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Chwae, Yong‐,Joon,Lee, Jae Myun,Kim, Eun Joon,Lee, Seung Tae,Soh, Jae‐,Won,Kim, Jongsun Nature Publishing Group 2007 Immunology and Cell Biology Vol.85 No.3
<P>Inhibitory killer Ig‐like receptor (KIR) expression was upregulated by protein kinase C (PKC) activation in stable Jurkat clones that express KIR or CD8KIR fusion proteins. PKC‐induced KIR upregulation was mediated by the cytoplasmic tail of KIR and regulated at the post‐transcriptional level. PKC inhibition, metabolic labeling and colocalization studies demonstrated that the activation of the conventional PKCs upregulated surface and cellular KIR levels by stimulating the maturation processes in endoplasmic reticulum–Golgi and by promoting the recycling of surface KIR through sorting endosomes. Similar studies also revealed that KIR was secreted to plasma membrane through lytic granules in a PKC<I>δ</I>‐dependent manner. Consequently, PKC<I>δ</I> inhibition caused the formation of giant perinuclear granules, which trapped KIR and FasL as well as CPE and Lamp1.</P>
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Association of Killer Cell Ig-like Receptor (KIR) with an Adaptor Protein Shc
Cho, Hyun-Il,Chwae, Yong-Joon,Park, Sang-Myun,Kim, Jong-Sun The Korean Association of Immunobiologists 2006 Immune Network Vol.6 No.2
Background: Cytotoxic function of killer cells is inhibited by specific recognition of class I MHC molecules on target cells by inhibitory killer Ig-like receptors (KIR) expressed on NK cells and some cytotoxic T cells. The inhibitory effect of KIR is accomplished by recruitment of SH2-containing protein tyrosine phosphatase (SHP) to the phosphotyrosine residues in the cytoplasmic tail. Methods: By in vitro coprecipitation experiments and transfection analysis, we investigated the association of KIR with an adaptor protein Shc in Jurkat T cells. Results: The cytoplasmic tail of KIR appeared to associate with an adaptor protein Shc in Jurkat T celilysates. Similar in vitro experiments showed that phosphorylated KIR cytoplasmic tail bound SHP-1 and Shc in Jurkat T cell lysates. The association of KIR with Shc was further confirmed by transfection analysis in 293T cells. Interestingly, however, Shc appeared to be replaced by SHP-2 upon engagement of KIR in 293T cells. Conclusion: Our data indicate that KIR associate with an adaptor protein Shc in Jurkat T cells, and suggest that KIR might have an additional role which is mediated by this adaptor protein.
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Jung, Jaesung,Hwang, Seong Gyu,Chwae, Yong-Joon,Park, Sun,Shin, Ho-Joon,Kim, Kyongmin American Society for Microbiology 2014 Journal of virology Vol.88 No.16
<P>Phosphorylation of serines 157, 164, and 172 within the carboxyl-terminal SPRRR motif of the hepatitis B virus (HBV) core (C) protein modulates HBV replication at multiple stages. Threonine 162 and serines 170 and 178, located within the carboxyl-terminal conserved RRRS/T motif of HBV C protein, have been proposed to be protein kinase A phosphorylation sites. However, <I>in vivo</I> phosphorylation of these residues has never been observed, and their contribution to HBV replication remains unknown. In this study, [<SUP>32</SUP>P]orthophosphate labeling of cells expressing C proteins followed by immunoprecipitation with anti-HBc antibody revealed that threonine 162 and serines 170 and 178 are phosphoacceptor residues. A triple-alanine-substituted mutant, mimicking dephosphorylation of all three residues, drastically decreased pregenomic RNA (pgRNA) encapsidation, thereby decreasing HBV DNA synthesis. In contrast, a triple-glutamate-substituted mutant, mimicking phosphorylation of these residues, decreased DNA synthesis without significantly decreasing encapsidation. Neither triple mutant affected C protein expression or core particle assembly. Individual alanine substitution of threonine 162 significantly decreased minus-strand, plus-strand, and relaxed-circular DNA synthesis, demonstrating that this residue plays multiple roles in HBV DNA synthesis. Double-alanine substitution of serines 170 and 178 reduced HBV replication at multiple stages, indicating that these residues also contribute to HBV replication. Thus, in addition to serines 157, 164, and 172, threonine 162 and serines 170 and 178 of HBV C protein are also phosphorylated in cells, and phosphorylation and dephosphorylation of these residues play multiple roles in modulation of HBV replication.</P><P><B>IMPORTANCE</B> Threonine 162, within the carboxyl-terminal end of the hepatitis B virus (HBV adw) core (C) protein, has long been ignored as a phosphoacceptor, even though it is highly conserved among mammalian hepadnaviruses and in the overlapping consensus RxxS/T, RRxS/T, and TP motifs. Here we show, for the first time, that in addition to the well-known phosphoacceptor serines 157, 164, and 172 in SPRRR motifs, threonine 162 and serines 170 and 178 in the RRRS/T motif are phosphorylated in cells. We also show that, like serines 157, 164, and 172, phosphorylated and dephosphorylated threonine 162 and serines 170 and 178 contribute to multiple steps of HBV replication, including pgRNA encapsidation, minus-strand and plus-strand DNA synthesis, and relaxed-circular DNA synthesis. Of these residues, threonine 162 is the most important. Furthermore, we show that phosphorylation of C protein is required for efficient completion of HBV replication.</P>
