• Journal of the Korean Mathematical Society
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• v.47 no.4
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• pp.789-804
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• 2010

We here investigate an existence and uniqueness of the nontrivial, nonnegative solution of a nonlinear ordinary differential equation: $$[\mid(w^m)]'\mid^{p-2}(w^m)']'\;+\;{\beta}rw'\;+\;{\alpha}w\;+\;(w^q)'\;=\;0$$ satisfying a specific decay rate: $lim_{r\rightarrow\infty}\;r^{\alpha/\beta}w(r)$ = 0 with $\alpha$ := (p - 1)/[pd-(m+1)(p-1)] and $\beta$:= [q-m(p-1)]/[pd-(m+1)(p-1)]. Here m(p-1) > 1 and m(p - 1) < q < (m+1)(p-1). Such a solution arises naturally when we study a very singular solution for a doubly degenerate equation with nonlinear convection: $$u_t\;=\;[\mid(u^m)_x\mid^{p-2}(u^m)_x]_x\;+\;(u^q)x$$ defined on the half line.

• BMB Reports
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• v.47 no.3
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• pp.167-172
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• 2014

Reactivating the p53 pathway in tumors is an important strategy for anticancer therapy. In response to diverse cellular stresses, the tumor suppressor p53 mediates apoptosis in a transcription-independent and transcription-dependent manner. Although extensive studies have focused on the transcription-dependent apoptotic pathway of p53, the transcription-independent apoptotic pathway of p53 has only recently been discovered. Molecular interactions between p53 and Bcl-2 family proteins in the mitochondria play an essential role in the transcription-independent apoptosis of p53. This review describes the structural basis for the transcription-independent apoptotic pathway of p53 and discusses its potential application to anticancer therapy.

• Journal of the Korean Mathematical Society
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• v.47 no.4
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• pp.845-860
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• 2010

In this paper, using the Nehari manifold approach and some variational techniques, we discuss the multiplicity of positive solutions for the p(x)-Laplacian problems with non-negative weight functions and prove that an elliptic equation has at least two positive solutions.

• Bulletin of the Korean Mathematical Society
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• v.47 no.5
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• pp.951-960
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• 2010

We provide the set of left-invariant minimal unit vector fields on the semi-direct product $\mathbb{R}^n\;{\rtimes}_p\mathbb{R}$, where P is a nonsingular diagonal matrix and on the 7 classes of 4-dimensional solvable Lie groups of the form $\mathbb{R}^3\;{\rtimes}_p\mathbb{R}$ which are unimodular and of type (R).

• Mass Spectrometry Letters
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• v.3 no.1
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• pp.10-14
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• 2012

Artificially oxidized cysteine residues in peroxiredoxin 6 (Prx6) were detected by electrospray interface capillary liquid chromatography-linear ion trap mass spectrometry after the preparation of two-dimensional gel electrophoresis (2D-GE). We used Prx6 as a model protein because it possesses only two cysteine residues at the 47th and 91st positions. The spot of Prx6 on 2D-GE undergoes a basic (isoelectric point, pI 6.6) to acidic (pI 6.2) shift by exposure to peroxide due to selective overoxidation of the active-site cysteine Cys-47 but not of Cys-91. However, we detected a tryptic peptide containing cysteine sulfonic acid at the 47th position from the basic spot and a peptide containing both oxidized Cys-47 and oxidized Cys-91 from the acidic spot of Prx6 after the separation by 2D-GE. We prepared two types of oxidized Prx6s: carrying oxidized Cys-47 (single oxidized Prx6), and other carrying both oxidized Cys-47 and Cys-91 (double oxidized Prx6). Using these oxidized Prx6s, the single oxidized Prx6 and double oxidized Prx6 migrated to pIs at 6.2 and 5.9, respectively. These results suggest that oxidized Cys-47 from the basic spot and oxidized Cys-91 from the acidic spot are generated by artificial oxidation during sample handling processes after isoelectric focusing of 2D-GE. Therefore, it is important to make sure of the origin of cysteine oxidation, if it is physiological or artificial, when an oxidized cysteine residue(s) is identified.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.19
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• pp.8413-8422
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• 2014

