• Molecules and Cells
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• v.26 no.1
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• pp.100-105
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• 2008

Glycogen synthase kinase $3{\beta}$ (GSK $3{\beta}$) is a serine/threonine kinase that phosphorylates substrates such as ${\beta}$-catenin and is involved in a variety of biological processes, including embryonic development, metabolism, tumorigenesis, and cell death. Here, we present evidence that human GSK $3{\beta}$ is associated with Fe65, which has the characteristics of an adaptor protein, possessing a WW domain, and two phosphotyrosine interaction domains, PID1 and PID2. The GSK $3{\beta}$ catalytic domain also contains a putative WW domain binding motif ($^{371}PPLA^{374}$), and we observed, using a pull down approach and co-immunoprecipitation, that it interacts physically with Fe65 via this motif. In addition, we detected co-localization of GSK $3{\beta}$ and Fe65 by confocal microscopy, and this co-localization was disrupted by mutation of the putative WW domain binding motif of GSK $3{\beta}$. Finally, in transient transfection assays interaction of GSK $3{\beta}$ (wt) with Fe65 induced substantial cell apoptosis, whereas interaction with the GSK $3{\beta}$ AALA mutant ($^{371}AALA^{374}$) did not, and we noted that phosphorylation of the Tyr 216 residue of the GSK $3{\beta}$ AALA mutant was significantly reduced compared to that of GSK $3{\beta}$ wild type. Thus, our observations indicate that GSK $3{\beta}$ binds to Fe65 through its $^{371}PPLA^{374}$ motif and that this interaction regulates apoptosis and phosphorylation of Tyr 216 of GSK $3{\beta}$.

• The Korean Journal of Applied Statistics
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• v.21 no.5
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• pp.835-843
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• 2008

In this paper, we investigate a Bayesian inference for software reliability models based on mean value functions which take the form of the mixture of beta distribution functions. The posterior simulation via the Markov chain Monte Carlo approach is used to produce estimates of posterior properties. Its applicability is illustrated with two real data sets. We compute the predictive distribution and the marginal likelihood of various models to compare the performance of them. The model comparison results show that the model based on the beta-mixture performs better than other models.

• Bulletin of the Korean Chemical Society
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• v.22 no.8
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• pp.897-902
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• 2001

The protein back-extraction processes were discussed from the viewpoint of the micelle-micelle interaction. Bovine serum albumin (BSA) suppressing the cluster formation of reverse micelle (positive value of ${\beta}pr)$ has the high back-extra cted fraction (Eb), but cytochrome c enhancing the formation of reverse micelle (negative value of ${\beta}pr)$ has the low back-extracted fraction, relatively. We have also examined quantitatively the effects of alcohol addition and protein solubilization on the percolation process of reverse micelle. The alcohols suppressing the formation of micellar cluster (high values of ${\beta}t)$, remarkably improved the back-extraction rates of BSA and cytochrome c. The values of ${\beta}t$, defined by the variation of percolation process, and the back-extraction behavior of proteins have a good linear correlation. These results indicate that the micelle-micelle interaction or micellar clustering plays an important role in the back-extraction process of proteins.

• Journal of the Korean Statistical Society
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• v.34 no.3
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• pp.235-244
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• 2005

In recent years, theoretical properties of Bayesian nonparametric survival models have been studied and the conclusion is that although there are pathological cases the popular prior processes have the desired asymptotic properties, namely, the posterior consistency and the Bernstein-von Mises theorem. In this study, through a simulation experiment, we study the finite sample properties of the Bayes estimator and compare it with the frequentist estimators. To our surprise, we conclude that in most situations except that the prior is highly concentrated at the true parameter value, the Bayes estimator performs worse than the frequentist estimators.

