• Journal of Microbiology and Biotechnology
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• 제1권2호
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• pp.96-101
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• 1991

Phenotypic changes after plasmid curing experiment suggested that the bacteriocin production phenotype ($Bac^{+}$) might be linked to a chromosomal DNA and the mucin production phenotype ($Muc^{+}$) might be linked to a 62.5 kilobase (kb) plasmid (pMUC62) in Lactobacillus plantarum 27 isolated from meat starter culture. The non-mucoid ($Muc^{-}$) variants were missing pMUC62 but they produced bacteriocin as the wild strain ($Bac^{+}$). There was no difference in antibiotic resistance and sugar fermentation patterns between the wild strain ($Bac^{+}$ $Muc^{+}$) and the nonmucoid ($Bac^{+}$ $Muc^{-}$) variants. Antimicrobial spectrum of bacteriocin produced by both wild strain and $Muc^{-}$ variant of Lb. plantarum 27 included strains of Pediococcus acidilactici (A, M, H), Pediococcus sp. isolated from meat, Lactobacillus sp. isolated from meat, Lb. plantarum NCDO 955 and Staphylococcus aureus 485. Neither of the tested Gram negative bacteria were inhibited by bacteriocin. Antimicrobial activity of crude bacteriocin was retained after autoclaving, DNase or catalase treatment and exposure from pHs 4 to 9 but was lost after treating with several proteolytic enzymes and exposure at pH 10.

• Plant Breeding and Biotechnology
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• 제5권4호
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• pp.363-370
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• 2017

In this study, Quercus acutissima seedlings were subjected to drought for 30 days then analyzed to determine their response to water deficit. The growth phenotype, chlorophyll fluorescence response, fresh weight, dry weight, photosynthetic pigment levels, soluble sugar content, and malondialdehyde (MDA) were measured to evaluate the effects of drought on plant growth and physiology. The growth phenotype was observed by infrared (IR) digital thermal imaging after 30 days of drought treatment. The maximum, average, and minimum temperatures of drought-treated plant leaves were $1-2^{\circ}C$ higher than those of the control. In contrast, the fresh and dry weights of the dehydrated leaves were generally lower than those of the control. There were no significant differences between treatments in terms of chlorophyll a, chlorophyll b, total chlorophyll, and carotenoid levels. Nevertheless, for the drought treatment, the $F_v/F_m$ and $F_v/F_o$ ratios (chlorophyll fluorescence response) were lower than those for the control. Therefore, photosynthetic activity was lower in the dehydrated plants than the control. The drought-stressed Q. acutissima S0536 had lower soluble sugar (glucose and fructose) and higher MDA levels than the controls. These findings may explain the early growth and physiological responses of Q. acutissima to dehydration and facilitate the selection of drought-resistant tree families.

• 한국작물학회:학술대회논문집
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• 한국작물학회 2017년도 9th Asian Crop Science Association conference
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• pp.174-174
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• 2017

To cope with phosphate (Pi) deficient stress, plants modulate various physiological and developmental processes, such as gene expression, Pi uptake and translocation, and root architecture changes. Here, we report the identification and characterization of novel activation-tagged mutant involved in Pi starvation signaling in Arabidopsis. The hpd (${\underline{h}ypersensitive}$ to ${\underline{P}i}$ $ {\underline{d}eficiency}$) mutant exhibits enhanced phosphate uptake and altered root architectural change under Pi starvation compared to wild type. Expression analysis of auxin-responsive DR5::GUS reporter gene in hpd mutant indicated that auxin translocation in roots under Pi starvation are suppressed in hpd mutant plants. Impaired auxin translocation in roots of hpd mutant was attributable to abnormal root architecture changes in Pi starvation conditions. Our results indicated that abnormal auxin translocation in hpd mutant might be due to mis-regulation of auxin efflux carrier proteins, PIN-FORMED (PIN) 1, and 2 under Pi starvation conditions. Not only expression levels but also expression domains of PIN proteins were altered in hpd mutant in response to Pi starvation. Molecular genetic analysis of hpd mutant revealed that the mutant phenotype is caused by the lesion in ENHANCED SILENCING PHENOTYPE4 (ESP4) gene whose function is proposed in mRNA 3'-end processing. The results suggest that mRNA processing plays crucial roles in Pi homeostasis as well as developmental reprograming in response to Pi deprivation in Arabidopsis.