Background: To investigate the relationship of five TP53 polymorphisms (p.P47S, p.R72P, PIN3 ins16bp, p.R213R and r.13494g>a) with the esophageal cancer (EC) risk in North Indians. Materials and Methods: Genotyping of p.P47S, p.R72P, PIN3 ins16bp, p.R213R and r.13494g>a polymorphisms of TP53 in 136 sporadic EC patients and 136 controls using polymerase chain reaction and PCR-RFLP. Results: The frequencies of genotype RR, RP and PP of p.R72P polymorphism were 16.91 vs 26.47%, 58.82 vs 49.27% and 24.27 vs 24.27% among patients and controls respectively. We observed significantly increased frequency of RP genotype in cases as compared to controls (OR=1.87, 95% CI, 1.01-3.46, p=0.05). The frequencies of genotype A1A1, A1A2 and A2A2 of PIN3 ins16bp polymorphism were 69.12 vs 70.59%, 27.20 vs 25% and 3.68 vs 4.41% among patients and controls. There was no significant difference among genotype and allele distribution between patients and controls. The frequencies of genotype GG, GA and AA of r.13494g>a polymorphism were 62.50 vs 64.70%, 34.56 vs 30.15% and 2.94 vs 5.15% among patients and controls respectively. No significant difference between genotype and allele frequency was observed in the patients and controls. For p.P47S and p.R213R polymorphisms, all the cases and controls had homozygous wild type genotype. The RP-A1A1-GG genotype combination shows significant risk for EC (OR=2.01, 95%CI: 1.01-3.99, p=0.05). Conclusions: Among the five TP53 polymorphisms investigated, only p.R72P polymorphism may contributes to EC susceptibility.

• BMB Reports
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• v.30 no.3
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• pp.182-187
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• 1997

The NADPH oxidase of phagocytes catalyzes the reduction of oxygen to $O_2^-$ at the expense of NADPH. The enzyme is dormant in resting neutrophils and becomes activated on stimulation. During activation, $p47^{phox}\;(\underline{ph}agocyte\;\underline{ox}idase\;factor)$, a cytosolic oxidase subunit, becomes extensively phosphorylated at a number of serines located between S303-S379. Oxidase activation can also be achieved by the addition of phosphorylated recombinant $p47^{phox}$ by protein kinase C in the cell-free system in the presence of $GTP{\gamma}S$. The cell-free activation is inhibited by wortmannin and LY294002. specific inhibitors of phosphatidylinositol 3kinase (PI 3-kinasel) These results indicate that PI 3-kinase may playa pivotal role in the activation of NADPH oxidase.

• Journal of the Korean Institute of Telematics and Electronics D
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• v.35D no.5
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• pp.80-86
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• 1998

Material characterizations were performed for In$_{0.53}Ga_{0.47}As/In$_{0.52}Al_{0.48}$/As MQWs grown on InP substrates by low-temperature modlecular beam epitaxy. MQW samples were grwon at different temperatures of 200.deg.C, 300.deg. C and 500.deg. C, and doped with 10$^{18}$ cm$^{3}$ Be. High resolution x-ray diffraction measurement showed the change in crystal qualities according to growth temperature. Hall measurement showed the changes in carrier concentrations and mobilities for different growth temperatures. The optical properties of MQW samples were investigated with photoluminescence and fourier-transform infrared spectroscopy measurements.

• Proceedings of the Korean Institute of Electrical and Electronic Material Engineers Conference
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• 2007.06a
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• pp.256-256
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• 2007

As a candidate for lead-free piezoelectric materials, dense ($(Na_{0.47}K_{0.47}Li_{0.06})NbO_3$ (LNKN6) ceramics were developed by conventional sintering process. Sintering temperature was lowered by adding $Li_2O$ as a sintering aid. Abnormal grain growth in the LNKN6 ceramics was observed with varying $Li_2O$ content. The electrical properties of LNKN6 ceramics were investigated as a function of $Li_2O$ concentration. When the sample sintered at $1000^{\circ}C$ for 4h with the addition of 1 mol% $Li_2O$, electromechanical coupling factor ($k_p$) and piezoelectric coefficient ($d_{33}$) of LNKN6 ceramics were found to reach the highest values of 0.40 and 184 pC/N, respectively.

• Genomics & Informatics
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• v.20 no.2
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• pp.24.1-24.8
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• 2022

Hypomyelinating leukodystrophy type 2 (HLD2), is an inherited genetic disease of the central nervous system caused by recessive mutations in the gap junction protein gamma 2 (GJC2/GJA12). HLD2 is characterized by nystagmus, developmental delay, motor impairments, ataxia, severe speech problem, and hypomyelination in the brain. The GJC2 sequence encodes connexin 47 protein (Cx47). Connexins are a group of membrane proteins that oligomerize to construct gap junctions protein. In the present study, a novel missense mutation gene c.760G>A (p.Val254Met) was identified in a patient with HLD2 by performing whole exome sequencing. Following the discovery of the new mutation in the proband, we used Sanger sequencing to analyze his affected sibling and parents. Sanger sequencing verified homozygosity of the mutation in the proband and his affected sibling. The autosomal recessive inheritance pattern was confirmed since Sanger sequencing revealed both healthy parents were heterozygous for the mutation. PolyPhen2, SIFT, PROVEAN, and CADD were used to evaluate the function prediction scores of detected mutations. Cx47 is essential for oligodendrocyte function, including adequate myelination and myelin maintenance in humans. Novel mutation p.Val254Met is located in the second extracellular domain of Cx47, both extracellular loops are highly conserved and probably induce intramolecular disulfide interactions. This novel mutation in the Cx47 gene causes oligodendrocyte dysfunction and HLD2 disorder.