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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 46, Issue 12 - Dec 2013
Volume 46, Issue 11 - Nov 2013
Volume 46, Issue 10 - Oct 2013
Volume 46, Issue 9 - Sep 2013
Volume 46, Issue 8 - Aug 2013
Volume 46, Issue 7 - Jul 2013
Volume 46, Issue 6 - Jun 2013
Volume 46, Issue 5 - May 2013
Volume 46, Issue 4 - Apr 2013
Volume 46, Issue 3 - Mar 2013
Volume 46, Issue 2 - Feb 2013
Volume 46, Issue 1 - Jan 2013
Selecting the target year
Single-molecule fluorescence in situ hybridization: Quantitative imaging of single RNA molecules
Kwon, Sunjong ;
BMB Reports , volume 46, issue 2, 2013, Pages 65~72
DOI : 10.5483/BMBRep.2013.46.2.016
In situ detection of RNAs is becoming increasingly important for analysis of gene expression within and between intact cells in tissues. International genomics efforts are now cataloging patterns of RNA transcription that play roles in cell function, differentiation, and disease formation, and they are demon-strating the importance of coding and noncoding RNA transcripts in these processes. However, these techniques typically provide ensemble averages of transcription across many cells. In situ hybridization-based analysis methods complement these studies by providing information about how expression levels change between cells within normal and diseased tissues, and they provide information about the localization of transcripts within cells, which is important in understanding mechanisms of gene regulation. Multi-color, single-molecule fluorescence in situ hybridization (smFISH) is particularly useful since it enables analysis of several different transcripts simultaneously. Combining smFISH with immunofluorescent protein detection provides additional information about the association between transcription level, cellular localization, and protein expression in individual cells.
Mouse models of polycystic kidney disease induced by defects of ciliary proteins
Ko, Je Yeong ; Park, Jong Hoon ;
BMB Reports , volume 46, issue 2, 2013, Pages 73~79
DOI : 10.5483/BMBRep.2013.46.2.022
Polycystic kidney disease (PKD) is a common hereditary disorder which is characterized by fluid-filled cysts in the kidney. Mutation in either PKD1, encoding polycystin-1 (PC1), or PKD2, encoding polycystin-2 (PC2), are causative genes of PKD. Recent studies indicate that renal cilia, known as mechanosensors, detecting flow stimulation through renal tubules, have a critical function in maintaining homeostasis of renal epithelial cells. Because most proteins related to PKD are localized to renal cilia or have a function in ciliogenesis. PC1/PC2 heterodimer is localized to the cilia, playing a role in calcium channels. Also, disruptions of ciliary proteins, except for PC1 and PC2, could be involved in the induction of polycystic kidney disease. Based on these findings, various PKD mice models were produced to understand the roles of primary cilia defects in renal cyst formation. In this review, we will describe the general role of cilia in renal epithelial cells, and the relationship between ciliary defects and PKD. We also discuss mouse models of PKD related to ciliary defects based on recent studies.
Altered expression of adrenocorticotropic hormone in the epileptic gerbil hippocampus following spontaneous seizure
Oh, Yun-Jung ; Kim, Heung-No ; Jeong, Ji-Heon ; Park, Dae-Kyoon ; Park, Kyung-Ho ; Ko, Jeong-Sik ; Kim, Duk-Soo ;
BMB Reports , volume 46, issue 2, 2013, Pages 80~85
DOI : 10.5483/BMBRep.2013.46.2.149
We investigated the temporal alterations of adrenocorticotropic hormone (ACTH) immunoreactivity in the hippocampus after seizure onset. Expression of ACTH was observed within inter-neurons in the pre-seizure group of seizure sensitive gerbils, whereas its immunoreactivities were rarely detected in seizure resistant gerbil. Three hr after the seizure, ACTH immunoreac-tivity was significantly increased in interneurons within all hippocampal regions. On the basis of their localization and morphology through immunofluorescence staining, these cells were identified as
-containing interneurons. At the 12 hr postictal period, ACTH expression in these regions was down-regulated, in a similar manner to the pre-seizure group of gerbils. These findings support the increase in ACTH synthesis that contributes to a reduction of corticotrophin-releasing factor via the negative feedback system which in turn provides an opportunity to enhance the excitability of GABAergic interneurons. Therefore, ACTH may play an important role in the reduction of excitotoxicity in all hippocampal regions.
