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A biosynthetic pathway for hexanoic acid production in Kluyveromyces marxianus
Cheon, Y.,Kim, J.S.,Park, J.B.,Heo, P.,Lim, J.H.,Jung, G.Y.,Seo, J.H.,Park, J.H.,Koo, H.M.,Cho, K.M.,Park, J.B.,Ha, S.J.,Kweon, D.H. Elsevier Science Publishers 2014 Journal of biotechnology Vol.182 No.-
Hexanoic acid can be used for diverse industrial applications and is a precursor for fine chemistry. Although some natural microorganisms have been screened and evolved to produce hexanoic acid, the construction of an engineered biosynthetic pathway for producing hexanoic acid in yeast has not been reported. Here we constructed hexanoic acid pathways in Kluyveromyces marxianus by integrating 5 combinations of seven genes (AtoB, BktB, Crt, Hbd, MCT1, Ter, and TES1), by which random chromosomal sites of the strain are overwritten by the new genes from bacteria and yeast. One recombinant strain, H4A, which contained AtoB, BktB, Crt, Hbd, and Ter, produced 154mg/L of hexanoic acid from galactose as the sole substrate. However, the hexanoic acid produced by the H4A strain was re-assimilated during the fermentation due to the reverse activity of AtoB, which condenses two acetyl-CoAs into a single acetoacetyl-CoA. This product instability could be overcome by the replacement of AtoB with a malonyl CoA-acyl carrier protein transacylase (MCT1) from Saccharomyces cerevisiae. Our results suggest that Mct1 provides a slow but stable acetyl-CoA chain elongation pathway, whereas the AtoB-mediated route is fast but unstable. In conclusion, hexanoic acid was produced for the first time in yeast by the construction of chain elongation pathways comprising 5-7 genes in K. marxianus.
Optimization of batch dilute-acid hydrolysis for biohydrogen production from red algal biomass
Park, J.H.,Cheon, H.C.,Yoon, J.J.,Park, H.D.,Kim, S.H. Pergamon Press ; Elsevier Science Ltd 2013 INTERNATIONAL JOURNAL OF HYDROGEN ENERGY - Vol.38 No.14
Marine algae are promising alternative sources for bioenergy including hydrogen. Their polymeric structure, however, requires a pretreatment such as dilute-acid hydrolysis prior to fermentation. This study aimed to optimize the control variables of batch dilute-acid hydrolysis for dark hydrogen fermentation of algal biomass. The powder of Gelidium amansii was hydrolyzed at temperatures of 120-180 <SUP>o</SUP>C, solid/liquid (S/L) ratios of 5-15% (w/v), and H<SUB>2</SUB>SO<SUB>4</SUB> concentrations of 0.5-1.5% (w/w), and then fed to batch hydrogen fermentation. Among the three control variables, hydrolysis temperature was the most significant for hydrogen production as well as for hydrolysis efficiency. The maximum hydrogen production performance of 0.51 L H<SUB>2</SUB>/L/hr and 37.0 mL H<SUB>2</SUB>/g dry biomass was found at 161-164 <SUP>o</SUP>C hydrolysis temperature, 12.7-14.1% S/L ratio, and 0.50% H<SUB>2</SUB>SO<SUB>4</SUB>. The optimized dilute-acid hydrolysis would enhance the feasibility of the red algal biomass as a suitable substrate for hydrogen fermentation.
Kim, S. Y.,Cheon, S. Y.,Kim, E. J.,Lee, J. H.,Kam, E. H.,Kim, J. M.,Park, M.,Koo, B. N. Springer Science + Business Media 2017 Neurochem Res Vol.42 No.5
<P>Tissue plasminogen activator (tPA) is the only recommended pharmacological treatment for acute ischemic stroke. However, tPA can induce intracerebral hemorrhage by blood-brain barrier breakdown through an increase in matrix metalloproteinases (MMPs). Previously, we showed that isoflurane postconditioning reduced intracranial hemorrhage following tPA treatment after cerebral ischemia. Here, we investigated the mechanism by which isoflurane postconditioning reduces tPA-induced MMP-2 and MMP-9 activation following hypoxia/reoxygenation (H/R) in brain endothelial cells. Mouse brain endothelial cells (bEnd.3) were exposed to 6 h of oxygen-glucose deprivation and 3 h of reoxygenation with tPA. Cells were treated with isoflurane for 1 h of the reoxygenation condition and the effect of isoflurane postconditioning on MMP-2 and MMP-9 activation was assessed. Involvement of low-density lipoprotein receptor-related protein (LRP), which is a receptor for tPA, and the extracellular signal-regulated kinase (ERK) and NF-kappa B pathway in isoflurane postconditioning was assessed using LRP inhibitor (receptor-associated protein, RAP) and ERK-1/2 inhibitor (PD98059). Isoflurane postconditioning decreased tPA-induced MMP-2 and MMP-9 activation under H/R. tPA treatment under H/R increased expression of LRP and the active form of NF-kappa B. Isoflurane postconditioning suppressed LRP expression, increased ERK-1/2 activation, and suppressed MMP-2 and MMP-9 activation, comparable to the effect of RAP. Activation of ERK-1/2, inhibition of NF-kappa B activation, and suppression of MMP-2 and MMP-9 activation by isoflurane postconditioning were abolished with PD98059 treatment. These finding indicate that isoflurane postconditioning inhibits tPA-induced MMP-2 and MMP-9 activation following H/R via the LRP/ERK/NF-kappa B pathway in bEnd.3.</P>
