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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 43, Issue 12 - Dec 2010
Volume 43, Issue 11 - Nov 2010
Volume 43, Issue 10 - Oct 2010
Volume 43, Issue 9 - Sep 2010
Volume 43, Issue 8 - Aug 2010
Volume 43, Issue 7 - Jul 2010
Volume 43, Issue 6 - Jun 2010
Volume 43, Issue 5 - May 2010
Volume 43, Issue 4 - Apr 2010
Volume 43, Issue 3 - Mar 2010
Volume 43, Issue 2 - Feb 2010
Volume 43, Issue 1 - Jan 2010
Selecting the target year
Overview of personalized medicine in the disease genomic era
Hong, Kyung-Won ; Oh, Berm-Seok ;
BMB Reports , volume 43, issue 10, 2010, Pages 643~648
DOI : 10.5483/BMBRep.2010.43.10.643
Sir William Osler (1849-1919) recognized that "variability is the law of life, and as no two faces are the same, so no two bodies are alike, and no two individuals react alike and behave alike under the abnormal conditions we know as disease". Accordingly, the traditional methods of medicine are not always best for all patients. Over the last decade, the study of genomes and their derivatives (RNA, protein and metabolite) has rapidly advanced to the point that genomic research now serves as the basis for many medical decisions and public health initiatives. Genomic tools such as sequence variation, transcription and, more recently, personal genome sequencing enable the precise prediction and treatment of disease. At present, DNA-based risk assessment for common complex diseases, application of molecular signatures for cancer diagnosis and prognosis, genome-guided therapy, and dose selection of therapeutic drugs are the important issues in personalized medicine. In order to make personalized medicine effective, these genomic techniques must be standardized and integrated into health systems and clinical workflow. In addition, full application of personalized or genomic medicine requires dramatic changes in regulatory and reimbursement policies as well as legislative protection related to privacy. This review aims to provide a general overview of these topics in the field of personalized medicine.
Epigenetic modification is linked to Alzheimer`s disease: is it a maker or a marker?
Lee, Jung-Hee ; Ryu, Hoon ;
BMB Reports , volume 43, issue 10, 2010, Pages 649~655
DOI : 10.5483/BMBRep.2010.43.10.649
Alzheimer`s disease (AD) is the most common age-dependent neurodegenerative disorder and shows progressive memory loss and cognitive decline. Intraneuronal filaments composed of aggregated hyperphosphorylated tau protein, called neurofibrillary tangles, along with extracellular accumulations of amyloid
), called senile plaques, are known to be the neuropathological hallmarks of AD. In light of recent studies, epigenetic modification has emerged as one of the pathogenic mechanisms of AD. Epigenetic changes encompass an array of molecular modifications to both DNA and chromatin, including transcription factors and cofactors. In this review, we summarize how DNA methylation and changes to DNA chromatin packaging by post-translational histone modification are involved in AD. In addition, we describe the role of SIRTs, histone deacetylases, and the effect of SIRT-modulating drugs on AD. Lastly, we discuss how amyloid precursor protein (APP) intracellular domain (AICD) regulates neuronal transcription. Our understanding of the epigenomes and transcriptomes of AD may warrant future identification of novel biological markers and beneficial therapeutic targets for AD.
Possible roles of amyloid intracellular domain of amyloid precursor protein
Chang, Keun-A ; Suh, Yoo-Hun ;
BMB Reports , volume 43, issue 10, 2010, Pages 656~663
DOI : 10.5483/BMBRep.2010.43.10.656
Amyloid precursor protein (APP), which is critically involved in the pathogenesis of Alzheimer`s disease (AD), is cleaved by gamma/epsilon-secretase activity and results in the generation of different lengths of the APP Intracellular C-terminal Domain (AICD). In spite of its small size and short half-life, AICD has become the focus of studies on AD pathogenesis. Recently, it was demonstrated that AICD binds to different intracellular binding partners (`adaptor protein`), which regulate its stability and cellular localization. In terms of choice of adaptor protein, phosphorylation seems to play an important role. AICD and its various adaptor proteins are thought to take part in various cellular events, including regulation of gene transcription, apoptosis, calcium signaling, growth factor, and
pathway activation, as well as the production, trafficking, and processing of APP, and the modulation of cytoskeletal dynamics. This review discusses the possible roles of AICD in the pathogenesis of neurodegenerative diseases including AD.
