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CNBP acts as a key transcriptional regulator of sustained expression of interleukin-6
Lee, Eunhye,Lee, Taeyun A.,Kim, Ji Hyun,Park, Areum,Ra, Eun A.,Kang, Sujin,Choi, Hyun jin,Choi, Junhee L.,Huh, Hyunbin D.,Lee, Ji Eun,Lee, Sungwook,Park, Boyoun Oxford University Press 2017 Nucleic acids research Vol.45 No.6
<P><B>Abstract</B></P><P>The transcription of inflammatory genes is an essential step in host defense activation. Here, we show that cellular nucleic acid-binding protein (CNBP) acts as a transcription regulator that is required for activating the innate immune response. We identified specific CNBP-binding motifs present in the promoter region of sustained inflammatory cytokines, thus, directly inducing the expression of target genes. In particular, lipopolysaccharide (LPS) induced <I>cnbp</I> expression through an NF-κB-dependent manner and a positive autoregulatory mechanism, which enables prolonged <I>il-6</I> gene expression. This event depends strictly on LPS-induced CNBP nuclear translocation through phosphorylation-mediated dimerization. Consequently, <I>cnbp</I>-depleted zebrafish are highly susceptible to <I>Shigella flexneri</I> infection <I>in vivo</I>. Collectively, these observations identify CNBP as a key transcriptional regulator required for activating and maintaining the immune response.</P>
Lee, Siyoung,Kim, Eunsom,Jhun, Hyunjhung,Hong, Jaewoo,Kwak, Areum,Jo, Seunghyun,Bae, Suyoung,Lee, Jongho,Kim, Busun,Lee, Jungmin,Youn, Sulah,Kim, Somi,Kim, Miyeon,Kim, Hyunwoo,Lee, Youngmin,Choi, Dong American Society for Biochemistry and Molecular Bi 2016 The Journal of biological chemistry Vol.291 No.28
<P>Although it has been established that diabetes increases susceptibility to infections, the role of insulin (INS) in the immune response is unknown. Here, we investigated the immunological function of INS. Proinsulin dimer (pINSd) was a potent immune stimulus that induced inflammatory cytokines, but mature INS was unable to induce an immune response. An affinity-purified rabbit polyclonal antibody raised against mature IL-1α recognized IL-1α and pINS but failed to detect mature INS and IL-1β. Analysis of the pINS sequence revealed the existence of an INS/IL-1α motif in the C-peptide of pINS. Surprisingly, the INS/IL-1α motif was recognized by monoclonal antibody raised against IL-1α. Deleting the INS/IL-1α motif in pINSd and IL-1α changed their activities. To investigate the pINSd receptor, the reconstitution of IL-1 receptor 1 (IL-1R1) in Wish cells restored pINSd activity that was reversed by an IL-1R antagonist. These data suggested that pINSd needs IL-1R1 for inflammatory cytokine induction. Mouse embryo fibroblast cells of IL-1R1-deficient mice further confirmed that pINSd promotes immune responses through IL-1R1.</P>
Suicidal Ideation of the Elderly According to Their Involvement in Grandchild Care
Jeewon Lee,Areum Lee,Doeun Lee,Han-Young Jung,Shin-gyeom Kim,Soyoung Irene Lee 대한신경정신의학회 2019 PSYCHIATRY INVESTIGATION Vol.16 No.8
The purpose of the present study was to examine the severity of suicidal ideation of the older adults according to the amount of involvement in grandchild care. Data for this research were drawn from a cross-sectional study conducted on community-dwelling adults aged 65 years or older. The 922 participants were divided into three groups according to their involvement in grandchild care: 18.5% had provided daily care, 12.4% had provided occasional care, and 69.1% had never cared for their grandchildren. ANCOVA analysis showed that the scores for depression was significantly lower in the group which took care of their grandchildren occasionally compared to the other two groups. The scores for suicidal ideation was significantly higher in the group which had never taken care of their grandchildren compared to the other two groups. Current study suggests that grandparenting may have a positive effect on suicidal ideation of the older adults.
Impact of sleep restriction on the structural brain network
Lee, Min-Hee,Lee, Youngjin,Hwang, Yoon Ho,Min, Areum,Han, Bong Soo,Kim, Dong Youn Wolters Kluwer Health | Lippincott Williams Wilkin 2016 NEUROREPORT - Vol.27 No.18
<P>Sleep restriction (SR) is defined as the condition of not having enough sleep, and it can cause brain injury. In this study, we examined the impact of SR on the structural brain network. We obtained diffusion MRI (dMRI) data for the SR group of fourteen participants who got less than or equal to 5.5 h of sleep for the last 1 month and normal group of the same number of participants who got 7 h of sleep. We constructed the structural brain networks from the dMRI data and analyzed them using graph theoretical approaches. In comparison with the normal group, the SR group showed higher vulnerability to the targeted node attack and alterations of regional efficiency in the brain regions such as the bilateral orbital part of the frontal gyri, superior occipital gyri, left insula, fusiform, right supplementary motor area, and cingulate gyrus. These findings indicate that SR may cause the reduction of the potential alternative neuronal pathways in the brain and rewiring of neuronal fibers in the structural brain networks, which may result in potential functional impairments, as well as alterations of the structural brain connectivity. Therefore, investigating the structural brain network offers new insight into how SR influences the human brain. Copyright (C) 2016 Wolters Kluwer Health, Inc. All rights reserved.</P>
Lee, Siyoung,Choi, Dong-Ki,Kwak, Areum,Kim, Sinae,Nguyen, Tam Thanh,Gil, Gaae,Kim, Eunhye,Yoo, Kwang Ha,Kim, In Ae,Lee, Youngmin,Jhun, Hyunjhung,Chan, Edward D.,Bai, Xiyuan,Kim, Hyunwoo,Kim, Yong-Sung 한국조명·전기설비학회 2017 한국조명·전기설비학회 학술대회논문집 Vol. No.