Probability that the k-gcd of products of positive integers is B-friable
Cheon, J.H.,Kim, D. Academic Press 2016 Journal of number theory Vol.168 No.-
<P>In 1849, Dirichlet [5] proved that the probability that two positive integers are relatively prime is 1/zeta(2). Later, it was generalized into the case that positive integers have no nontrivial kth power common divisor. In this paper, we further generalize this result: the probability that the gcd of m products of n positive integers is B-friable is Pi(p>B) [1-{1 - (1 - 1/p)(n)}(m)] for m >= 2. We show that it is lower bounded by 1/zeta(s) for some s > 1 if B > n(m/m-1), which completes the heuristic proof in the cryptanalysis of cryptographic multilinear maps by Cheon et al. [2]. We extend this result to the case of k-gcd: the probability is Pi(p>B) [1 - {1 - (1 - 1/p)(n) (1 + H-n(1)/p + ... + H-n(k-1)/p(k-1))}(m)], where H-n(i) = (n+i-1/i). (C) 2016 Elsevier Inc. All rights reserved.</P>
Cheon, Y.J.,Lee, H.K.,Kim, H.G. Pergamon Press ; Elsevier Science Ltd 2017 International journal of solids and structures Vol.125 No.-
Most cohesive zone models for the simulation of crack growth in ductile metals do not reflect continuum constitutive laws on traction-separation relationships across cohesive crack surfaces. In this study, a continuously-deforming material layer associated with a ductile failure process of void nucleation, growth and coalescence is converted into a separating pair of cohesive crack surfaces resisted by cohesive tractions. Representative volume elements of damageable and undamageable material layers are used to extract the porous portion of the deformation in the failure process zone, which is reduced to a cohesive law based on continuum damage mechanics. The failure process zone height is determined by matching the J-integral evaluated from the results of crack growth simulations using cohesive elements with that evaluated from the displacements measured in crack growth experiments. The present approach provides an efficient and effective way to estimate cohesive laws of ductile metals by combining experimental tests and numerical simulations of a cracked specimen.
Cheon, J. H.,Kim, J. Y.,Lee, B.-M.,Kim, H. S.,Yoon, S. INTERNATIONAL INSTITUTE OF ANTICANCER RESEARCH 2017 Anticancer research Vol.37 No.12
<P>The present study was designed to identify conditions that could increase the sensitivity of resistant cancer cells to antimitotic drugs. We investigated whether a Janus kinase 2 (JAK2) inhibitor used in clinical trials, XL019, sensitizes antimitotic drug-resistant KBV20C cells. XL019 reduced cellular viability and increased apoptosis in vincristine-treated KBV20C cells, independently of the JAK/signal transducer and activator of transcription (STAT) pathway. Based on the ATP-binding cassette protein B1 [ABCB1, P-glycoprotein (P-gp)] inhibitory assay, we demonstrated that XL019 functions as a P-gp inhibitor in drug-resistant KBV20C cells. Considering that another JAK2 inhibitor, CEP-33779, also inhibited P-gp and sensitized drug-resistant cancer cells in a previous study, we concluded that JAK2 inhibitors can be used as P-gp inhibitors in drug-resistant cancer cells. Fluorescence-activated cell sorting, western blot, and annexin V analyses were used to further investigate the mechanism of action of XL019 in vincristine-treated KBV20C cells. XL019 induced early apoptosis of KBV20C cells in response to vincristine treatment via increased G(2) phase arrest. Moreover, G(2) phase arrest and apoptosis of cells co-treated with vincristine and XL019 resulted from the up-regulation of phosphorylated retinoblastoma protein (pRb), p21, and the DNA-damage protein, phosphorylated H2A histone family, member X (pH2AX). Additionally, the P-gp-inhibitory effect of XL019 was less than that of CEP-33779, and a more than 2-fold higher dose was required to sensitize vincristine-treated KBV20C cells. Furthermore, lower doses of XL019 were required to sensitize KBV20C cells to a degree similar to that obtained with the established P-gp inhibitor verapamil, suggesting that XL019 has higher specificity than verapamil. Our results showed that JAK2 inhibitors inhibited P-gp action via a direct binding mechanism, which was similar to that of verapamil. These findings indicate that JAK2 inhibitors may be promising therapeutics for the treatment of cancer that is resistant to antimitotic drugs.</P>