• Journal of the Korean Chemical Society
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• v.25 no.2
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• pp.61-66
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• 1981

A method for calculation of the contribution of $\pi$ bonding molecular orbitals to the dipole moments for octahedral [M(III)$A_3B_3$] type complexes has been developed [M(III) = Ti(III), V(III), Cr(III), Fe(III) or Co(III); A = O or N; B = N, S or Cl]. The contribution of ${\pi}$ bonding molecular orbitals to the dipole moments is found to be smaller than that of ${\sigma}$ bonding molecular orbitals but this contribution may not be negligible even for chelate complexes in which delocalization of ${\pi}$ electron is assumed. The calculated dipole moments (u = $u_{\sigma}$ + $u_{\pi}$) are closer to the experimental values than those for the case where only ${\sigma}$ bonds are assumed to be formed.

• Molecules and Cells
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• v.41 no.6
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• pp.532-544
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• 2018

Gastrointestinal stromal tumours (GIST) are the most common mesenchymal tumors of the gastrointestinal (GI) tract. In order to investigate a new treatment fot GIST, we hypothesized the effect of miR-374b targeting PTEN gene-mediated PI3K/Akt signal transduction pathway on proliferation and apoptosis of human gastrointestinal stromal tumor (GIST) cells. We obtained GIST tissues and adjacent normal tissues from 143 patients with GIST to measure the levels of miR-374b, PTEN, PI3K, Akt, caspase9, Bax, MMP2, MMP9, ki67, PCNA, P53 and cyclinD1. Finally, cell viability, cell cycle and apoptosis were detected. According to the KFGG analysis of DEGs, PTEN was involved in a variety of signaling pathways and miRs were associated with cancer development. The results showed that MiR-374b was highly expressed, while PTEN was downregulated in the GIST tissues. The levels of miR-374b, PI3K, AKT and PTEN were related to tumor diameter and pathological stage. Additionally, miR-374b increased the mRNA and protein levels of PI3K, Akt, MMP2, MMP9, P53 and cyclinD1, suggesting that miR-374b activates PI3K/Akt signaling pathway in GIST-T1 cells. Moreover, MiR374b promoted cell viability, migration, invasion, and cell cycle entry, and inhibited apoptosis in GIST cells. Taken together, the results indicated that miR-374b promotes viability and inhibits apoptosis of human GIST cells by targeting PTEN gene through the PI3K/Akt signaling pathway. Thus, this study provides a new potential target for GIST treatment.

• Journal of the Chungcheong Mathematical Society
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• v.23 no.2
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• pp.323-333
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• 2010

The biproduct bialgebra has been generalized to generalized biproduct bialgebra $B{\times}^L_H\;D$ in [5]. Let (D, B) be an admissible pair and let D be a bialgebra. We show that if generalized biproduct bialgebra $B{\times}^L_H\;D$ is a Hopf algebra with antipode s, then D is a Hopf algebra and the identity $id_B$ has an inverse in the convolution algebra $Hom_k$(B, B). We show that if D is a Hopf algebra with antipode $s_D$ and $s_B$ in $Hom_k$(B, B) is an inverse of $id_B$ then $B{\times}^L_H\;D$ is a Hopf algebra with antipode s described by $s(b{\times}^L_H\;d)={\Sigma}(1_B{\times}^L_H\;s_D(b_{-1}{\cdot}d))(s_B(b_0){\times}^L_H\;1_D)$. We show that the mapping system $B{\leftrightarrows}^{{\Pi}_B}_{j_B}\;B{\times}^L_H\;D{\rightleftarrows}^{{\pi}_D}_{i_D}\;D$ (where $j_B$ and $i_D$ are the canonical inclusions, ${\Pi}_B$ and ${\pi}_D$ are the canonical coalgebra projections) characterizes $B{\times}^L_H\;D$. These generalize the corresponding results in [6].