Evaluation of chemopreventive effects of Thymoquinone on cell surface glycoconjugates and cytokeratin expression during DMBA induced hamster buccal pouch carcinogenesis
Rajkamal, G. ; Suresh, K. ; Sugunadevi, G. ; Vijayaanand, M.A. ; Rajalingam, K. ;
BMB Reports , volume 43, issue 10, 2010, Pages 664~669
DOI : 10.5483/BMBRep.2010.43.10.664
The present study aimed to investigate the membrane stabilizing effect of Thymoquinone (TQ) on cell surface glycoconjugates and cytokeratin expression against DMBA induced hamster buccal pouch carcinogenesis. 0.5% DMBA painting (three times per week) in hamster buccal pouches for 14 weeks resulted in the formation of well developed oral squamous cell carcinoma. We observed 100% tumor formation with marked abnormalities of glycoconjugates status in tumor bearing hamsters as compared to control animals. Oral administration of TQ at a dose of 30 mg/kg body weight, to DMBA painted hamsters on alternate days for 14 weeks, reduced the tumor formation as well as protected the levels of cell surface glycoconjugates in DMBA painted hamsters. The present study thus suggests that TQ has potent chemopreventive efficacy as well as protected the abnormalities on cell surface glycoconjugates during DMBA induced hamster buccal pouch carcinogenesis.
A novel method for predicting protein subcellular localization based on pseudo amino acid composition
Ma, Junwei ; Gu, Hong ;
BMB Reports , volume 43, issue 10, 2010, Pages 670~676
DOI : 10.5483/BMBRep.2010.43.10.670
In this paper, a novel approach, ELM-PCA, is introduced for the first time to predict protein subcellular localization. Firstly, Protein Samples are represented by the pseudo amino acid composition (PseAAC). Secondly, the principal component analysis (PCA) is employed to extract essential features. Finally, the Elman Recurrent Neural Network (RNN) is used as a classifier to identify the protein sequences. The results demonstrate that the proposed approach is effective and practical.
Dendritic localization and a cis-acting dendritic targeting element of Kv4.2 mRNA
Jo, Anna ; Nam, Yeon-Ju ; Oh, Jun-Young ; Cheon, Hyo-Soon ; Jeromin, Andreas ; Lee, Jin-A ; Kim, Hyong-Kyu ;
BMB Reports , volume 43, issue 10, 2010, Pages 677~682
DOI : 10.5483/BMBRep.2010.43.10.677
Kv4.2, a pore-forming
-subunit of voltage-gated A-type potassium channels, is expressed abundantly in the soma and dendrites of hippocampal neurons, and is responsible for somatodendritic
current. Recent studies have suggested that changes in the surface levels of Kv4.2 potassium channels might be relevant to synaptic plasticity. Although the function and expression of Kv4.2 protein have been extensively studied, the dendritic localization of Kv4.2 mRNA is not well described. In this study, Kv4.2 mRNAs were shown to be localized in the dendrites near postsynaptic regions. The dendritic transport of Kv4.2 mRNAs were mediated by microtubule-based movement. The 500 nucleotides of specific regions within the 3`-untranslated region of Kv4.2 mRNA were found to be necessary and sufficient for its dendritic localization. Collectively, these results suggest that the dendritic localization of Kv4.2 mRNAs might regulate the dendritic surface level of Kv4.2 channels and synaptic plasticity.
Protective effects of carnosine and homocarnosine on ferritin and hydrogen peroxide-mediated DNA damage
Kang, Jung-Hoon ;
BMB Reports , volume 43, issue 10, 2010, Pages 683~687
DOI : 10.5483/BMBRep.2010.43.10.683
Previous studies have shown that one of the primary causes of increased iron content in the brain may be the release of excess iron from intracellular iron storage molecules such as ferritin. Free iron generates ROS that cause oxidative cell damage. Carnosine and related compounds such as endogenous histidine dipetides have antioxidant activities. We have investigated the protective effects of carnosine and homocarnosine against oxidative damage of DNA induced by reaction of ferritin with
. The results show that carnosine and homocarnosine prevented ferritin/
-mediated DNA strand breakage. These compounds effectively inhibited ferritin/
-mediated hydroxyl radical generation and decreased the mutagenicity of DNA induced by the ferritin/
reaction. Our results suggest that carnosine and related compounds might have antioxidant effects on DNA under pathophysiological conditions leading to degenerative damage such as neurodegenerative disorders.
Preventable effect of L-threonate, an ascorbate metabolite, on androgen-driven balding via repression of dihydrotestosteroneinduced dickkopf-1 expression in human hair dermal papilla cells
Kwack, Mi-Hee ; Ahn, Ji-Sup ; Kim, Moon-Kyu ; Kim, Jung-Chul ; Sung, Young-Kwan ;
BMB Reports , volume 43, issue 10, 2010, Pages 688~692
DOI : 10.5483/BMBRep.2010.43.10.688
In a previous study, we recently claimed that dihydrotestosterone (DHT)-inducible dickkopf-1 (DKK-1) expression is one of the key factors involved in androgen-potentiated balding. We also demonstrated that L-ascorbic acid 2-phosphate (Asc 2-P) represses DHT-induced DKK-1 expression in cultured dermal papilla cells (DPCs). Here, we investigated whether or not L-threonate could attenuate DHT-induced DKK-1 expression. We observed via RT-PCR analysis and enzyme-linked immunosorbent assay that DHT-induced DKK-1 expression was attenuated in the presence of L-threonate. We also found that DHT-induced activation of DKK-1 promoter activity was significantly repressed by L-threonate. Moreover, a co-culture system featuring outer root sheath (ORS) keratinocytes and DPCs showed that DHT inhibited the growth of ORS cells, which was then significantly reversed by L-threonate. Collectively, these results indicate that L-threonate inhibited DKK-1 expression in DPCs and therefore is a good treatment for the prevention of androgen-driven balding.