Tetrahydropteridines possess antioxidant roles to guard against glucose-induced oxidative stress in Dictyostelium discoideum
Park, Seon-Ok ; Kim, Hye-Lim ; Lee, Soo-Woong ; Park, Young Shik ;
BMB Reports , volume 46, issue 2, 2013, Pages 86~91
DOI : 10.5483/BMBRep.2013.46.2.128
Glucose effects on the vegetative growth of Dictyostelium discoideum Ax2 were studied by examining oxidative stress and tetrahydropteridine synthesis in cells cultured with different concentrations (0.5X, 7.7 g
; 1X, 15.4 g
; 2X, 30.8 g
) of glucose. The growth rate was optimal in 1X cells (cells grown in 1X glucose) but was impaired drastically in 2X cells, below the level of 0.5X cells. There were glucose-dependent increases in reactive oxygen species (ROS) levels and mitochondrial dysfunction in parallel with the mRNA copy numbers of the enzymes catalyzing tetrahydropteridine synthesis and regeneration. On the other hand, both the specific activities of the enzymes and tetrahydropteridine levels in 2X cells were lower than those in 1X cells, but were higher than those in 0.5X cells. Given the antioxidant function of tetrahydropteridines and both the beneficial and harmful effects of ROS, the results suggest glucose-induced oxidative stress in Dictyostelium, a process that might originate from aerobic glycolysis, as well as a protective role of tetrahydropteridines against this stress.
Egr-1 regulates the transcription of the BRCA1 gene by etoposide
Shin, Soon Young ; Kim, Chang Gun ; Lee, Young Han ;
BMB Reports , volume 46, issue 2, 2013, Pages 92~96
DOI : 10.5483/BMBRep.2013.46.2.202
The breast cancer susceptibility gene BRCA1 encodes a nuclear protein, which functions as a tumor suppressor and is involved in gene transcription and DNA repair processes. Many families with inherited breast and ovarian cancers have mutations in the BRCA1 gene. However, only a few studies have reported on the mechanism underlying the regulation of BRCA1 expression in humans. In this study, we investigated the transcriptional regulation of BRCA1 in HeLa cells treated with etoposide. We found that three Egr-1-binding sequences (EBSs) were located at -1031, -1005, and -385 within the enhancer region of the BRCA1 gene. Forced expression of Egr-1 stimulated the BRCA1 promoter activity. EMSA data showed that Egr-1 bound directly to the EBS within the BRCA1 gene. Knockdown of Egr-1 through the expression of a small hairpin RNA (shRNA) attenuated etoposide-induced BRCA1 promoter activity. We conclude that Egr-1 targets the BRCA1 gene in HeLa cells exposed to etoposide.
Somatic mutation patterns and compound response in cancers
He, Ningning ; Kim, Nayoung ; Yoon, Sukjoon ;
BMB Reports , volume 46, issue 2, 2013, Pages 97~102
DOI : 10.5483/BMBRep.2013.46.2.226
The use of various cancer cell lines can recapitulate known tumor-associated mutations and genetically define cancer subsets. This approach also enables comparative surveys of associations between cancer mutations and drug responses. Here, we analyzed the effects of ~40,000 compounds on cancer cell lines that showed diverse mutation-dependent sensitivity profiles. Over 1,000 compounds exhibited unique sensitivity on cell lines with specific mutational genotypes, and these compounds were clustered into six different classes of mutation-oriented sensitivity. The present analysis provides new insights into the relationship between somatic mutations and selectivity response of chemicals, and these results should have applications related to predicting and optimizing thera-peutic windows for anti-cancer agents.
Elevated RalA activity in the hippocampus of PI3Kγ knock-out mice lacking NMDAR-dependent long-term depression
Sim, Su-Eon ; Lee, Hye-Ryeon ; Kim, Jae-Ick ; Choi, Sun-Lim ; Bakes, Joseph ; Jang, Deok-Jin ; Lee, Kyungmin ; Han, Kihoon ; Kim, Eunjoon ; Kaang, Bong-Kiun ;
BMB Reports , volume 46, issue 2, 2013, Pages 103~106
DOI : 10.5483/BMBRep.2013.46.2.143
Phosphoinositide 3-kinases (PI3Ks) play key roles in synaptic plasticity and cognitive functions in the brain. We recently found that genetic deletion of
, the only known member of class IB PI3Ks, results in impaired N-methyl-D-aspartate receptor-dependent long-term depression (NMDAR-LTD) in the hippocampus. The activity of RalA, a small GTP-binding protein, increases following NMDAR-LTD inducing stimuli, and this increase in RalA activity is essential for inducing NMDAR-LTD. We found that RalA activity increased significantly in
knockout mice. Furthermore, NMDAR-LTD-inducing stimuli did not increase RalA activity in
knockout mice. These results suggest that constitutively increased RalA activity occludes further increases in RalA activity during induction of LTD, causing impaired NMDAR-LTD. We propose that
regulates the activity of RalA, which is one of the molecular mechanisms inducing NMDAR-dependent LTD.