• Journal of Forest and Environmental Science
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• v.13 no.1
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• pp.143-152
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• 1997

The decayed wood by Fomes pini (Thore) Lloyd required a smaller H factor than the sound wood for pulping to permanganate number 20. The H factors for the decayed wood pulping by the kraft and soda processes were reduced by 15% and 17%, respectively, in the presence of 1% anthraquinone. The wood components degraded by fungi are normally more readily solubilized in alkali than the corresponding components in sound wood. The nonphenolic ${\beta}$-O-4 type lignin model compound, veratrylglycerol-${\beta}$-guaiacyl ether(I), and phenolic model compound, syringylglycerol-${\beta}$-syringyl ether(III), were degraded by the white-rot fungi to yield ${\alpha}$-guaiacoxy-${\beta}$-hydroxypropioveratrone(II) from the former and ${\alpha}$-syringyloxy-${\beta}$-hydroxypropiosyringone(IV) from the latter. Structures of the degradation products indicated that C ${\alpha}$-oxidation could occur with white-rot fungi. It has been shown that the alkaline cleavage of ${\beta}$-aryl ether bonds in the lignin units is accelerated by the presence of ${\alpha}$-carbonyl groups.

• Biomolecules & Therapeutics
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• v.25 no.1
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• pp.12-25
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• 2017

G protein-coupled receptors (GPCRs) are a family of cell-surface proteins that play critical roles in regulating a variety of pathophysiological processes and thus are targeted by almost a third of currently available therapeutics. It was originally thought that GPCRs convert extracellular stimuli into intracellular signals through activating G proteins, whereas ${\beta}$-arrestins have important roles in internalization and desensitization of the receptor. Over the past decade, several novel functional aspects of ${\beta}$-arrestins in regulating GPCR signaling have been discovered. These previously unanticipated roles of ${\beta}$-arrestins to act as signal transducers and mediators of G protein-independent signaling have led to the concept of biased agonism. Biased GPCR ligands are able to engage with their target receptors in a manner that preferentially activates only G protein- or ${\beta}$-arrestin-mediated downstream signaling. This offers the potential for next generation drugs with high selectivity to therapeutically relevant GPCR signaling pathways. In this review, we provide a summary of the recent studies highlighting G protein- or ${\beta}$-arrestin-biased GPCR signaling and the effects of biased ligands on disease pathogenesis and regulation.

• International Journal of Oral Biology
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• v.38 no.3
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• pp.121-126
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• 2013

Tumor necrosis factor alpha ($TNF{\alpha}$) is a multifunctional inflammatory cytokine that regulates various cellular and biological processes. Increased levels of $TNF{\alpha}$ have been implicated in a number of human diseases including diabetes and arthritis. Sympathetic nervous system stimulation via the beta2-adrenergic receptor (${\beta}2AR$) in osteoblasts suppresses osteogenic activity. We previously reported that $TNF{\alpha}$ upregulates ${\beta}2AR$ expression in murine osteoblastic cells and that this modulation is associated with $TNF{\alpha}$ inhibition of osteoblast differentiation. In our present study, we explored whether $TNF{\alpha}$ induces ${\beta}2AR$ expression in human osteoblasts and then identified the downstream signaling pathway. Our results indicated that ${\beta}2AR$ expression was increased in Saos-2 and C2C12 cells by $TNF{\alpha}$ treatment, and that this increase was blocked by the inhibition of NF-${\kappa}B$ activation. Chromatin immunoprecipitation and luciferase reporter assay results indicated that NF-${\kappa}B$ directly binds to its cognate elements on the ${\beta}2AR$ promoter and thereby stimulates ${\beta}2AR$ expression. These findings suggest that the activation of $TNF{\alpha}$ signaling in osteoblastic cells leads to an upregulation of ${\beta}2AR$ and also that $TNF{\alpha}$ induces ${\beta}2AR$ expression in an NF-${\kappa}B$-dependent manner.