Three novel germline mutations in MLH1 and MSH2 in families with Lynch syndrome living on Jeju island, Korea
Kim, Young-Mee ; Choe, Chang-Gyu ; KimCho, So-Mi ; Jung, In-Ho ; Chang, Won-Young ; Cho, Moon-Jae ;
BMB Reports , volume 43, issue 10, 2010, Pages 693~697
DOI : 10.5483/BMBRep.2010.43.10.693
Hereditary non-polyposis colorectal cancer (HNPCC) is an autosomal dominant syndrome characterized by predisposition to early-onset cancers. HNPCC is caused by heterozygous loss-of-function mutations within the mismatch repair genes MLH1, MSH2, MSH6, PMS1, and PMS2. We genotyped the MLH1 and MSH2 genes in patients suffering from Lynch syndrome and in 11 unrelated patients who were diagnosed with colorectal cancer and had subsequently undergone surgery. Five Lynch syndrome patients carried germline mutations in MLH1 or MSH2. Two of these were identified as known mutations in MLH1: deletion of exon 10 and a point mutation (V384D). The remaining three patients exhibited novel mutations: a duplication (937_942dupGAAGTT) in MLH1; deletion of exons 8, 9, and 10; and a point mutation in MLH1 (F396I) combined with multiple missense mutations in MSH2 (D295G, K808E, Q855P, and I884T). The findings underline the importance of efficient pre-screening of conspicuous cases.
Susceptibility for breast cancer in young patients with short rare minisatellite alleles of BORIS
Yoon, Se-Lyun ; Kim, Dae-Cheol ; Cho, Se-Heon ; Lee, Sang-Yeop ; Chu, In-Sun ; Heo, Jeong-Hoon ; Leem, Sun-Hee ;
BMB Reports , volume 43, issue 10, 2010, Pages 698~703
DOI : 10.5483/BMBRep.2010.43.10.698
In this study, we characterized two blocks of minisatellites in the 5` upstream region of the BORIS gene (BORIS-MS1, -MS2). BORIS-MS2 was found to be polymorphic; therefore, this locus could be useful as a marker for DNA fingerprinting. We assessed the association between BORIS-MS2 and breast cancer by a case-control study with 428 controls and 793 breast cancers cases. Rare alleles in the younger group (age, <40) were associated with a statistically significant increased risk of breast cancer (odds ratio, 4.84; 95% confidence interval, 1.06-22.22; and P
Swedish mutation within amyloid precursor protein modulates global gene expression towards the pathogenesis of Alzheimer`s disease
Shin, Jong-Yeon ; Yu, Saet-Byeol ; Yu, Un-Young ; Ahnjo, Sang-Mee ; Ahn, Jung-Hyuck ;
BMB Reports , volume 43, issue 10, 2010, Pages 704~709
DOI : 10.5483/BMBRep.2010.43.10.704
The Swedish mutation (K595N/M596L) of amyloid precursor protein (APP-swe) has been known to increase abnormal cleavage of cellular APP by Beta-secretase (BACE), which causes tau protein hyperphosphorylation and early-onset Alzheimer`s disease (AD). Here, we analyzed the effect of APP-swe in global gene expression using deep transcriptome sequencing technique. We found 283 genes were down-regulated and 348 genes were up-regulated in APP-swe expressing H4-swe cells compared to H4 wild-type cells from a total of approximately 74 million reads of 38 base pairs from each transcriptome. Two independent mechanisms such as kinase and phosphatase signaling cascades leading hyperphosphorylation of tau protein were regulated by the expression of APP-swe. Expressions of catalytic subunit as well as several regulatory subunits of protein phosphatases 2A were decreased. In contrast, expressions of tau-phosphorylating glycogen synthase kinase
), cyclin dependent kinase 5 (CDK5), and cAMP-dependent protein kinase A (PKA) catalytic subunit were increased. Moreover, the expression of AD-related Aquaporin 1 and presenilin 2 expression was regulated by APP-swe. Taken together, we propose that the expression of APP-swe modulates global gene expression directed to AD pathogenesis.