<P>The induction of interleukin (IL)-32 in bone marrow (BM) inflammation is crucial in graft versus host disease (GvHD) that is a common side effect of allogeneic BM transplantation. Clinical trials on α-1 antitrypsin (AAT) in patients with GvHD are based on the preliminary human and mouse studies on AAT reducing the severity of GvHD. Proteinase 3 (PR3) is an IL-32-binding protein that was isolated from human urine. IL-32 primarily induces inflammatory cytokines in myeloid cells, probably due to PR3 expression on the membrane of the myeloid lineage cells. The inhibitory activity of AAT on serine proteinases may explain the anti-inflammatory effect of AAT on GvHD. However, the anti-inflammatory activity of AAT on BM cells remains unclear. Mouse BM cells were treated with IL-32γ and different inflammatory stimuli to investigate the anti-inflammatory activity of AAT. Recombinant AAT-Fc fusion protein inhibited IL-32γ-induced IL-6 expression in BM cells, but failed to suppress that induced by other stimuli. In addition, the binding of IL-32γ to PR3 was abrogated by AAT-Fc. The data suggest that the specific anti-inflammatory effect of AAT in mouse BM cells is due to the blocking of IL-32 binding to membrane PR3.</P>
Lee, Areum,Lee, Sang Sook,Jung, Won Yong,Park, Hyun Ji,Lim, Bo Ra,Kim, Hyun-Soon,Ahn, Jun Cheul,Cho, Hye Sun MDPI 2016 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Vol.17 No.7
<P>Alternative splicing (AS) is an important molecular mechanism by which single genes can generate multiple mRNA isoforms. We reported previously that, in <I>Oryza sativa</I>, the <I>cyclophilin 19-4</I> (<I>OsCYP19-4.1</I>) transcript was significantly upregulated in response to cold stress, and that transgenic plants were cold tolerant. Here we show that, under cold stress, <I>OsCYP19-4</I> produces eight transcript variants by intron retention and exon skipping, resulting in production of four distinct protein isoforms. The OsCYP19-4 AS isoforms exhibited different cellular localizations in the epidermal cells: in contrast to OsCYP19-4.1, the OsCYP19-4.2 and OsCYP19-4.3 proteins were primarily targeted to guard and subsidiary cells, whereas OsCYP19-4.5, which consists largely of an endoplasmic reticulum (ER) targeting signal, was co-localized with the RFP-BiP marker in the ER. In OsCYP19-4.2, the key residues of the PPIase domain are altered; consistent with this, recombinant OsCYP19-4.2 had significantly lower PPIase activity than OsCYP19-4.1 in vitro. Specific protein-protein interactions between OsCYP19-4.2/3 and AtRCN1 were verified in yeast two-hybrid (Y2H) and bimolecular fluoresence complementation (BiFC assays), although the OsCYP19-4 isoforms could not bind each other. Based on these results, we propose that two OsCYP19-4 AS isoforms, OsCYP19-4.2 and OsCYP19-4.3, play roles linking auxin transport and cold stress via interactions with RCN1.</P>
Engineering of Sulfolobus acidocaldarius for Hemicellulosic Biomass Utilization
( Areum Lee ),( Hyeju Jin ),( Jaeho Cha ) 한국미생물생명공학회 2022 Journal of microbiology and biotechnology Vol.32 No.5
The saccharification of cellulose and hemicellulose is essential for utilizing lignocellulosic biomass as a biofuel. While cellulose is composed of glucose only, hemicelluloses are composed of diverse sugars such as xylose, arabinose, glucose, and galactose. Sulfolobus acidocaldarius is a good potential candidate for biofuel production using hemicellulose as this archaeon simultaneously utilizes various sugars. However, S. acidocaldarius has to be manipulated because the enzyme that breaks down hemicellulose is not present in this species. Here, we engineered S. acidocaldarius to utilize xylan as a carbon source by introducing xylanase and β-xylosidase. Heterologous expression of β-xylosidase enhanced the organism’s degradability and utilization of xylooligosaccharides (XOS), but the mutant still failed to grow when xylan was provided as a carbon source. S. acidocaldarius exhibited the ability to degrade xylan into XOS when xylanase was introduced, but no further degradation proceeded after this sole reaction. Following cell growth and enzyme reaction, S. acidocaldarius successfully utilized xylan in the synergy between xylanase and β-xylosidase.