• Microbiology and Biotechnology Letters
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• v.45 no.4
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• pp.277-283
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• 2017

To produce sweet liquor without artificial sweeteners, 8 traditional rice pre-treatment methods (juk, beombeok, seolgitteok, gumeongtteok, mulsongpyeon, injeolmi, gaetteok, and godubap) were analyzed in this study. The formation of sugars with the help of ${\alpha}$-amylase, ${\beta}$-amylase, and glucoamylase using nuruk as a substrate has been previously confirmed. During the early stages of the pre-treatment processes, the amount of maltose produced (in descending order of its concentration) by ${\alpha}$-amylase was observed to be as follows: gaetteok > seolgitteok > beombeok > mulsongpyeon > juk > injeolmi > gumeongtteok > godubap. However, changes in maltose concentrations with respect to the pre-treatment processes after 48 hours were observed to be as follows: injeolmi > beombeok = godubap > gumeongtteok > gaetteok = mulsongpyeon > seolgitteok > juk. Maltose produced using either ${\alpha}$-amylase or ${\beta}$-amylase showed similar results. Glucoamylase produced 10 mg/ml of glucose during the godubap process, which was the highest amount of glucose among all the methods. Moreover, when ${\alpha}$-amylase, ${\beta}$-amylase, and glucoamylase were used concurrently, glucoamylase increased glucose production in the later stages. Therefore, the possibility of producing sweet liquor without employing artificial sweeteners was confirmed, even if the amount of sugar in the liquor varied with the pre-treatment process.

• KSBB Journal
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• v.22 no.5
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• pp.328-335
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• 2007

In this work ursolic acid (UA), a poorly water-soluble compound, was inclusion complexed with 2-hydroxypropyl-$\beta$-cyclodextrin (HP-$\beta$-CD) by various methods such as kneading, solvent evaporation and two types of supercritical fluid processes. The solubility and characteristics of these UA/HP-$\beta$-CD complexes were investigated by scanning electron microscopy, x-ray diffraction and HPLC. The water solubilities of the two complexes obtained from solvent evaporation and ASES processes were observed to increase up to 6$\sim$240 folds and 12$\sim$56 folds, respectively, compared with that of unprocessed UA. The stability of UA/HP-$\beta$-CD complex samples in cosmetic formulations was examined at various temperatures for one month. The UA/HP-$\beta$-CD complex prepared by solvent evaporation was found to be most stable among all the cosmetic formulations tested in our experiments.

• IMMUNE NETWORK
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• v.13 no.5
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• pp.213-217
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• 2013

Enterotoxigenic Bacteroides fragilis (ETBF) is a human gut commensal bacteria that causes inflammatory diarrhea and colitis. ETBF also promotes colorectal tumorigenesis in the Min mouse model. The key virulence factor is a secreted metalloprotease called B. fragilis toxin (BFT). BFT induces E-cadherin cleavage, cell rounding, activation of the ${\beta}$-catenin pathway and secretion of IL-8 in colonic epithelial cells. However, the precise mechanism by which these processes occur and how these processes are interrelated is still unclear. E-cadherin form homophilic interactions which tethers adjacent cells. Loss of E-cadherin results in detachment of adjacent cells. Prior studies have suggested that BFT induces IL-8 expression by inducing E-cadherin cleavage; cells that do not express E-cadherin do not secrete IL-8 in response to BFT. In the current study, we found that HT29/C1cells treated with dilute trypsin solution induced E-cadherin degradation and IL-8 secretion, consistent with the hypothesis that E-cadherin cleavage causes IL-8 secretion. However, physical damage to the cell monolayer did not induce IL-8 secretion. We also show that EDTA-mediated disruption of E-cadherin interactions without E-cadherin degradation was sufficient to induce IL-8 secretion. Finally, we determined that HT29/C1 cells treated with LiCl (${\beta}$-catenin activator) induced IL-8 secretion in a dose-dependent and time-dependent manner. Taken together, our results suggest that BFT induced IL-8 secretion may occur by the following process: E-cadherin cleavage, disruption of cellular interactions, activation of the ${\beta}$-catenin pathway and IL-8 expression. However, we further propose that E-cadherin cleavage per se may not be required for BFT induced IL-8 secretion.