• BMB Reports
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• v.48 no.5
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• pp.239-240
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• 2015

Dysregulation of cytokine expression causes inflammatory diseases or chronic infection conditions. We have identified that Tat-activating regulatory DNA-binding protein-43 (TDP-43) is involved in cytokine RNA processing in order to promote an optimal immune response. The interaction of TDP-43 with spliceosomal components from the Cajal body leads to the formation of a novel sub-nuclear body called the Interleukin (IL)-6 and IL-10 Splicing Activating Compartment (InSAC). TDP-43 binds to the IL-6 and IL-10 RNAs in a sequence-dependent manner. In cell-based studies, we observed that lipopoly-saccharide (LPS) stimulation induces the formation of the InSAC through TDP-43 ubiquitination, thereby influencing the processing and expression levels of IL-6 RNA. Moreover, TDP-43 knockdown in vivo results in a decrease in IL-6 production and its RNA splicing and stability. Thus, these findings demonstrate that the InSAC is linked to the activation and modulation of the immune response. [BMB Reports 2015; 48(5): 239-240]

• IMMUNE NETWORK
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• v.2 no.3
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• pp.150-157
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• 2002

Background: Although Tat plays a role as a potent transactivator in the viral gene expression from the Human Immunodeficiency Virus type 1 long terminal repeat (HIV-1 LTR), it does not function efficiently in rodent cells implying the absence of a human specific factor essential for Tat-medicated transactivation in rodent cells. In previous experiments, we demonstrated that one of chimeric forms of TAR (transacting responsive element) of HIV-1 LTR compensated the restriction in rodent cells. Methods: To characterize the nature of the compensation, we tested the effects of several upstream binding factors of HIV-1 LTR by simple substitution, and also examined the role of the configuration of the upstream binding factor(s) indirectly by constructing spacing mutants that contained insertions between Sp1 and TATA box on Tat-mediated transactivation. Results: Human Sp1 had no effect whereas its associated factors displayed differential effects in human and rodent cells. In addition, none of the spacing mutants tested overcame the restriction in rodent cells. Rather, when the secondary structure of the chimeric HIV-1 TAR construct was destroyed, the compensation in rodent cells was disappeared. Interestingly, the proper interaction between Sp1 and TATA box binding proteins, which is essential for Tat-dependent transcription, was dispensable in rodent cells. Conclusion: This result suggests that the human-specific Tat cofactor acts to allow Tat to interact effectively in a ribonucleoprotein complex that includes Tat, cellular factors, and TAR RNA, rather than be associated with the HIV-1 LTR upstream DNA binding factors.

• 한국전산유체공학회:학술대회논문집
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• 2009.11a
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• pp.97-102
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• 2009

Translocation of biopolymers such as DNA and RNA through a nano-pore is an important process in biotechnology applications. The translocation process of a biopolymer through an artificial nano-pore in the presence of a fluid solvent is simulated. The polymer motion is simulated by Langevin molecular dynamics (MD) techniques while the solvent dynamics are taken into account by lattice-Boltzmann method (LBM). The hydrodynamic interactions are considered explicitly by coupling the polymer and solvent through the frictional and the random forces. From simulation results we found that the hydrodynamic interactions between polymer and solvent speed-up the translocation process. The translocation time ${\tao}_T$ scales with the chain length N as ${{\tau}_T}^{\propto}N^{\alpha}$. The value of scaling exponents($\alpha$) obtained from our simulations are $1.29{\pm}0.03$ and $1.41{\pm}0.03$, with and without hydrodynamic interactions, respectively. Our simulation results are in good agreement with the experimentally observed value of $\alpha$, which is equal to $1.27{\pm}0.03$, particularly when hydrodynamic interaction effects are taken into account.

• Biotechnology and Bioprocess Engineering:BBE
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• v.9 no.1
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• pp.23-34
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• 2004

Escherichia coli transcription termination factor Rho catalyzes the unwinding of RNA/DNA duplex in reactions that are coupled to ATP binding and hydrolysis. Fluorescence stopped-flow methods using ATP and the fluorescent 2'(3')-O-( N-methylanthraniloyl) derivatives (mant-derivatives) of ATP and ADP were used to probe the kinetics of nucleotide binding to and dissociation from the Rho-RNA complex. Presteady state nucleotide binding kinetics provides evidence for the presence of negative cooperativity in nucleotide binding among the multiple nucleotide binding sites on Rho hexamer. The binding of the first nucleotide to the Rho-RNA complex occurs at a bimolecular rate of 3.6${\times}$10$\^$6/ M$\^$-1/ sec$\^$-1/ whereas the second nucleotide binds at a slower rate of 4.7${\times}$10$\^$5/ M$\^$-1/ sec$\^$-1/ at 18$^{\circ}C$, RNA complexed with Rho affects the kinetics of nucleotide interaction with the active sites through conformational changes to the Rho hexamer, allowing the incoming nucleotide to be more accessible to the sites. Adenine nucleotide binding and dissociation is more favorable when RNA is bound to Rho, whereas ATP binding and dissociation step in the absence of RNA occurs significantly slower, at a rate ∼70- and ∼40-fold slower than those observed with the Rho-RNA complex, respectively.