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Jo, Guk Heui,Bö,gler, Oliver,Chwae, Yong-Joon,Yoo, Heon,Lee, Seung Hoon,Park, Jong Bae,Kim, Youn-Jae,Kim, Jong Heon,Gwak, Ho-Shin Korean Cancer Association 2015 Cancer Research and Treatment Vol.47 No.2
<P><B>Purpose</B></P><P>Radiation-induced autophagy has been shown to play two different roles, in malignant glioma (MG) cells, cytocidal or cytoprotective. However, neither the role of radiation-induced autophagy for cell death nor the existence of autophagy-induced apoptosis, a well-known cell-death pathway after irradiation, has been verified yet.</P><P><B>Materials and Methods</B></P><P>We observed both temporal and dose-dependent response patterns of autophagy and apoptosis to radiation in MG cell lines. Additionally, we investigated the role of autophagy in apoptosis through knockdown of autophagy-related proteins.</P><P><B>Results</B></P><P>Autophagic activity measured by staining of acidic vesicle organelles and Western blotting of LC-3 protein increased in proportion to radiation dose from day 1 to 5 after irradiation. Apoptosis measured by annexin-V staining and Western blotting of cleaved poly(ADP-ribose) polymerase demonstrated relatively late appearance 3 days after irradiation that increased for up to 7 days. Blocking of pan-caspase (Z-VAD-FMK) did not affect apoptosis after irradiation, but silencing of Atg5 effectively reduced radiation-induced autophagy, which decreased apoptosis significantly. Inhibition of autophagy in Atg5 knockdown cells was shown to be beneficial for cell survival. Stable transfection of GFP-LC3 cells was observed after irradiation. Annexin-V was localized in cells bearing GFP-LC3 punctuated spots, indicating autophagy in immunofluorescence. Some of these punctuated GFP-LC3 bearing cells formed conglomerated spots and died in final phase.</P><P><B>Conclusion</B></P><P>These findings suggest that autophagy appears earlier than apoptosis after irradiation and that a portion of the apoptotic population that appears later is autophagy-dependent. Thus, autophagy is a pathway to cell death after irradiation of MG cells.</P>
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( Zahra Zahid Piracha ),( Hyun Woong Lee ),( Umar Saeed ),( Jumi Kim ),( Hyeonjoong Kwon ),( Yong-joon Chwae ),( Jin Hong Lim ),( Sun Park ),( Ho-joon Shin ),( Kyongmin Kim ) 대한간학회 2020 춘·추계 학술대회 (KASL) Vol.2020 No.1
Aims: Sirtuin 2 (Sirt2), an NAD+-dependent protein deacetylase, deacetylates tubulin, AKT, and other proteins. Previously, we showed that Sirt2 isoform 1 (Sirt2.1) increased replication of hepatitis B virus (HBV). Methods: Here, we show that HBV replication upregulates expression of Sirt2 primary and alternatively spliced transcripts, and their respective isoforms 1, 2, and 5. Since Sirt2 isoform 5 (Sirt2.5) is a catalytically inactive nuclear protein with a splicedout nuclear export signal (NES), we speculated that its different localization may affect its activity. Results: Overexpression of Sirt2.5 reduced expression of HBV mRNAs, replicative intermediate DNAs, and covalently closed circular DNA (cccDNA), an activity opposite to that of Sirt2.1 and Sirt2.2. Unlike the Sirt2.1-AKT interaction, the Sirt2.5-AKT interaction was weakened by HBV replication. Unlike Sirt2.1, Sirt2.5 activated the AKT/GSK-3ß/ß-catenin signaling pathway very weakly and independently of HBV replication. When the NES and an N-terminal truncated catalytic domain were added to the Sirt2.5 construct, it localized in the cytoplasm and increased HBV replication (like Sirt2.1 and Sirt2.2). Chromatin immunoprecipitation assays revealed that more Sirt2.5 was recruited to cccDNA than Sirt2.1. Also, recruitment of histone lysine methyltransferases (HKMTs) such as SETDB1 and SUV39H1, EZH2, and PR-Set7, and their respective transcriptional repressive markers H3K9me3, H3K27me3, and H4K20me1, to cccDNA increased in Sirt2.5-overexpressing cells. Among these, the Sirt2.5-PR-Set7 and -SETDB1 interactions increased upon HBV replication. Conclusions: These results demonstrate that Sirt2.5 reduces cccDNA levels and viral transcription through epigenetic modification of cccDNA via direct and/or indirect association with HKMTs, thereby exhibiting anti-HBV activity.
