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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 45, Issue 12 - Dec 2012
Volume 45, Issue 11 - Nov 2012
Volume 45, Issue 10 - Oct 2012
Volume 45, Issue 9 - Sep 2012
Volume 45, Issue 8 - Aug 2012
Volume 45, Issue 7 - Jul 2012
Volume 45, Issue 6 - Jun 2012
Volume 45, Issue 5 - May 2012
Volume 45, Issue 4 - Apr 2012
Volume 45, Issue 3 - Mar 2012
Volume 45, Issue 2 - Feb 2012
Volume 45, Issue 1 - Jan 2012
Selecting the target year
Tumor-associated autoantibodies as diagnostic and prognostic biomarkers
Heo, Chang-Kyu ; Bahk, Young Yil ; Cho, Eun-Wie ;
BMB Reports , volume 45, issue 12, 2012, Pages 677~685
DOI : 10.5483/BMBRep.2012.45.12.236
In the process of tumorigenesis, normal cells are remodeled to cancer cells and protein expression patterns are changed to those of tumor cells. A newly formed tumor microenvironment elicits the immune system and, as a result, a humoral immune response takes place. Although the tumor antigens are undetectable in sera at the early stage of tumorigenesis, the nature of an antibody amplification response to antigens makes tumor-associated autoantibodies as promising early biomarkers in cancer diagnosis. Moreover, the recent development of proteomic techniques that make neo-epitopes of tumor-associated autoantigens discovered concomitantly has opened a new area of 'immuno-proteomics', which presents tumor-associated autoantibody signatures and confers information to redefine the process of tumorigenesis. In this article, the strategies recently used to identify and validate serum autoantibodies are outlined and tumor-associated antigens suggested until now as diagnostic/prognostic biomarkers in various tumor types are reviewed. Also, the meaning of autoantibody signatures and their clinical utility in personalized medicine are discussed.
Mouse genetics: Catalogue and scissors
Sung, Young Hoon ; Baek, In-Jeoung ; Seong, Je Kyung ; Kim, Jin-Soo ; Lee, Han-Woong ;
BMB Reports , volume 45, issue 12, 2012, Pages 686~692
DOI : 10.5483/BMBRep.2012.45.12.242
Phenotypic analysis of gene-specific knockout (KO) mice has revolutionized our understanding of in vivo gene functions. As the use of mouse embryonic stem (ES) cells is inevitable for conventional gene targeting, the generation of knockout mice remains a very time-consuming and expensive process. To accelerate the large-scale production and phenotype analyses of KO mice, international efforts have organized global consortia such as the International Knockout Mouse Consortium (IKMC) and International Mouse Phenotype Consortium (IMPC), and they are persistently expanding the KO mouse catalogue that is publicly available for the researches studying specific genes of interests in vivo. However, new technologies, adopting zinc-finger nucleases (ZFNs) or Transcription Activator-Like Effector (TALE) Nucleases (TALENs) to edit the mouse genome, are now emerging as valuable and effective shortcuts alternative for the conventional gene targeting using ES cells. Here, we introduce the recent achievement of IKMC, and evaluate the significance of ZFN/TALEN technology in mouse genetics.
Structure and catalytic mechanism of human protein tyrosine phosphatome
Kim, Seung Jun ; Ryu, Seong Eon ;
BMB Reports , volume 45, issue 12, 2012, Pages 693~699
DOI : 10.5483/BMBRep.2012.45.12.240
Together with protein tyrosine kinases (PTKs), protein tyrosine phosphatases (PTPs) serve as hallmarks in cellular signal transduction by controlling the reversible phosphorylation of their substrates. The human genome is estimated to encode more than 100 PTPs, which can be divided into eleven sub-groups according to their structural and functional characteristics. All the crystal structures of catalytic domains of sub-groups have been elucidated, enabling us to understand their precise catalytic mechanism and to compare their structures across all sub-groups. In this review, I describe the structure and mechanism of catalytic domains of PTPs in the structural context.
Involvement of protein tyrosine phosphatases in adipogenesis: New anti-obesity targets?