• BMB Reports
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• v.32 no.2
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• pp.119-126
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• 1999

The SH3 domain of PLC-${\gamma}1$ has been known to induce DNA synthesis. However, little is known about the putative effector proteins that associate with the domain. In this report, we provide evidence that the SH3 domain of PLC-${\gamma}1$ associates with Shc, which has been implicated in the activation of p21Ras in response to many growth factors. The association between Shc and PLC-${\gamma}1$ is enhanced either by v-Src-induced transformation or EGF-stimulation in vivo and in vitro. Furthermore, from transient expression studies with COS-7 cells, we show that the SH3 domain of PLC-${\gamma}1$ is required for association with Shc in vivo, whereas tyrosyl phosphorylation of PLC-${\gamma}1$ is not. Taken together, we suggest that Shc might be involved in the PLC-${\gamma}1$-mediated signaling pathway.

• Journal of Microbiology and Biotechnology
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• v.13 no.6
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• pp.1008-1012
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• 2003

Symbiobacterium toebii has been reported as a thermophile exhibiting a commensal interaction with Geobacillus toebii. The distribution of the commensal thermophiles in various soils was investigated using a denaturing gradient gel electrophoresis (DGGE). Based on the DGGE analysis, the enrichment condition for the growth of Symbiobacterium sp. was found to also enrich populations of several other microbial spp. as well as Symbiobacterium sp. In the enrichment experiment, several different 16S rDNA sequences of commensal thermophiles were detected in all of the soil samples tested, indicating that commensal thermophiles are widely distributed in various soils.

• Journal of the Korean Magnetic Resonance Society
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• v.22 no.3
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• pp.64-70
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• 2018

Human Tid1, belonging to the family of the Hsp40/DnaJ, functions as a co-chaperone of cytosolic and mitochondrial Hsp70 proteins. In addition, the conserved J-domain and G/F-rich region of Tid1 has been suggested to interact with the p53 tumor suppressor protein, to translocate it to the mitochondria. Here, backbone NMR assignments were achieved for the putative p53-binding domain of Tid1. The obtained chemical shift information identified five ${\alpha}$-helices including four helices characteristic of J-domain, which are connected to a short ${\alpha}$-helix in the G/F-rich region via a flexible loop region. We expect that this structural information would contribute to our progressing studies to elucidate atomic structure and molecular interaction of the domain with p53.

• Environmental Mutagens and Carcinogens
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• v.26 no.2
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• pp.45-47
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• 2006

The reactive oxygen species (ROS) caused the damage of macro molecules, many degenerative disease and cancer, which was produced in process of the aerotropic metabolic pathway as well as in response to the various genotoxic stresses. Recently, redox systems including the number of antioxidant proteins such as catalase, glutathione peroxidase, heam-containing peroxidase, peroxiredoxin and superoxide dismutase (SOD) has been reported to have chemopreventive effects. Antioxidant proteins has been known to have the activity directly removing ROS and affecting the protein-protein interaction and cell signaling to induce the cellular responses. We need to understand the mechanism of antioxidants prevent DNA damage from oxidative stresses for researching the cancer prevention and providing the development of cancer therapeutic drug.

• Proceedings of the Korean Society for Bioinformatics Conference
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• 2004.11a
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• pp.77-85
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• 2004

A significant portion (about 8% in human genome) of mammalian mRNA sequences contains AU(Adenine and Uracil) rich elements or AREs at their 3' untranslated regions (UTR). These mRNA sequences are usually stable. ARE motifs are assorted into three classes. The importance of AREs in biology is that they make certain mRNA unstable. We analyzed the occurrences of AREs and Alu, and propose a possible mechanism on how human mRNA could acquire and keep A REs at its 3' UTR originated from Alu repeats. Interspersed in the human genome, Alu repeats occupy 5% of the 3' UTR of mRNA sequences. Alu has poly-adenine (poly-A) regions at the end that lead to poly -thymine (poly-T) regions at the end of its complementary Alu. It has been discovered that AREs are present at the poly -T regions. In the all ARE's classes, 27-40% of ARE repeats were found in the poly -T region of Alu with mismatch allowed within 10% of ARE's length from the 3' UTRs of the NCBI's reference m RNA sequence database. We report that Alu, which has been reported as a junk DNA element, is a source of AREs. We found that one third of AREs were derived from the poly -T regions of the complementary Alu.

• BMB Reports
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• v.48 no.9
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• pp.487-488
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• 2015

The ubiquitin-proteasome system and the autophagy lysosome system are the two major protein degradation machineries in eukaryotic cells. These two systems coordinate the removal of unwanted intracellular materials, but the mechanism by which they achieve this synchronization is largely unknown. The ubiquitination of substrates serves as a universal degradation signal for both systems. Our study revealed that the amino-terminal Arg, a canonical N-degron in the ubiquitin-proteasome system, also acts as a degradation signal in autophagy. We showed that many ER residents, such as BiP, contain evolutionally conserved arginylation permissive pro-N-degrons, and that certain inducers like dsDNA or proteasome inhibitors cause their translocation into the cytoplasm where they bind misfolded proteins and undergo amino-terminal arginylation by arginyl transferase 1 (ATE1). The amino-terminal Arg of BiP binds p62, which triggers p62 oligomerization and enhances p62-LC3 interaction, thereby stimulating autophagic delivery and degradation of misfolded proteins, promoting cell survival. This study reveals a novel ubiquitin-independent mechanism for the selective autophagy pathway, and provides an insight into how these two major protein degradation pathways communicate in cells to dispose the unwanted proteins. [BMB Reports 2015; 48(9): 487-488]