• The Korean Journal of Physiology and Pharmacology
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• v.4 no.6
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• pp.507-513
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• 2000

ErbB3/HER3 is a cell surface receptor which belongs to the ErbB/HER subfamily of receptor protein tyrosine kinases. When expressed in NIH/3T3 cells, ErbB3 can form heterodimeric coreceptor with endogenous ErbB2. Among known intracellular effectors of the ErbB2/ErbB3 are mitogen-activated protein kinase (MAPK) and phosphoinositide (PI) 3-kinase. In the present study, we studied relative contributions of above two distinct signaling pathways to the heregulin-induced mitogenic response via activated ErbB3. For this, clonal NIH-3T3 cell lines expressing wild-type ErbB3 and ErbB3 mutants were stimulated with $heregulin{\beta}_1$. While cyclin D1 level was markedly high and further increased by treatment of heregulin in cells expressing wild-type ErbB3, the elimination of either Shc binding or PI 3-kinase binding lowered both levels. This result was supported by the reduction of cyclin $D_1$ expression by preteatment with MAPK kinase inhibitor or PI 3-kinase inhibitor before stimulation with heregulin. In accordance with the cyclin $D_1$ expression, elimination of either Shc binding or PI 3-kinase binding reduced the heregulin-induced DNA synthesis and cell growth rate. Our results obtained by the comparison of wild-type and ErbB3 mutants indicate that the full induction of the cell cycle progression through $G_1/S$ phase by ErbB3 activation is dependent on both Shc/MAPK and PI 3-kinase signal transduction pathways.

• Bulletin of the Korean Mathematical Society
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• v.55 no.4
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• pp.1209-1219
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• 2018

We provide a direct proof of the following theorem of Kalton, Hollenbeck, and Verbitsky [7]: let H be the Hilbert transform and let a, b be real constants. Then for 1 < p < ${\infty}$ the norm of the operator aI + bH from $L^p(\mathbb{R})$ to $L^p(\mathbb{R})$ is equal to $$\({\max_{x{\in}{\mathbb{R}}}}{\frac{{\mid}ax-b+(bx+a){\tan}{\frac{\pi}{2p}}{\mid}^p+{\mid}ax-b-(bx+a){\tan}{\frac{\pi}{2p}}{\mid}^p}{{\mid}x+{\tan}{\frac{\pi}{2p}}{\mid}^p+{\mid}x-{\tan}{\frac{\pi}{2p}}{\mid}^p}}\)^{\frac{1}{p}}$$. Our proof avoids passing through the analogous result for the conjugate function on the circle, as in [7], and is given directly on the line. We also provide new approximate extremals for aI + bH in the case p > 2.

• Bulletin of the Korean Mathematical Society
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• v.46 no.1
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• pp.25-33
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• 2009

Let ${\pi}:E{\rightarrow}B$ be a Serre fibration with fibre F. We prove that if the inclusion map $i:F{\rightarrow}E$ has a left homotopy inverse r and ${\pi}:E{\rightarrow}B$ admits a cross section ${\rho}:B{\rightarrow}E$, then $G_n(E,F){\cong}{\pi}_n(B){\oplus}G_n(F)$. This is a generalization of the case of trivial fibration which has been proved by Lee and Woo in [8]. Using this result, we will prove that ${\pi}_n(X^A){\cong}{\pi}_n(X){\oplus}G_n(F)$ for the function space $X^A$ from a space A to a weak $H_*$-space X where the evaluation map ${\omega}:X^A{\rightarrow}X$ is regarded as a fibration.

• Molecules and Cells
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• v.41 no.12
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• pp.1008-1015
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• 2018

$I{\kappa}B$, a cytoplasmic inhibitor of nuclear factor-${\kappa}B$ ($NF-{\kappa}B$), is reportedly degraded via the proteasome. However, we recently found that long-term incubation with proteasome inhibitors (PIs) such as PS-341 or MG132 induces $I{\kappa}B{\alpha}$ degradation via an alternative pathway, lysosome, which results in $NF-{\kappa}B$ activation and confers resistance to PI-induced lung cancer cell death. To enhance the anti-cancer efficacy of PIs, elucidation of the regulatory mechanism of PI-induced $I{\kappa}B{\alpha}$ degradation is necessary. Here, we demonstrated that PI up-regulates nuclear factor (erythroid-derived 2)-like 2 (Nrf2) via both de novo protein synthesis and Kelch-like ECH-associated protein 1 (KEAP1) degradation, which is responsible for $I{\kappa}B{\alpha}$ degradation via macroautophagy activation. PIs increased the protein level of light chain 3B (LC3B, macroautophagy marker), but not lysosome-associated membrane protein 2a (Lamp2a, the receptor for chaperone-mediated autophagy) in NCI-H157 and A549 lung cancer cells. Pretreatment with macroautophagy inhibitor or knock-down of LC3B blocked PI-induced $I{\kappa}B{\alpha}$ degradation. PIs up-regulated Nrf2 by increasing its transcription and mediating degradation of KEAP1 (cytoplasmic inhibitor of Nrf2). Overexpression of dominant-negative Nrf2, which lacks an N-terminal transactivating domain, or knock-down of Nrf2 suppressed PI-induced LC3B protein expression and subsequent $I{\kappa}B{\alpha}$ degradation. Thus, blocking of the Nrf2 pathway enhanced PI-induced cell death. These findings suggest that Nrf2-driven induction of LC3B plays an essential role in PI-induced activation of the $I{\kappa}B$/$NF-{\kappa}B$ pathway, which attenuates the anti-tumor efficacy of PIs.

