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REFERENCE LINKING PLATFORM OF KOREA S&T JOURNALS
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Journal DOI :
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
Autophagy-Is it a preferred route for lifespan extension?
Dwivedi, Meenakshi ; Ahnn, Joo-Hong ;
BMB Reports , volume 42, issue 2, 2009, Pages 65~71
DOI : 10.5483/BMBRep.2009.42.2.065
Autophagy, which is a process of self eating, has gained interest in the past decade due to its both beneficial and controversial roles in various biological phenomena. The discovery of autophagy genes (ATG) in yeast has led to focused research designed to elucidate the mechanism and regulation of this process. The role of autophagy in a variety of biological phenomena, including human disease, is still the subject of debate. However, recent findings suggest that autophagy is a highly regulated process with both beneficial and negative effects. Indeed, studies conducted using various model organisms have demonstrated that increased autophagy leads to an extended lifespan. Despite these findings, it is still unknown if all pathways leading to extended lifespan converge at the process of autophagy or not. Here, an overview of modern developments related to the process of autophagy, its regulation and the molecular machinery involved is presented. In addition, this review focuses on one of the beneficial aspects of autophagy, its role in lifespan regulation.
Embryo-derived stem cells -a system is emerging
Binas, B. ;
BMB Reports , volume 42, issue 2, 2009, Pages 72~80
DOI : 10.5483/BMBRep.2009.42.2.072
In mammals, major progress has recently been made with the dissection of early embryonic cell specification, the isolation of stem cells from early embryos, and the production of embryonic-like stem cells from adult cells. These studies have overcome long-standing species barriers for stem cell isolation, have revealed a deeper than expected similarity of embryo cell types across species, and have led to a better understanding of the lineage identities of embryo-derived stem cells, most notably of mouse and human embryonic stem (ES) cells. Thus, it has now become possible to propose a species-overarching classification of embryo stem cells, which are defined here as pre- to early post-implantation conceptus-derived stem cell types that maintain embryonic lineage identities in vitro. The present article gives an overview of these cells and discusses their relationships with each other and the conceptus. Consequently, it is debated whether further embryo stem cell types await isolation, and the study of the earliest extraembryonically committed stem cells is identified as a promising new research field.
Microplate hybridization assay for detection of isoniazid resistance in Mycobacterium tuberculosis
Han, Hye-Eun ; Lee, In-Soo ; Hwang, Joo-Hwan ; Bang, Hye-Eun ; Kim, Yeun ; Cho, Sang-Nae ; Kim, Tae-Ue ; Lee, Hye-Young ;
BMB Reports , volume 42, issue 2, 2009, Pages 81~85
DOI : 10.5483/BMBRep.2009.42.2.081
Early and accurate detection of drug resistant Mycobacterium tuberculosis can improve both the treatment outcome and public health control of tuberculosis. A number of molecular-based techniques have been developed including ones using probe molecules that target drug resistance-related mutations. Although these techniques are highly specific and sensitive, mixed signals can be obtained when the drug resistant isolates are mixed with drug susceptible isolates. In order to overcome this problem, we developed a new drug susceptibility test (DST) for one of the most effective anti-tuberculosis drug, isoniazid. This technique employed a microplate hybridization assay that quantified signals from each probe molecule, and was evaluated using clinical isolates. The evaluation analysis clearly showed that the microplate hybridization assay was an accurate and rapid method that overcame the limitations of DST based on conventional molecular techniques.
Upregulation of smpd3 via BMP2 stimulation and Runx2
Chae, Young-Mi ; Heo, Sun-Hee ; Kim, Jae-Young ; Lee, Jae-Mok ; Ryoo, Hyun-Mo ; Cho, Je-Yoel ;
BMB Reports , volume 42, issue 2, 2009, Pages 86~90
DOI : 10.5483/BMBRep.2009.42.2.086
Deletion of smpd3 induces osteogenesis and dentinogenesis imperfecta in mice. smpd3 is highly elevated in the parietal bones of developing mouse calvaria, but not in sutural mesenchymes. Here, we examine the mechanism of smpd3 regulation, which involves BMP2 stimulation of Runx2. smpd3 mRNA expression increased in response to BMP2 treatment and Runx2 transfection in C2C12 cells. The Runx2-responsive element (RRE) encoded within the -562 to -557 region is important for activation of the smpd3 promoter by Runx2. Electrophoretic mobility shift assays revealed that Runx2 binds strongly to the -355 to -350 RRE and less strongly to the -562 to -557 site. Thus, the smpd3 promoter is activated by BMP2 and is directly regulated by the Runx2 transcription factor. This novel description of smpd3 regulation will aid further studies of bone development and osteogenesis.
