Korea Research Institute of Bioscience and Biotechnology
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Ent-peniciherqueinone suppresses acetaldehyde-induced cytotoxicity and oxidative stress by inducing ALDH and suppressing MAPK signaling
No full textStudies on ethanol-induced stress and acetaldehyde toxicity are actively being conducted, owing to an increase in alcohol consumption in modern society. In this study, ent-peniciherqueinone (EPQ) isolated from a Hawaiian volcanic soil-associated fungus Penicillium herquei FT729 was found to reduce the acetaldehyde-induced cytotoxicity and oxidative stress in PC12 cells. EPQ increased cell viability in the presence of acetaldehyde-induced cytotoxicity in PC12 cells. In addition, EPQ reduced cellular reactive oxygen species (ROS) levels and restored acetaldehyde-mediated disruption of mitochondrial membrane potential. Western blot analyses revealed that EPQ treatment increased protein levels of ROS-scavenging heme oxygenase-1 and superoxide dismutase, as well as the levels of aldehyde dehydrogenase (ALDH) 1, ALDH2, and ALDH3, under acetaldehyde-induced cellular stress. Finally, EPQ reduced acetaldehyde-induced phosphorylation of p38 and c-Jun N-terminal kinase, which are associated with ROS-induced oxidative stress. Therefore, our results demonstrated that EPQ prevents cellular oxidative stress caused by acetaldehyde and functions as a potent agent to suppress hangover symptoms and alcohol-related stress.
Variants of Candida antartica Lipase B and Their Use
No full text본 발명은 가수분해(hydrolysis), 에스터화 반응(esterification) 및 아미노화 반응(amidation) 활성별로 특화된 칸디다 안타티카 유래의 리파제 B(Candida antarctica lipase B, CalB)의 변이체 및 이의 이용에 관한 것이다. 본 발명에 따른 CalB의 변이체는 CalB에 비해 향상된 가수분해(hydrolysis), 에스터 반응(esterification) 및 아미노화 반응(amidation) 활성을 나타내므로, 이를 이용하여 지방산 또는 트리글리세라이드로부터 기능성 화장품용 오일인 왁스에스터와 유사세라마이드 생산 효율을 개선할 수 있다.국
Construction of high quality reference genome of Korean melon
No full text참외의 고품질 유전체 구축 및 분자마커 대량 발굴ABM440201
Genome editing 기술을 이용한 Bacillus균 시스템 재설계 기술 개발
No full textGenome editing 기술을 이용한 Bacillus균 시스템 재설계 기술 개발PRM102201
Study on the pathogenesis of neurodegenerative disease using in vivo model for neuronal dendritic dynamics
No full text신경수상돌기 동태 분석 모델 구축을 통한 뇌신경계질환 병인기전 연구KFM062181
Eudebeiolide B inhibits osteoclastogenesis and prevents ovariectomy-induced bone loss by regulating RANKL-induced NF-κB, c-Fos and calcium signaling
No full textEudebeiolide B is a eudesmane-type sesquiterpenoid compound isolated from Salvia plebeia R. Br., and little is known about its biological activity. In this study, we investigated the effects of eudebeiolide B on osteoblast differentiation, receptor activator nuclear factor-κB ligand (RANKL)-induced osteoclastogenesis in vitro and ovariectomy-induced bone loss in vivo. Eudebeiolide B induced the expression of alkaline phosphatase (ALP) and calcium accumulation during MC3T3-E1 osteoblast differentiation. In mouse bone marrow macrophages (BMMs), eudebeiolide B suppressed RANKL-induced osteoclast differentiation of BMMs and bone resorption. Eudebeiolide B downregulated the expression of nuclear factor of activated T-cells 1 (NFATc1) and c-fos, transcription factors induced by RANKL. Moreover, eudebeiolide B attenuated the RANKL-induced expression of osteoclastogenesis-related genes, including cathepsin K (Ctsk), matrix metalloproteinase 9 (MMP9) and dendrocyte expressed seven transmembrane protein (DC-STAMP). Regarding the molecular mechanism, eudebeiolide B inhibited the phosphorylation of Akt and NF-κB p65. In addition, it downregulated the expression of cAMP response element-binding protein (CREB), Bruton's tyrosine kinase (Btk) and phospholipase Cγ2 (PLCγ2) in RANKL-induced calcium signaling. In an ovariectomized (OVX) mouse model, intragastric injection of eudebeiolide B prevented OVX-induced bone loss, as shown by bone mineral density and contents, microarchitecture parameters and serum levels of bone turnover markers. Eudebeiolide B not only promoted osteoblast differentiation but inhibited RANKL-induced osteoclastogenesis through calcium signaling and prevented OVX-induced bone loss. Therefore, eudebeiolide B may be a new therapeutic agent for osteoclast-related diseases, including osteoporosis, rheumatoid arthritis and periodontitis.
