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REFERENCE LINKING PLATFORM OF KOREA S&T JOURNALS
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Korean Society for Biochemistry and Molecular Biology
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Volume & Issues
Volume 42, Issue 12 - Dec 2009
Volume 42, Issue 11 - Nov 2009
Volume 42, Issue 10 - Oct 2009
Volume 42, Issue 9 - Sep 2009
Volume 42, Issue 8 - Aug 2009
Volume 42, Issue 7 - Jul 2009
Volume 42, Issue 6 - Jun 2009
Volume 42, Issue 5 - May 2009
Volume 42, Issue 4 - Apr 2009
Volume 42, Issue 3 - Mar 2009
Volume 42, Issue 2 - Feb 2009
Volume 42, Issue 1 - Jan 2009
Selecting the target year
Mechanism of amyloidogenesis: nucleation-dependent fibrillation versus double-concerted fibrillation
Bhak, Ghi-Bom ; Choe, Young-Jun ; Paik, Seung-R. ;
BMB Reports , volume 42, issue 9, 2009, Pages 541~551
DOI : 10.5483/BMBRep.2009.42.9.541
Amyloidogenesis defines a condition in which a soluble and innocuous protein turns to insoluble protein aggregates known as amyloid fibrils. This protein suprastructure derived via chemically specific molecular self-assembly process has been commonly observed in various neurodegenerative disorders such as Alzheimer's, Parkinson's, and Prion diseases. Although the major culprit for the cellular degeneration in the diseases remains unsettled, amyloidogenesis is considered to be etiologically involved. Recent recognition of fibrillar polymorphism observed mostly from in vitro amyloidogeneses may indicate that multiple mechanisms for the amyloid fibril formation would be operated. Nucleation-dependent fibrillation is the prevalent model for assessing the self-assembly process. Following thermodynamically unfavorable seed formation, monomeric polypeptides bind to the seeds by exerting structural adjustments to the template, which leads to accelerated amyloid fibril formation. In this review, we propose another in vitro model of amyloidogenesis named double-concerted fibrillation. Here, two consecutive assembly processes of monomers and subsequent oligomeric species are responsible for the amyloid fibril formation of
-synuclein, a pathological component of Parkinson's disease, following structural rearrangement within the oligomers which then act as a growing unit for the fibrillation.
Posttranscriptional and posttranslational determinants of cyclooxygenase expression
Mbonye, Uri R. ; Song, In-Seok ;
BMB Reports , volume 42, issue 9, 2009, Pages 552~560
DOI : 10.5483/BMBRep.2009.42.9.552
Cyclooxygenases (COX-1 and COX-2) are ER-resident proteins that catalyze the committed step in prostanoid synthesis. COX-1 is constitutively expressed in many mammalian cells, whereas COX-2 is usually expressed inducibly and transiently. Abnormal expression of COX-2 has been implicated in the pathogenesis of chronic inflammation and various cancers; therefore, it is subject to tight and complex regulation. Differences in regulation of the COX enzymes at the posttranscriptional and posttranslational levels also contribute significantly to their distinct patterns of expression. Rapid degradation of COX-2 mRNA has been attributed to AU-rich elements (AREs) at its 3’UTR. Recently, microRNAs that can selectively repress COX-2 protein synthesis have been identified. The mature forms of these COX proteins are very similar in structure except that COX-2 has a unique 19-amino acid (19-aa) segment located near the C-terminus. This C-terminal 19-aa cassette plays an important role in mediation of the entry of COX-2 into the ER-associated degradation (ERAD) system, which transports ER proteins to the cytoplasm for degradation by the 26S proteasome. A second pathway for COX-2 protein degradation is initiated after the enzyme undergoes suicide inactivation following cyclooxygenase catalysis. Here, we discuss these molecular determinants of COX-2 expression in detail.