• Molecules and Cells
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• 제44권1호
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• pp.13-25
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• 2021

Apoptosis and compensatory proliferation, two intertwined cellular processes essential for both development and adult homeostasis, are often initiated by the mis-regulation of centrosomal proteins, damaged DNA, and defects in mitosis. Fly Anastral spindle 3 (Ana3) is a member of the pericentriolar matrix proteins and known as a key component of centriolar cohesion and basal body formation. We report here that ana3m19 is a suppressor of lethality induced by the overexpression of Sol narae (Sona), a metalloprotease in a disintegrin and metalloprotease with thrombospondin motif (ADAMTS) family. ana3m19 has a nonsense mutation that truncates the highly conserved carboxyl terminal region containing multiple Armadillo repeats. Lethality induced by Sona overexpression was completely rescued by knockdown of Ana3, and the small and malformed wing and hinge phenotype induced by the knockdown of Ana3 was also normalized by Sona overexpression, establishing a mutually positive genetic interaction between ana3 and sona. p35 inhibited apoptosis and rescued the small wing and hinge phenotype induced by knockdown of ana3. Furthermore, overexpression of Ana3 increased the survival rate of irradiated flies and reduced the number of dying cells, demonstrating that Ana3 actively promotes cell survival. Knockdown of Ana3 decreased the levels of both intra- and extracellular Sona in wing discs, while overexpression of Ana3 in S2 cells dramatically increased the levels of both cytoplasmic and exosomal Sona due to the stabilization of Sona in the lysosomal degradation pathway. We propose that one of the main functions of Ana3 is to stabilize Sona for cell survival and proliferation.

• Childhood Kidney Diseases
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• 제23권2호
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• pp.59-66
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• 2019

Background: Primary hyperoxaluria (PH), a rare inborn error of glyoxylate meta bolism causing overproduction of oxalate, is classified into three genetic subgroups: type 1-3 (PH1-PH3) caused by AGXT, GRHPR, and HOGA1 gene mutations, respectively. We performed a retrospective case series study of Korean pediatric patients with PH. Methods: In total, 11 unrelated pediatric patients were recruited and their phenotypes and genotypes were analyzed by a retrospective review of their medical records. Results: Mutational analyses revealed biallelic AGXT mutations (PH1) in nine patients and a single heterozygous GRHPR and HOGA1 mutation in one patient each. The c.33dupC was the most common AGXT mutation with an allelic frequency of 44%. The median age of onset was 3 months (range, 2 months-3 years), and eight patients with PH1 presented with end stage renal disease (ESRD). Patients with two truncating mutations showed an earlier age of onset and more frequent retinal involvement than patients with one truncating mutation. Among eight PH1 patients presenting with ESRD, five patients were treated with intensive dialysis followed by liver transplantation (n=5) with/without subsequent kidney transplantation (n=3). Conclusion: Most patients presented with severe infantile forms of PH. Patients with two truncating mutations displayed more severe phenotypes than those of patients with one truncating mutation. Sequential liver and kidney transplantation was adopted for PH1 patients presenting with ESRD. A larger nation-wide multicenter study is needed to confirm the genotype-phenotype correlations and outcomes of organ transplantation.

• Journal of Periodontal and Implant Science
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• 제32권4호
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• pp.733-744
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• 2002

The fibroblasts are the principal cells in the periodontal ligament of peridontium. As the periodontal ligament fibroblasts (PDLF) show similar phenotype with osteoblasts, the PDLF are thought to play an important role in alveolar bone remodeling. Cell-to-cell contacted signaling is crucial for osteoclast formation. Recently it has been reported that PDLJ enhance the bone resorbing activity of osteoclasts differentiated from hematopoietic preosteoclasts. The aims of this study were to $clarify\;^{1)}$ the mechanism of PDLF-induced osteoclastogenesis $and\;^{2)}$ whether we can use preosteoclast cell line instead of primary hematopoietic preosteoclast cells for studying the mechanism of PDLF-induced osteoclastogenesis. Osteoclastic differentiation of mouse macrophage cell line RAW264.7 was compared with that of mouse bone marrow-derived M-CSF dependent cell (MDBM), a well-known hematopoietic preosteoclast model, by examining, 1) osteoclast-specific gene expression such as calcitonin receptor, M-CSF receptor (c-fms), cathepsin K, receptoractivator nuclear factor kappa B (RANK) ,2) generation of TRAP(+) multinucleated cells (MNCs), and 3) generation of resorption pit on the $OAAS^{TM}$ plate. RAW264.7 cultured in the medium containing of soluble osteoclast differentiation Factor (sODF) showed similar phenotype with MDBM-derived osteoclasts, those are mRNA expression pattern of osteoclast-specific genes, TRAP(+) MNCs generation, and bone resorbing abivity. Formation of resorption pits by osteoclastic MNCs differentiated from sODF-treated RAW264.7, was completely blocked by the addition of osteoprotegerin (OPG), a soluble decoy receptor for ODF, to the sODF-containing culture me야um. The effects of PDLF on differentiation of RAW264.7 into　the TRAP(+) multinucleated osteoclast-like cells were examined using coculture system. PDLF were fxed with paraformaldehyde, followed by coculture with RAW264.7, which induced formation of TRAP(+) MNCs in the absence of additional treatment of sODF. When compared with untreated and fixed PDLF (fPDLF), IL-1 ${\beta}$-treated, or lipopolysaccha-ride-treated and then fixed PDLF showed two-folld increase in the supporting activity of osteoclastogenesis from RAW264.7 coculture system. There were no TRAP(+) MNCs formation in coculture system of RAW264.7 with PDLF of no fixation. These findigs suggested that we can replace the primary hematopoietic preosteoclasts for RAW264. 7 cell line for studying the mechanism of PDLF-induced osteoclastogenesis, and we hypothesize that PDLF control osteoclastogenesis through ODF expression which might be enhanced by inflammatory signals.