Bae, Kwang-Hee ; Kim, Won Kon ; Lee, Sang Chul ;
BMB Reports , volume 45, issue 12, 2012, Pages 700~706
DOI : 10.5483/BMBRep.2012.45.12.235
Obesity is a worldwide epidemic as well as being a major risk factor for diabetes, cardiovascular diseases and several types of cancers. Obesity is mainly due to the overgrowth of adipose tissue arising from an imbalance between energy intake and energy expenditure. Adipose tissue, primarily composed of adipocytes, plays a key role in maintaining whole body energy homeostasis. In view of the treatment of obesity and obesity-related diseases, it is critical to understand the detailed signal transduction mechanisms of adipogenic differentiation. Adipogenic differentiation is tightly regulated by many key signal cascades, including insulin signaling. These signal cascades generally transfer or amplify the signal by using serial tyrosine phosphorylations. Thus, protein tyrosine kinases and protein tyrosine phosphatases are closely related to adipogenic differentiation. Compared to protein tyrosine kinases, protein tyrosine phosphatases have received little attention in adipogenic differentiation. This review aims to highlight the involvement of protein tyrosine phosphatases in adipogenic differentiation and the possibility of protein tyrosine phosphatases as drugs to target obesity.
Roles of cysteine residues in the inhibition of human glutamate dehydrogenase by palmitoyl-CoA
Son, Hyo Jeong ; Ha, Seung Cheol ; Hwang, Eun Young ; Kim, Eun-A ; Ahn, Jee-Yin ; Choi, Soo Young ; Cho, Sung-Woo ;
BMB Reports , volume 45, issue 12, 2012, Pages 707~712
DOI : 10.5483/BMBRep.2012.45.12.156
Human glutamate dehydrogenase isozymes (hGDH1 and hGDH2) have been known to be inhibited by palmitoyl-CoA with a high affinity. In this study, we have performed the cassette mutagenesis at six different Cys residues (Cys59, Cys93, Cys119, Cys201, Cys274, and Cys323) to identify palmitoyl-CoA binding sites within hGDH2. Four cysteine residues at positions of C59, C93, C201, or C274 may be involved, at least in part, in the inhibition of hGDH2 by palmitoyl-CoA. There was a biphasic relationship, depending on the levels of palmitoyl-CoA, between the binding of palmitoyl-CoA and the loss of enzyme activity during the inactivation process. The inhibition of hGDH2 by palmitoyl-CoA was not affected by the allosteric inhibitor GTP. Multiple mutagenesis studies on the hGDH2 are in progress to identify the amino acid residues fully responsible for the inhibition by palmitoyl-CoA.
Ganglioside GM1 influences the proliferation rate of mouse induced pluripotent stem cells
Ryu, Jae-Sung ; Chang, Kyu-Tae ; Lee, Ju-Taek ; Lim, Malg-Um ; Min, Hyun-Ki ; Na, Yoon-Ju ; Lee, Su-Bin ; Moussavou, Gislain ; Kim, Sun-Uk ; Kim, Ji-Su ; Ko, Kinarm ; Ko, Kisung ; Hwang, Kyung-A ; Jeong, Eun-Jeong ; Lee, Jeong-Woong ; Choo, Young-Kug ;
BMB Reports , volume 45, issue 12, 2012, Pages 713~718
DOI : 10.5483/BMBRep.2012.45.12.138
Gangliosides play important roles in the control of several biological processes, including proliferation and transmembrane signaling. In this study, we demonstrate the effect of ganglioside GM1 on the proliferation of mouse induced pluripotent stem cells (miPSCs). The proliferation rate of miPSCs was lower than in mouse embryonic stem cells (mESCs). Fluorescence activated cell sorting analysis showed that the percentage of cells in the G2/M phase in miPSCs was lower than that in mESCs. GM1 was expressed in mESCs, but not miPSCs. To confirm the role of GM1 in miPSC proliferation, miPSCs were treated with GM1. GM1-treated miPSCs exhibited increased cell proliferation and a larger number of cells in the G2/M phase. Furthermore, phosphorylation of mitogen-activated protein kinases was increased in GM1-treated miPSCs.