Evidence for the association of peroxidases with the antioxidant effect of p-coumaric acid in endothelial cells exposed to high glucose plus arachidonic acid
Lee, Seung-Jin ; Mun, Gyeong-In ; An, Sang-Mi ; Boo, Yong-Chool ;
BMB Reports , volume 42, issue 9, 2009, Pages 561~567
DOI : 10.5483/BMBRep.2009.42.9.561
Although many plant-derived phenolic compounds display antioxidant effects in biological systems, their mechanism of action remains controversial. In this study, the mechanism by which p-coumaric acid (p-CA) performs its antioxidant action was investigated in bovine aortic endothelial cells under oxidative stress due to high levels of glucose (HG) and arachidonic acid (AA), a free fatty acid. p-CA prevented lipid peroxidation and cell death due to HG+AA without affecting the production of reactive oxygen species. The antioxidant effect of p-CA was not decreased by buthionine-(S,R)-sulfoximine, an inhibitor of cellular GSH synthesis. In contrast, pretreatment with p-CA caused the induction of peroxidases that decomposed t-butyl hydroperoxide in a p-CA-dependent manner. Furthermore, the antioxidant effect of p-CA was significantly mitigated by methimazole, which was shown to inhibit the catalytic activity of 'p-CA peroxidases' in vitro. Therefore, it is suggested that the induction of these previously unidentified 'p-CA peroxidases' is responsible for the antioxidant effect of p-CA.
Regulation of ANKRD9 expression by lipid metabolic perturbations
Wang, Xiaofei ; Newkirk, Robert F. ; Carre, Wilfrid ; Ghose, Purnima ; Igobudia, Barry ; Townsel, James G. ; Cogburn, Larry A. ;
BMB Reports , volume 42, issue 9, 2009, Pages 568~573
DOI : 10.5483/BMBRep.2009.42.9.568
Fatty acid oxidation (FAO) defects cause abnormal lipid accumulation in various tissues, which provides an opportunity to uncover novel genes that are involved in lipid metabolism. During a gene expression study in the riboflavin deficient induced FAO disorder in the chicken, we discovered the dramatic increase in mRNA levels of an uncharacterized gene, ANKRD9. No functions have been ascribed to ANKRD9 and its orthologs, although their sequences are well conserved among vertebrates. To provide insight into the function of ANKRD9, the expression of ANKRD9 mRNA in lipidperturbed paradigms was examined. The hepatic mRNA level of ANKRD9 was repressed by thyroid hormone (
) and fasting, elevated by re-feeding upon fasting. However, ANKRD9 mRNA level is reduced in response to apoptosis. Transient transfection assay with green fluorescent protein tagged- ANKRD9 showed that this protein is localized within the cytoplasm. These findings point to the possibility that ANKRD9 is involved in intracellular lipid accumulation.
Inhibitory effects of honokiol on LPS and PMA-induced cellular responses of macrophages and monocytes
Lee, Sang-Yeol ; Cho, Jae-Youl ;
BMB Reports , volume 42, issue 9, 2009, Pages 574~579
DOI : 10.5483/BMBRep.2009.42.9.574
The regulatory effects of honokiol on the cellular responses of macrophages and monocytes were evaluated. Specifically, we investigated the effects of honokiol with respect to lipopolysaccharide (LPS)-induced cytotoxicity, LPS- or phorbol-12-myristate-13-acetate (PMA)-mediated morphological changes, and relevant events (FITC-dextran-induced phagocytic uptake). Honokiol blocked the LPS-induced cytotoxicity of RAW264.7 cells in a dose-dependent manner. In addition, honokiol appeared to block the production of cytotoxic cytokines such as interleukin (IL)-
and tumor necrosis factor (TNF)-
, nitric oxide (NO), and reactive oxygen species (ROS). Moreover, honokiol strongly prevented the morphological changes in RAW 264.7 and U937 cells that were induced by LPS and PMA. The surface levels of marker proteins, which are up-regulated under the morphological changes of RAW264.7 and U937 cells, were also diminished. The data presented here strongly suggest that the honokiol modulates various cellular responses managed by macrophages and monocytes.