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Kim, Jong-Hyun,Sohn, Hae-Jin,Lee, Jinyoung,Yang, Hee-Jong,Chwae, Yong-Joon,Kim, Kyongmin,Park, Sun,Shin, Ho-Joon American Society for Microbiology 2013 Clinical and vaccine immunology Vol.20 No.7
<P><I>Naegleria fowleri</I>, a pathogenic free-living amoeba, causes fatal primary amoebic meningoencephalitis (PAM) in humans and animals. The <I>nfa1</I> gene (360 bp), cloned from a cDNA library of <I>N. fowleri</I>, produces a 13.1-kDa recombinant protein which is located on pseudopodia, particularly the food cup structure. The <I>nfa1</I> gene plays an important role in the pathogenesis of <I>N. fowleri</I> infection. To examine the effect of <I>nfa1</I> DNA vaccination against <I>N. fowleri</I> infection, we constructed a lentiviral vector (pCDH) expressing the <I>nfa1</I> gene. For the <I>in vivo</I> mouse study, BALB/c mice were intranasally vaccinated with viral particles of a viral vector expressing the <I>nfa1</I> gene. To evaluate the effect of vaccination and immune responses of mice, we analyzed the IgG levels (IgG, IgG1, and IgG2a), cytokine induction (interleukin-4 [IL-4] and gamma interferon [IFN-γ]), and survival rates of mice that developed PAM. The levels of both IgG and IgG subclasses (IgG1 and IgG2a) in vaccinated mice were significantly increased. The cytokine analysis showed that vaccinated mice exhibited greater IL-4 and IFN-γ production than the other control groups, suggesting a Th1/Th2 mixed-type immune response. In vaccinated mice, high levels of Nfa1-specific IgG antibodies continued until 12 weeks postvaccination. The mice vaccinated with viral vector expressing the <I>nfa1</I> gene also exhibited significantly higher survival rates (90%) after challenge with <I>N. fowleri</I> trophozoites. Finally, the <I>nfa1</I> vaccination effectively induced protective immunity by humoral and cellular immune responses in <I>N. fowleri</I>-infected mice. These results suggest that DNA vaccination using a viral vector may be a potential tool against <I>N. fowleri</I> infection.</P>
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The immune response induced by DNA vaccine expressing nfa1 gene against Naegleria fowleri
Kim, Jong-Hyun,Lee, Sang-Hee,Sohn, Hae-Jin,Lee, Jinyoung,Chwae, Yong-Joon,Park, Sun,Kim, Kyongmin,Shin, Ho-Joon Springer-Verlag 2012 Parasitology research Vol.111 No.6
<P>The pathogenic free-living amoeba, Naegleria fowleri, causes fatal primary amoebic meningoencephalitis in experimental animals and in humans. The nfa1 gene that was cloned from N. fowleri is located on pseudopodia, especially amoebic food cups and plays an important role in the pathogenesis of N. fowleri. In this study, we constructed and characterized retroviral vector and lentiviral vector systems for nfa1 DNA vaccination in mice. We constructed the retroviral vector (pQCXIN) and the lentiviral vector (pCDH) cloned with the egfp-nfa1 gene. The expression of nfa1 gene in Chinese hamster ovary cell and human primary nasal epithelial cell transfected with the pQCXIN/egfp-nfa1 vector or pCDH/egfp-nfa1 vector was observed by fluorescent microscopy and Western blotting analysis. Our viral vector systems effectively delivered the nfa1 gene to the target cells and expressed the Nfa1 protein within the target cells. To evaluate immune responses of nfa1-vaccinated mice, BALB/c mice were intranasally vaccinated with viral particles of each retro- or lentiviral vector expressing nfa1 gene. DNA vaccination using viral vectors expressing nfa1 significantly stimulated the production of Nfa1-specific IgG subclass, as well as IgG levels. In particular, both levels of IgG2a (Th1) and IgG1 (Th2) were significantly increased in mice vaccinated with viral vectors. These results show the nfa1-vaccination induce efficiently Th1 type, as well as Th2 type immune responses. This is the first report to construct viral vector systems and to evaluate immune responses as DNA vaccination in N. fowleri infection. Furthermore, these results suggest that nfal vaccination may be an effective method for treatment of N. fowleri infection.</P>
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