Novosphingobium aquimarinum sp. nov., isolated from seawater
No full textA novel Gram-stain-negative, aerobic, and rod-shaped bacterial strain, M24A2MT, was isolated from seawater in the Republic of Korea. On the basis of the 16S rRNA gene phylogeny, strain M24A2MT was found to be closely related to Novosphingobium pentaromativorans US6-1T and Novosphingobium mathurense SM117T with pair-wise sequence similarities of 97.4 and 96.9？%, respectively. Phylogenetic analysis of 16S rRNA sequences indicated that M24A2MT formed a branch with Novosphingobium pentaromativorans US6-1T and represented a member of the genus Novosphingobium. The predominant cellular fatty acids were C14？:？0 2-OH, summed feature 3 (C16？:？1ω7c and/or C16？:？1ω6c), and summed feature 8 (C18？:？1ω7c and/or C18？:？1ω6c). The polar lipids of strain M24A2MT consisted mainly of diphosphatidylglycerol, phosphatidylethanolamine, phosphatidylglycerol, phosphatidylcholine, one unidentified phospholipid, and two unidentified lipids. The respiratory quinone was ubiquinone Q-10. The genomic DNA G+C content was 63.9？%. Given the phenotypic characteristics along with the phylogenetic distinctness and chemotaxonomic features, strain M24A2MT is considered to represent a novel species within the genus Novosphingobium, for which the name Novosphingobium aquimarinum sp. nov. is proposed. The type strain of Novosphingobium aquimarinum sp. nov. is M24A2MT (=KCTC 72894T=JCM 33983T).
Methyl lucidone induces apoptosis and G2/M phase arrest via the PI3K/Akt/NF-κB pathway in ovarian cancer cells
No full textContext: Methyl lucidone (ML) from the dried fruit of Lindera erythrocarpa Makino (Lauraceae) exhibits cytotoxic effects in various cancer cell lines. However, its effects on ovarian cancer cells remain unknown.Objective: This study evaluates the mechanism of ML-induced apoptosis, cell cycle distribution in ovarian cells.Materials and methods: The cytotoxic effect of ML (2.5-80 μM) on OVCAR-8 and SKOV-3 cells was evaluated by MTS assay for 24 and 48？h. Apoptosis and cell cycle arrest were analysed by flow cytometry. PCR, western blot analyses were performed to examine the related signalling pathways.Results: ML induced significant cellular morphological changes and apoptosis in ovarian cancer cells, leading to an antiproliferative effect (IC50？=？33.3-54.7 μM for OVCAR-8 and 48.8-60.7 μM for SKOV-3 cells). Treatment with ML induced cleavage of caspase-3/9 and PARP and release of cytochrome c from the mitochondria. Moreover, ML downregulated the expression of Bcl-2 and Bcl-xL and induced cell cycle arrest in the G2/M phase. Additionally, ML suppressed the expression of cyclin-A/B and promoted that of the cyclin-dependent kinase inhibitors p21 and p27. The expression of death receptors was not altered. Interestingly, ML also inhibited the activity of PI3K/Akt and NF-κB.Discussion and conclusions: ML caused G2/M phase arrest and apoptosis in ovarian cancer cells by activating intrinsic apoptotic pathways and suppressing the PI3K/Akt survival pathway. ML may be a potential anticancer agent to suppress ovarian cancer proliferation; thus, to improve the survival rate of cancer patients.