Signal crosstalk between estrogen and peroxisome proliferator-activated receptor α on adiposity
Kim, Bang-Hyun ; Won, Young-Suk ; Kim, Dae-Yong ; Kim, Bora ; Kim, Eun-Young ; Yoon, Mi-Jung ; Oh, Goo-Taeg ;
BMB Reports , volume 42, issue 2, 2009, Pages 91~95
DOI : 10.5483/BMBRep.2009.42.2.091
Peroxisome proliferator-activated receptor
and estrogen are believed to be involved in metabolic changes leading to obesity. To test this relationship, we divided female wildtype and PPAR
-deficient mice fed on a high fat diet into the following groups: mock-operated, ovariectomized (OVX), and
-treated. The visceral white adipose tissue and plasma cholesterol levels were increased significantly in wild type OVX and decreased in the
-treated group, but interestingly not in PPAR
-deficient mice. The mRNA levels of lipoprotein lipase in adipose tissue were also increased in only wild type OVX and decreased significantly in
-treated mice. These novel results suggest the possibility of signaling crosstalk between PPAR
, causing obesity in vivo.
Activation of apoptotic protein in U937 cells by a component of turmeric oil
Lee, Yong-Kyu ;
BMB Reports , volume 42, issue 2, 2009, Pages 96~100
DOI : 10.5483/BMBRep.2009.42.2.096
Aromatic (ar)-turmerone from turmeric oil displays anti-tumorigenesis activity that includes inhibited cell proliferation. This study investigated ar-turmerone-mediated apoptotic protein activation in human lymphoma U937 cells. Ar-turmerone treatment inhibited U937 cell viability in a concentration-dependent fashion, with inhibition exceeding 84%. Moreover, the treatment produced nucleosomal DNA fragmentation and the percentage of sub-diploid cells increased in a concentration-dependent manner; both are hallmarks of apoptosis. The apoptotic effect of ar-turmerone was associated with the induction of Bax and p53 proteins, rather than Bcl-2 and p21. Activation of mitochondrial cytochrome c and caspase-3 demonstrated that the activation of caspases accompanied the apoptotic effect of ar-turmerone, which mediated cell death. These results suggest that the apoptotic effect of ar-turmerone on U937 cells may involve caspase-3 activation through the induction of Bax and p53, rather than Bcl-2 and p21.
Arabidopsis AMY1 expressions and early flowering mutant phenotype
Jie, Wang ; Dashi, Yu ; XinHong, Guo ; Xuanming, Liu ;
BMB Reports , volume 42, issue 2, 2009, Pages 101~105
DOI : 10.5483/BMBRep.2009.42.2.101
The homozygous T-DNA mutant of the AMY1 gene in Arabidopsis was identified and importantly, shown to cause an early flowering phenotype. We found that the disruption of AMY1 enhanced expression of CO and FT. The expression analyses of genes related to starch metabolism revealed that expression of the AGPase small subunit APS1 in the wild type was higher than in the amy1 mutant. However, there were no significant differences in expression levels of the AGPase large subunit genes ApL1, AMY2, or AMY3 between wild type and the amy1 mutant. Expression profiling showed that AMY1 was highly expressed in leaves, stems, and flowers, and expressed less in leafstalks and roots. Furthermore, the level of AMY1 mRNA was highly elevated with age and in senescing leaves. RT-PCR analyses showed that the expression of AMY1 was induced by heat shock, GA, and ABA, while salt stress had no apparent effect on its expression.