• Korean Journal Plant Pathology
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• v.14 no.3
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• pp.217-219
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• 1998

Of over 100 accessions of pepper tested, MC 4 and MC 5, PBC631, PI322727, PI358812, PBC066, Kerting, PI322726, PI369994, PI377688, CMS-B, PI322728, and Jatilaba showed similarly high level of resistance to bacterial wilt (Ralstonia solanacearum).

• BMB Reports
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• v.33 no.2
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• pp.120-125
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• 2000

M2PI is an active single chain mini-proinsulin with a 9-residue linker containing the turn-forming sequence 'YPGDV' between the B- and A-chains, but which retains about 50% of native insulin receptor binding activity. The refolding efficiency of M2PI is higher than proinsulin by 20-40% at alkaline pH, and native insulin is generated by the enzymatic conversion of M2PI. The solution structure of M2PI was determined by NMR spectroscopy. The global structure of M2PI is similar to that of native insulin, but the flexible linker between the B- and A-chains perturbed the N-terminal A-chain and C-terminal B-chain. The helix in the N-terminal A-chain is partly perturbed and the ${\beta}$-turn in the B-chain is disrupted in M2PI. However, the linker between the two chains was completely disordered indicating that the designed turn was not formed under the experimental conditions (20% acetic acid). Considering the fact that an insulin analogue, directly cross-linked between the C-terminus of the B-chain and the N-terminus of the A-chain, has negligible binding activity, a flexible linker between the two chains is sufficient to keep binding activity of M2PI, but the perturbed secondary structures are detrimental to receptor binding.

• Proceeding of EDISON Challenge
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• 2014.03a
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• pp.399-408
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• 2014

신약을 개발하거나 단백질 구조를 예측하는데 Molecular Mechanics (MM)의 방법을 사용한다. 하지만, MM 만으로는 자연현상에서 일어나는 결과를 정확하게 기술하기 어렵다. 본 연구는 기존의 MM 방법으로는 정확히 예측이 불가능한 비 공유결합 중 하나인 ${\pi}-{\pi}$ interaction을 양자역학 계산을 통해 정확한 예측이 가능한지 알아보았다. ${\pi}-{\pi}$ interaction이란 생채 내, 의약 화합물에서 발견되는 결합이기 때문에, 단백질과 결합하는 구조의 예측에 중요하다고 할 수 있다. 본 실험은 ${\pi}-{\pi}$ interaction을 갖는 Sandwich, T shape, 그리고 Parallel displaced 세 가지 모형과 각각의 모형 아래에 분자를 하나 더 쌓은 모형을 추가하여 양자역학 재산을 수행하였다. 양자역학 계산은 DFT의 세가지 함수 M06_2X, M05_2X, B3LYP를 이용하였다. 실험결과에서 세 가지 함수가 각기 다른 결과를 보였는데, 상대적으로 B3LYP의 경우에는 세가지 모델에서 모두 제대로 된 에너지 변화를 계산하지 못하였으며, M06_2X와 M05_2X의 결과에서는 거리에 따른 ${\pi}-{\pi}$ interaction 에너지의 변화를 정확하게 계산하였다. 이러한 결과를 바탕으로, 양자역학의 방법을 통해 MM에서는 예측이 불가능한 ${\pi}-{\pi}$ interaction을 계산 할 수 있고 이 부분을 고려하여 화합물 간의 결합구조를 예측을 향상시킬 수 있다.