Inhibition of methionine sulfoxide reduction by dimethyl sulfoxide
Kwak, Geun-Hee ; Choi, Seung-Hee ; Kim, Jae-Ryong ; Kim, Hwa-Young ;
BMB Reports , volume 42, issue 9, 2009, Pages 580~585
DOI : 10.5483/BMBRep.2009.42.9.580
Dimethyl sulfoxide (DMSO) is widely used in chemistry and biology as a solvent and as a cryoprotectant. It is also used as a pharmaceutical agent for the treatment of interstitial cystitis and rheumatoid arthritis. Previous reports described DMSO as being reduced by methionine-S-sulfoxide reductase (MsrA). However, little is known about the DMSO reduction capability of methionine-R-sulfoxide reductase (MsrB) or its effect on the catalysis of methionine sulfoxide reduction. We show that mammalian MsrB2 and MsrB3 were unable to reduce DMSO. This compound inhibited MsrB2 activity but did not inhibit MsrB3 activity. We further determined that DMSO functions as an inhibitor of MsrA and MsrB2 in the reduction of methionine sulfoxides via different inhibition mechanisms. DMSO competitively inhibited MsrA activity but acted as a non-competitive inhibitor of MsrB2 activity. Our study also demonstrated that DMSO inhibits in vivo methionine sulfoxide reduction in yeast and mammalian cells.
Different modes of antibiotic action of homodimeric and monomeric bactenecin, a cathelicidin-derived antibacterial peptide
Lee, Ju-Yeon ; Yang, Sung-Tae ; Kim, Hyo-Jeong ; Lee, Seung-Kyu ; Jung, Hyun-Ho ; Shin, Song-Yub ; Kim, Jae-Il ;
BMB Reports , volume 42, issue 9, 2009, Pages 586~592
DOI : 10.5483/BMBRep.2009.42.9.586
The bactenecin is an antibacterial peptide with an intramolecular disulfide bond. We recently found that homodimeric bactenecin exhibits more potent antibacterial activity than the monomeric form and retains its activity at physiological conditions. Here we assess the difference in the modes of antibiotic action of homodimeric and monomeric bactenecins. Both monomeric and dimeric bactenecins almost completely killed both Staphylococcus aureus and E. coli within 10-30 min at concentrations of
. However, exposure to liposomes elicited an increase in the fluorescence quantum yield from a tryptophan-containing monomeric analog, while the homodimeric analog showed a significant reduction in fluorescence intensity. Moreover, unlike the monomer, the homodimer displayed apparent membrane-lytic activity enabling release of various sized dyes from liposomes, and rapidly and fully depolarized the S. aureus membrane. Together, our results suggest that homodimeric bactenecin forms pores in the bacterial membrane, while monomeric one penetrates through the membrane to target intracellular molecules/organelles.
Analysis of microRNA expression profiles during the cell cycle in synchronized HeLa cells
Zhou, Jue-Yu ; Ma, Wen-Li ; Liang, Shuang ; Zeng, Ye ; Shi, Rong ; Yu, Hai-Lang ; Xiao, Wei-Wei ; Zheng, Wen-Ling ;
BMB Reports , volume 42, issue 9, 2009, Pages 593~598
DOI : 10.5483/BMBRep.2009.42.9.593
Cell cycle progression is regulated by both transcriptional and post-transcriptional mechanisms. MicroRNAs (miRNAs) emerge as a new class of small non-coding RNA regulators of cell cycle as recent evidence suggests. It is hypothesized that expression of specific miRNAs oscillates orderly along with cell cycle progression. However, the oscillated expression patterns of many candidate miRNAs have yet to be determined. Here, we describe miRNA expression profiling in double-thymidine synchronized HeLa cells as cell cycle progresses. Twenty-five differentially expressed miRNAs were classified into five groups based on their cell cycle-dependent expression patterns. The cyclic expression of six miRNAs (miR-221, let-7a, miR-21, miR-34a, miR-24, miR-376b) was validated by real-time quantitative RT-PCR (qRT-PCR). These results suggest that specific miRNAs, along with other key factors are required for maintaining and regulating proper cell cycle progression. The study deepens our understanding on cell cycle regulation.
Autophagy inhibition through PI3K/Akt increases apoptosis by sodium selenite in NB4 cells
Ren, Yun ; Huang, Fang ; Liu, Yuan ; Yang, Yang ; Jiang, Qian ; Xu, Caimin ;
BMB Reports , volume 42, issue 9, 2009, Pages 599~604
DOI : 10.5483/BMBRep.2009.42.9.599
Selenium possesses the chemotherapeutic feature by inducing apoptosis in cancer cell with trivial side effects on normal cells. However, the mechanism in which is not clearly understood. Emerging evidence indicates the overlaps between the autophagy and the apoptosis. In this study, we have investigated the role of autophagy in selenium-induced apoptosis in NB4 cells. We find that autophagy is suppressed in NB4 cells treated by sodium selenite, as measured by electron microscope, acridine orange staining and western blot. Moreover, selenite combined with autophagy inhibitor contributes to the up-regulation of apoptosis, while the PI3K/Akt signaling pathway is down- regulated. Consistently, when the inhibitor of PI3K was applied, the autophagic level significantly decreased. In summary, sodium selenite increases NB4 cell apoptosis by autophagy inhibition through PI3K/Akt, and the inhibition of autophagy contributes to the up-regulation of apoptosis.