HER2 induces expression of leptin in human breast epithelial cells
Cha, Yujin ; Kang, Youjin ; Moon, Aree ;
BMB Reports , volume 45, issue 12, 2012, Pages 719~723
DOI : 10.5483/BMBRep.2012.45.12.164
A close association between the obesity hormone leptin and breast cancer progression has been suggested. The present study investigated the molecular mechanism for enhanced leptin expression in breast cancer cells and its functional significance in breast cancer aggressiveness. We examined whether leptin expression level is affected by the oncoprotein human epidermal growth factor receptor2 (HER2), which is overexpressed in ~30% of breast tumors. Here, we report, for the first time, that HER2 induces transcriptional activation of leptin in MCF10A human breast epithelial cells. We also showed that p38 mitogen-activated protein kinase signaling was involved in leptin expression induced by HER2. We showed a crucial role of leptin in the invasiveness of HER2-MCF10A cells using an siRNA molecule targeting leptin. Taken together, the results indicate a molecular link between HER2 and leptin, providing supporting evidence that leptin represents a target for breast cancer therapy.
The effects of Caffeoylserotonin on inhibition of melanogenesis through the downregulation of MITF via the reduction of intracellular cAMP and acceleration of ERK activation in B16 murine melanoma cells
Kim, Hye-Eun ; Ishihara, Atsushi ; Lee, Seong-Gene ;
BMB Reports , volume 45, issue 12, 2012, Pages 724~729
DOI : 10.5483/BMBRep.2012.45.12.039
In this study, we evaluated the anti-melanogenesis effects of Caffeoylserotonin (CaS) in B16 melanoma cells. Treatment with CaS reduced the melanin content and tyrosinase (TYR) activity in B16 melanoma cells in a dose-dependent manner. CaS inhibited the expression of melanogenesis-related proteins, including microphthalmia-associated transcription factor (MITF), TYR, and tyrosinase-related protein-1 (TRP-1), but not TRP-2.
-MSH is known to interact with melanocortin 1 receptor (MC1R) thus activating adenylyl cyclase and increasing intracellular cyclic AMP (cAMP) levels. Furthermore, cAMP activates extracellular signal-regulated kinase 2 (ERK2) via phosphorylation, which phosphorylates MITF, thereby targeting the transcription factor to proteasomes for degradation. The CaS reduced intracellular cAMP levels to unstimulated levels and activated ERK phosphorylation within 30 min. The ERK inhibitor PD98059 abrogated the suppressive effect of CaS on
-MSH-induced melanogenesis. Based on this study, the inhibitory effects of CaS on melanogenesis are derived from the downregulation of MITF signaling via the inhibition of intracellular cAMP levels, as well as acceleration of ERK activation.
p13 from group II baculoviruses is a killing-associated gene
Lu, Nan ; Du, Enqi ; Liu, Yangkun ; Qiao, Hong ; Yao, Lunguang ; Pan, Zishu ; Lu, Songya ; Qi, Yipeng ;
BMB Reports , volume 45, issue 12, 2012, Pages 730~735
DOI : 10.5483/BMBRep.2012.45.12.058
p13 gene was first described in Leucania separata multinuclear polyhedrosis virus (Ls-p13) several years ago, but the function of P13 protein has not been experimentally investigated to date. In this article, we indicated that the expression of p13 from Heliothis armigera single nucleocapsid nucleopolyhedrovirus (Ha-p13) was regulated by both early and late promoter. Luciferase assay demonstrated that the activity of Ha-p13 promoter with hr4 enhancer was more than 100 times in heterologous Sf9 cells than that in nature host Hz-AM1 cells. Both Ls-P13 and Ha-P13 are transmembrane proteins. Confocal microscopic analysis showed that both mainly located in the cytoplasm membrane at 48 h. Results of RNA interference indicated that Ha-p13 was a killing-associated gene for host insects H. armigera. The AcMNPV acquired the mentioned killing activity and markedly accelerate the killing rate when expressing Ls-p13. In conclusion, p13 is a killing associated gene in both homologous and heterologous nucleopolyhedrovirus.