Dual roles of ULK1 (unc-51 like autophagy activating kinase 1) in cytoprotection against lipotoxicity
No full textSaturated fatty acid (SFA)-induced lipotoxicity is caused by the accumulation of reactive oxygen species (ROS), which is associated with damaged mitochondria. Moreover, lipotoxicity is crucial for the progression of nonalcoholic steatohepatitis (NASH). Autophagy is required for the clearance of protein aggregates or damaged mitochondria to maintain cellular metabolic homeostasis. The NFE2L2/NRF2 (nuclear factor, erythroid 2 like 2)-KEAP1 (kelch like ECH associated protein 1) pathway is essential for the elimination of ROS. ULK1 (unc-51 like autophagy activating kinase 1; yeast Atg1) is involved in the initiation of autophagy; however, its role in lipotoxicity-induced cell death in hepatocytes and mouse liver has not been elucidated. We now show that ULK1 potentiates the interaction between KEAP1 and the autophagy adaptor protein SQSTM1/p62, thereby mediating NFE2L2 activation in a manner requiring SQSTM1-dependent autophagic KEAP1 degradation. Furthermore, ULK1 is required for the autophagic removal of damaged mitochondria and to enhance binding between SQSTM1 and PINK1 (PTEN induced kinase 1). This study demonstrates the molecular mechanisms underlying the cytoprotective role of ULK1 against lipotoxicity. Thus, ULK1 could represent a potential therapeutic target for the treatment of NASH.Abbreviations: ACTB: actin beta; CM-H2DCFDA:5-(and-6)-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate; CQ: chloroquine; CUL3: cullin 3; DMSO: dimethyl sulfoxide; GSTA1: glutathione S-transferase A1; HA: hemagglutinin; Hepa1c1c7: mouse hepatoma cells; HMOX1/HO-1: heme oxygenase 1; KEAP1: kelch like ECH associated protein 1; LPS: lipopolysaccharides; MAP1LC3/LC3: microtubule-associated protein 1 light chain 3; MAPK8/JNK: mitogen-activated protein kinase 8; MEF: mouse embryonic fibroblast; MFN1: mitofusin 1; MTT: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide; NASH: nonalcoholic steatohepatitis; NFE2L2/NRF2: nuclear factor, erythroid 2 like 2; NQO1: NAD(P)H quinone dehydrogenase 1; PA: palmitic acid; PARP: poly (ADP-ribose) polymerase 1; PINK1: PTEN induced kinase 1; PRKAA1/2: protein kinase AMP-activated catalytic subunits alpha1/2; PRKN/PARK2: parkin RBR E3 ubiquitin protein ligase; PRKC/PKC: protein kinase C; RBX1: ring-box 1; ROS: reactive oxygen species; SFA: saturated fatty acid; siRNA: small interfering RNA; SQSTM1/p62: sequestosome 1; TOMM20: translocase of outer mitochondrial membrane 20; TUBA: tubulin alpha; TUNEL: terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling; ULK1: unc-51 like autophagy activating kinase 1.
Biomolecules from municipal and food industry wastes: an overview
No full textBiological wastes generated from food and fruit processing industries, municipal markets, and water treatment facilities are a major cause of concern for Health Departments and Environmentalists around the world. Conventional means of managing these wastes such as transportation, treatment, and disposal, are proving uneconomical. The need is to develop green and sustainable technologies to circumvent this ever-growing and persistent problem. In this article, the potential of diverse microbes to metabolize complex organic rich biowastes into a variety of bioactive compounds with diverse biotechnological applications have been presented. An integrated strategy has been proposed that can be commercially exploited for the recovery of value-adding products ranging from bioactive compounds, chemical building blocks, energy rich chemicals, biopolymers and materials, which results in a self-sustaining circular bioeconomy with nearly zero waste generation and complete degradation.