Enhanced functional and structural properties of high-density lipoproteins from runners and wrestlers compared to throwers and lifters
Lee, Hwa-Hyung ; Park, Jeong-Euy ; Choi, In-Ho ; Cho, Kyung-Hyun ;
BMB Reports , volume 42, issue 9, 2009, Pages 605~610
DOI : 10.5483/BMBRep.2009.42.9.605
Plasma high-density lipoprotein cholesterol (HDL-C) levels are inversely correlated with the risk of cardiovascular disease, and are known to increase with repetitive exercise. In the current study, HDL fractions from athletes' sera were isolated and compared as a function of the type of sport (runners [n = 10], throwers [n = 10], wrestlers [n = 10], and weight lifters [n = 8]), and as an age- and gender-matched reference group (n = 14). Among athletes, HDL from runners had the strongest antioxidant activity. Immunodetection showed that runners and wrestlers had the highest levels of apoA-I and lowest levels of apoA-II in their HDL. Electron microscopy also revealed that HDL2 of runners and wrestlers were the largest in size. In conclusion, although all athlete groups had significantly better serum lipid/lipoprotein profiles than the reference group, runners and wrestlers had the most desirable lipoprotein function and structure, including antioxidant activity, HDL-associated enzyme activities and increased particle size.
Expression of dehydration responsive element-binding protein-3 (DREB3) under different abiotic stresses in tomato
Islam, Mohammad Saiful ; Wang, Myeong-Hyeon ;
BMB Reports , volume 42, issue 9, 2009, Pages 611~616
DOI : 10.5483/BMBRep.2009.42.9.611
We investigated the expression pattern of dehydration responsive element-binding protein-3 in tomato under different abiotic stresses. Full length LeDREB3 cDNA was isolated from tomato plant, followed by phylogenetic analysis based on deduced amino acid sequences that revealed significant sequence similarity to DREB proteins belonging to diverse families of plant species. Southern blot analysis showed duplicate copies of LeDREB3 in the tomato genome while organ-specific expression profiling indicated constitutive expression of LeDREB3 in all tested organs, which was particularly strong in flower. LeDREB3 expression was significantly induced by Nacl, drought, low temperature and
. Moreover, LeDREB3 was slightly regulated by treatment with ABA and MV. These observations suggest that the LeDREB3 gene may be involved in the response of the tomato plant to stress.
Identification of epistasis in ischemic stroke using multifactor dimensionality reduction and entropy decomposition
Park, Jung-Dae ; Kim, Youn-Young ; Lee, Chae-Young ;
BMB Reports , volume 42, issue 9, 2009, Pages 617~622
DOI : 10.5483/BMBRep.2009.42.9.617
We investigated the genetic associations of ischemic stroke by identifying epistasis of its heterogeneous subtypes such as small vessel occlusion (SVO) and large artery atherosclerosis (LAA). Epistasis was analyzed with 24 genes in 207 controls and 271 patients (SVO = 110, LAA = 95) using multifactor dimensionality reduction and entropy decomposition. The multifactor dimensionality reduction analysis with any of 1- to 4-locus models showed no significant association with LAA (P > 0.05). The analysis of SVO, however, revealed a significant association in the best 3-locus model with P10L of TGF-
, C1013T of SPP1, and R485K of F5 (testing balanced accuracy = 63.17%, P < 0.05). Subsequent entropy analysis also revealed that such heterogeneity was present and quite a large entropy was estimated among the 3 loci for SVO (5.43%), but only a relatively small entropy was estimated for LAA (1.81%). This suggests that the synergistic epistasis model might contribute specifically to the pathogenetsis of SVO, which implies a different etiopathogenesis of the ischemic stroke subtypes.