In-silico and In-vitro based studies of Streptomyces peucetius CYP107N3 for oleic acid epoxidation
Bhattarai, Saurabh ; Niraula, Narayan Prasad ; Sohng, Jae Kyung ; Oh, Tae-Jin ;
BMB Reports , volume 45, issue 12, 2012, Pages 736~741
DOI : 10.5483/BMBRep.2012.45.12.080
Certain members of the cytochromes P450 superfamily metabolize polyunsaturated long-chain fatty acids to several classes of oxygenated metabolites. An approach based on in silico analysis predicted that Streptomyces peucetius CYP107N3 might be a fatty acid-metabolizing enzyme, showing high homology with epoxidase enzymes. Homology modeling and docking studies of CYP107N3 showed that oleic acid can fit directly into the active site pocket of the double bond of oleic acid within optimum distance of
from the Fe. In order to confirm the epoxidation activity proposed by in silico analysis, a gene coding CYP107N3 was expressed in Escherichia coli. The purified CYP107N3 was shown to catalyze
epoxidation of oleic acid in vitro to 9,10-epoxy stearic acid confirmed by ESI-MS, HPLC-MS and GC-MS spectral analysis.
Antiapoptotic effects of Phe140Asn, a novel human granulocyte colony-stimulating factor mutant in H9c2 rat cardiomyocytes
Chung, Hee Kyoung ; Ko, Eun Mi ; Kim, Sung Woo ; Byun, Sung-June ; Chung, Hak-Jae ; Kwon, Moosik ; Lee, Hwi-Cheul ; Yang, Byoung-Chul ; Han, Deug-Woo ; Park, Jin-Ki ; Hong, Sung-Gu ; Chang, Won-Kyong ; Kim, Kyung-Woon ;
BMB Reports , volume 45, issue 12, 2012, Pages 742~747
DOI : 10.5483/BMBRep.2012.45.12.095
Granulocyte colony-stimulating factor (G-CSF) is used for heart failure therapy and promotes myocardial regeneration by inducing mobilization of bone marrow stem cells to the injured heart after myocardial infarction; however, this treatment has one weakness in that its biological effect is transient. In our previous report, we generated 5 mutants harboring N-linked glycosylation to improve its antiapoptotic activities. Among them, one mutant (Phe140Asn) had higher cell viability than wild-type hG-CSF in rat cardiomyocytes, even after treatment with an apoptotic agent (
). Cells treated with this mutant significantly upregulated the antiapoptotic proteins, and experienced reductions in caspase 3 activity and PARP cleavage. Moreover, the total number of apoptotic cells was dramatically lower in cultures treated with mutant hG-CSF. Taken together, these results suggest that the addition of an N-linked glycosylation was successful in improving the antiapoptotic activity of hG-CSF, and that this mutated product will be a feasible therapy for patients who have experienced heart failure.
Rationalization of allosteric pathway in Thermus sp. GH5 methylglyoxal synthase
Zareian, Shekufeh ; Khajeh, Khosro ; Pazhang, Mohammad ; Ranjbar, Bijan ;
BMB Reports , volume 45, issue 12, 2012, Pages 748~753
DOI : 10.5483/BMBRep.2012.45.12.11-138
A sequence of 10 amino acids at the C-terminus region of methylglyoxal synthase from Escherichia coli (EMGS) provides an arginine, which plays a crucial role in forming a salt bridge with a proximal aspartate residue in the neighboring subunit, consequently transferring the allosteric signal between subunits. In order to verify the role of arginine, the gene encoding MGS from a thermophile species, Thermus sp. GH5 (TMGS) lacking this arginine was cloned with an additional 30 bp sequence at the 3'-end and then expressed in form of a fusion TMGS with a 10 residual segment at the C-terminus (
). The resulting recombinant enzyme showed a significant increase in cooperativity towards phosphate, reflected by a change in the Hill coefficient (nH) from 1.5 to 1.99. Experiments including site directed mutagenesis for Asp-10 in TMGS and
, two dimentional structural survey, fluorescence and irreversible thermoinactivation were carried out to confirm this pathway.