Analysis and characterization of the functional TGFβ receptors required for BMP6-induced osteogenic differentiation of mesenchymal progenitor cells
Zhang, Yan ; Zhang, De-Ying ; Zhao, Yan-Fang ; Wang, Jin ; He, Juan-Wen ; Luo, Jinyong ;
BMB Reports , volume 46, issue 2, 2013, Pages 107~112
DOI : 10.5483/BMBRep.2013.46.2.141
Although BMP6 is highly capable of inducing osteogenic differentiation of mesenchymal progenitor cells (MPCs), the molecular mechanism involved remains to be fully elucidated. Using dominant negative (dn) mutant form of type I and type II
receptors, we demonstrated that three dn-type I receptors (dnALK2, dnALK3, dnALK6), and three dn-type II receptors (dnBMPRII, dnActRII, dnActRIIB), effectively diminished BMP6-induced osteogenic differentiation of MPCs. These findings suggested that ALK2, ALK3, ALK6, BMPRII, ActRII and ActRIIB are essential for BMP6-induced osteogenic differentiation of MPCs. However, MPCs in this study do not express ActRIIB. Moreover, RNA interference of ALK2, ALK3, ALK6, BMPRII and ActRII inhibited BMP6-induced osteogenic differentiation in MPCs. Our results strongly suggested that BMP6-induced osteogenic differentiation of MPCs is mediated by its functional
receptors including ALK2, ALK3, ALK6, BMPRII, and ActRII.
Overexpression of TTRAP inhibits cell growth and induces apoptosis in osteosarcoma cells
Zhou, Caihong ; Shen, Qi ; Xue, Jinglun ; Ji, Chaoneng ; Chen, Jinzhong ;
BMB Reports , volume 46, issue 2, 2013, Pages 113~118
DOI : 10.5483/BMBRep.2013.46.2.150
TTRAP is a multi-functional protein that is involved in multiple aspects of cellular functions including cell proliferation, apoptosis and the repair of DNA damage. Here, we demonstrated that the lentivirus-mediated overexpression of TTRAP significantly inhibited cell growth and induced apoptosis in osteosarcoma cells. The ectopic TTRAP suppressed the growth and colony formation capacity of two osteosarcoma cell lines, U2OS and Saos-2. Cell apoptosis was induced in U2OS cells and the cell cycle was arrested at G2/M phase in Saos-2 cells. Exogenous expression of TTRAP in serum-starved U2OS and Saos-2 cells induced an increase in caspase-3/-7 activity and a decrease in cyclin B1 expression. In comparison with wild-type TTRAP, mutations in the 5`-tyrosyl-DNA phosphodiesterase activity of TTRAP, in particular
, showed decreased inhibitory activity on cell growth. These results may aid in clarifying the physiological functions of TTRAP, especially its roles in the regulation of cell growth and tumorigenesis.
Salsolinol, a catechol neurotoxin, induces oxidative modification of cytochrome c
Kang, Jung Hoon ;
BMB Reports , volume 46, issue 2, 2013, Pages 119~123
DOI : 10.5483/BMBRep.2013.46.2.220
Methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline (salsolinol), an endogenous neurotoxin, is known to perform a role in the pathogenesis of Parkinson`s disease (PD). In this study, we evaluated oxidative modification of cytochrome c occurring after incubation with salsolinol. When cytochrome c was incubated with salsolinol, protein aggregation increased in a dose-dependent manner. The formation of carbonyl compounds and the release of iron were obtained in salsolinol-treated cytochrome c. Salsolinol also led to the release of iron from cytochrome c. Reactive oxygen species (ROS) scavengers and iron specific chelator inhibited the salsolinol-mediated cytochrome c modification and carbonyl compound formation. It is suggested that oxidative damage of cytochrome c by salsolinol might induce the increase of iron content in cells, subsequently leading to the deleterious condition which was observed. This mechanism may, in part, provide an explanation for the deterioration of organs under neurodegenerative disorders such as PD.
Transduced PEP-1-FK506BP ameliorates corneal injury in Botulinum toxin A-induced dry eye mouse model
Kim, Dae Won ; Lee, Sung Ho ; Ku, Sae Kwang ; Cho, Soo Hyun ; Cho, Sung-Woo ; Yoon, Ga Hyeon ; Hwang, Hyun Sook ; Park, Jinseu ; Eum, Won Sik ; Kwon, Oh-Shin ; Choi, Soo Young ;
BMB Reports , volume 46, issue 2, 2013, Pages 124~129
DOI : 10.5483/BMBRep.2013.46.2.272
FK506 binding protein 12 (FK506BP) belongs to a family of immunophilins, and is involved in multiple biological processes. However, the function of FK506BP in corneal disease remains unclear. In this study, we examined the protective effects on dry eye disease in a Botulinum toxin A (BTX-A) induced mouse model, using a cell-permeable PEP-1-FK506BP protein. PEP-1-FK506BP efficiently transduced into human corneal epithelial cells in a time- and dose-dependent manner, and remained stable in the cells for 48 h. In addition, we demonstrated that topical application of PEP-1-FK506BP was transduced into mouse cornea and conjunctiva by immunohistochemistry. Furthermore, topical application of PEP-1-FK506BP to BTX-A-induced mouse model markedly inhibited expression levels of pro-inflammatory cytokines such as interleukin-
), tumor necrosis factor-
) and macrophage inhibitory factor (MIF) in corneal and conjunctival epithelium. These results suggest PEP-1-FK506BP as a potential therapeutic agent for dry eye diseases.