• Genomics & Informatics
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• 제18권2호
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• pp.20.1-20.4
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• 2020

Accessible negative results are relevant for researchers and clinicians not only to limit their search space but also to prevent the costly re-exploration of research hypotheses. However, most biomedical relation extraction datasets do not seek to distinguish between a false and a negative relation among two biomedical entities. Furthermore, datasets created using distant supervision techniques also have some false negative relations that constitute undocumented/ unknown relations (missing from a knowledge base). We propose to improve the distinction between these concepts, by revising a subset of the relations marked as false on the phenotype-gene relations corpus and give the first steps to automatically distinguish between the false (F), negative (N), and unknown (U) results. Our work resulted in a sample of 127 manually annotated FNU relations and a weighted-F1 of 0.5609 for their automatic distinction. This work was developed during the 6th Biomedical Linked Annotation Hackathon (BLAH6).

• 한국작물학회지
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• 제27권2호
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• pp.111-115
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• 1982

속간교잡을 실시함에 있어서 교배방법 및 교배촉진 물질로 알려진 EACA와 $GA_3$의 처리가 결실율 향상에 미치는 영향을 구명하고 교배시기에 있어서 뢰수분과 노화수분중 어떤 처리가 교잡종 생산에 유리한가를 검토하여 생장조절제인 EACA와 $GA_3$를 함께 처리한 구와 EACA만을 처리한 구를 두고 생장조절제의 효과도 아울러 구명코저 시험한 바 그 결과를 요약하면 다음과 같다. 1. 대맥$\times$소맥 속간교잡을 실시할 때는 노화수분의 결실율(4.5%)이 뢰수분보다 훨씬 높았다. 그러나 배형성율은 오히려 뢰수분쪽이 높았다. 2. $GA_3$ 처리 효과는 크게 인정되었으나 EACA 단독 효과는 인정되지 않았다. 3. 대맥$\times$소맥을 속간교잡하여 2개체의 형태적으로 소맥쪽을 더 닮은 식물체를 얻었으며 이는 생육이 진행될수록 더욱 소맥과 유사하였다. 이밖에도 시험관내에서 얼마간 자란 9개의 식물체도 얻을 수 있었다.

• BMB Reports
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• 제51권7호
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• pp.350-355
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• 2018

HnRNPK is a multifunctional protein that participates in chromatin remodeling, transcription, RNA splicing, mRNA stability and translation. Here, we uncovered the function of hnRNPK in regulating the proliferation and differentiation of myoblasts. hnRNPK was mutated in the C2C12 myoblast cell line using the CRISPR/Cas9 system. A decreased proliferation rate was observed in hnRNPK-mutated cells, suggesting an impaired proliferation phenotype. Furthermore, increased G2/M phase, decreased S phase and increased sub-G1 phase cells were detected in the hnRNPK-mutated cell lines. The expression analysis of key cell cycle regulators indicated mRNA of Cyclin A2 was significantly increased in the mutant myoblasts compared to the control cells, while Cyclin B1, Cdc25b and Cdc25c were decreased sharply. In addition to the myoblast proliferation defect, the mutant cells exhibited defect in myotube formation. The myotube formation marker, myosin heavy chain (MHC), was decreased sharply in hnRNPK-mutated cells compared to control myoblasts during differentiation. The deficiency in hnRNPK also resulted in the repression of Myog expression, a key myogenic regulator during differentiation. Together, our data demonstrate that hnRNPK is required for myoblast proliferation and differentiation and may be an essential regulator of myoblast function.

• IMMUNE NETWORK
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• 제24권2호
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• pp.14.1-14.26
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• 2024

The inflammatory response during cutaneous leishmaniasis (CL) involves immune and non-immune cell cooperation to contain and eliminate Leishmania parasites. The orchestration of these responses is coordinated primarily by CD4⁺ T cells; however, the disease outcome depends on the Th cell predominant phenotype. Although Th1 and Th2 phenotypes are the most addressed as steers for the resolution or perpetuation of the disease, Th17 cell activities, especially IL-17 release, are recognized to be vital during CL development. Th17 cells perform vital functions during both acute and chronic phases of CL. Overall, Th17 cells induce the migration of phagocytes (neutrophils, macrophages) to the infection site and CD8⁺ T cells and NK cell activation. They also provoke granzyme and perforin secretion from CD8⁺ T cells, macrophage differentiation towards an M2 phenotype, and expansion of B and Treg cells. Likewise, immune cells from the inflammatory infiltrate have modulatory activities over Th17 cells involving their differentiation from naive CD4⁺ T cells and further expansion by generating a microenvironment rich in optimal cytokines such as IL-1β, TGF-β, IL-6, and IL-21. Th17 cell activities and synergies are crucial for the resistance of the infection during the early and acute stages; however, if unchecked, Th17 cells might lead to a chronic stage. This review discusses the synergies between Th17 cells and the inflammatory infiltrate and how these interactions might destine the course of CL.