The bio-complex "reaction pattern in vertebrate cells" reduces cytokine-induced cellular adhesion molecule mRNA expression in human endothelial cells by attenuation of NF-kappaB translocation
Ronnau, Cindy ; Liebermann, Herbert E. H. ; Helbig, Franz ; Staudt, Alexander ; Felix, Stephan B. ; Ewert, Ralf ; Landsberger, Martin ;
BMB Reports , volume 42, issue 2, 2009, Pages 106~112
DOI : 10.5483/BMBRep.2009.42.2.106
The bio-complex "reaction pattern in vertebrate cells"(RiV) is mainly represented by characteristic exosome-like particles - probably as reaction products of cells to specific stress. The transcription factor NF-kappaB plays a central role in inflammation. We tested the hypothesis that RiV particle preparations (RiV-PP) reduce cellular adhesion molecule (CAM) expression (ICAM-1, VCAM-1, E-selectin) by the attenuation of NF-kappaB translocation in human umbilical vein endothelial cells (HUVEC). After 4 hours, pre-incubation of HUVEC with RiV-PP before stimulation with TNF-alpha significantly reduced ICAM-1 (65.5
10.3%) and VCAM-1 (71.1
12.3%) mRNA expression compared to TNF-alpha-treated cells (100%, n=7). ICAM-1 surface expression was significantly albeit marginally reduced in RiV/TNF-alpha- treated cells (92.0
5.6%, n=4). No significant effect was observed on VCAM-1 surface expression. In RiV/TNF-alpha-treated cells (n=4), NF-kappaB subunits p50 (85.7
4.1%) and p65 (85.0
1.8%) nuclear translocation was significantly reduced. RiV-PP may exert an anti-inflammatory effect in HUVEC by reducing CAM mRNA expression via attenuation of p50 and p65 translocation.
Expression, subcellular localization, and antioxidant role of mammalian methionine sulfoxide reductases in Saccharomyces cerevisiae
Kwak, Geun-Hee ; Kim, Jae-Ryong ; Kim, Hwa-Young ;
BMB Reports , volume 42, issue 2, 2009, Pages 113~118
DOI : 10.5483/BMBRep.2009.42.2.113
Despite the growing body of evidence suggesting a role for MsrA in antioxidant defense, little is currently known regarding the function of MsrB in cellular protection against oxidative stress. In this study, we overexpressed the mammalian MsrB and MsrA genes in Saccharomyces cerevisiae and assessed their subcellular localization and antioxidant functions. We found that the mitochondrial MsrB3 protein (MsrB3B) was localized to the cytosol, but not to the mitochondria, of the yeast cells. The mitochondrial MsrB2 protein was detected in the mitochondria and, to a lesser extent, the cytosol of the yeast cells. In this study, we report the first evidence that MsrB3 overexpression in yeast cells protected them against
-mediated cell death. Additionally, MsrB2 overexpression also provided yeast cells with resistance to oxidative stress, as did MsrA overexpression. Our results show that mammalian MsrB and MsrA proteins perform crucial functions in protection against oxidative stress in lower eukaryotic yeast cells.
Knockdown of endogenous SKIP gene enhanced insulin-induced glycogen synthesis signaling in differentiating C2C12 myoblasts
Xiong, Qi ; Deng, Chang-Yan ; Chai, Jin ; Jiang, Si-Wen ; Xiong, Yuan-Zhu ; Li, Feng-E ; Zheng, Rong ;
BMB Reports , volume 42, issue 2, 2009, Pages 119~124
DOI : 10.5483/BMBRep.2009.42.2.119
produced by the activated PI3-kinase is a key lipid second messenger in cell signaling downstream of insulin. Skeletal muscle and kidney-enriched inositol phosphatase (SKIP) identified as a 5'-inositol phosphatase that hydrolyzes PI(3,4,5)
, negatively regulates the insulin-induced glycogen synthesis in skeletal muscle. However the mechanism by which this occurs remains unclear. To elucidate the function of SKIP in glycogen synthesis, we employed RNAi techniques to knockdown the SKIP gene in differentiating C2C12 myoblasts. Insulininduced phosphorylation of Akt (protein kinase B) and GSK-3
(Glycogen synthase kinase), subsequent dephosphorylation of glycogen synthase and glycogen synthesis were increased by inhibiting the expression of SKIP, whereas the insulin-induced glycogen synthesis was decreased by overexpression of WT-SKIP. Our results suggest that SKIP plays a negative regulatory role in Akt/ GSK-3
/GS (glycogen synthase) pathway leading to glycogen synthesis in myocytes.