the two proteins were colocalized in the cell periphery and cytoplasm. The 190th leucine of rpS3, and the 118th histidine and the 120th serine of nm23-H1 play key roles in the interaction of two proteins, respectively. The expression of rpS3 reduced the secretion of MMP-9 and the invasive potential in HT1080 cells. Additionally, the phosphorylated ERK was reduced by the expression of rpS3. In MCF7 cells, where the ERK pathway is inactivated and MMPs are not secreted and the ERK pathway can be activated by PMA, the PMA-induced ERK phosphorylation was reduced by the expression of rpS3. However, the L190A mutant of rpS3, which did not interact with nm23-H1, did not inhibit the invasive potential, the secretion of MMP-9, and the activation of the ERK pathway in HT1080 cells and PMA-activated MCF7 cells. These results suggest that rpS3 inhibits invasion via blocking the ERK pathway and MMP-9 secretion; the results also suggest that the interaction of rpS3 and nm23-H1 appears to be critical in this inhibition.
    Biochimica et Biophysica Acta 09/2006; 1763(8):823-32. · 4.66 Impact Factor
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    ABSTRACT: The hepatitis B virus core protein consists of an amino-terminal capsid-assembly domain and a carboxyl-terminal RNA-binding domain. By using the yeast two-hybrid system, two Hsp40/DnaJ chaperone-family proteins, Hdj1 and hTid1, that interact with the carboxyl-terminal region (aa 94-185) of the core protein were identified. Hdj1 is the prototype member of the family and hTid1 is the human homologue of the Drosophila tumour-suppressor protein Tid56. Binding of the viral core protein with the Hsp40 proteins was confirmed by affinity chromatography and immunoprecipitation of transiently expressed proteins. Moreover, in a sucrose gradient, the precursor form of hTid1 co-sedimented with capsid-like particles composed of the full-length core protein. Unlike the general perception of the role of the cellular chaperone proteins in assisting viral protein folding and thus enhancing virus replication, ectopic expression of Hdj1 and hTid1 suppressed replication of HBV in transfected human hepatoma cells. Conversely, RNA interference-mediated knock-down of hTid1 resulted in increased HBV replication. It was found that both Hsp40 proteins specifically accelerated degradation of the viral core and HBx proteins. Our results suggest that the cellular chaperones, through destabilization of viral proteins, exert inhibitory functions on virus replication and hence may play suppressive roles in hepatocellular carcinoma.
    Journal of General Virology 08/2006; 87(Pt 7):1883-91. · 3.13 Impact Factor

Publication Stats

915 Citations
258.87 Total Impact Points

Institutions

  • 2002–2013
    • Korea University
      • • Department of Life Sciences
      • • Department of Physics
      Sŏul, Seoul, South Korea
  • 2012
    • Sookmyung Women's University
      • College of Pharmacy
      Seoul, Seoul, South Korea
  • 2007–2012
    • Radiation Health Research Institute
      Sŏul, Seoul, South Korea
  • 2006–2012
    • Hallym University
      • College of Medicine
      Seoul, Seoul, South Korea
  • 2004–2010
    • Korea Institute of Science and Technology
      • • Center for Functional Connectomics
      • • Biomedical Research Institute
      Seoul, Seoul, South Korea
  • 2009
    • University of Seoul
      Sŏul, Seoul, South Korea
  • 2008
    • Pusan National University
      • Department of Biological Sciences
      Pusan, Busan, South Korea