• Biomolecules & Therapeutics
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• v.31 no.3
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• pp.340-349
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• 2023

Mad2B (Mad2L2), the human homolog of the yeast Rev7 protein, is a regulatory subunit of DNA polymerase ζ that shares sequence similarity with the mitotic checkpoint protein Mad2A. Previous studies on Mad2B have concluded that it is a mitotic checkpoint protein that functions by inhibiting the anaphase-promoting complex/cyclosome (APC/C). Here, we demonstrate that Mad2B is activated in response to cisplatin-induced DNA damage. Mad2B co-localizes at nuclear foci with DNA damage markers, such as proliferating cell nuclear antigen and gamma histone H2AX (γ-H2AX), following cisplatin-induced DNA damage. However, unlike Mad2A, the binding of Mad2B to Cdc20 does not inhibit the activity of APC/C in vitro. In contrast to Mad2A, Mad2B does not localize to kinetochores or binds to Cdc20 in spindle assembly checkpoint-activated cells. Loss of the Mad2B protein leads to damaged nuclei following cisplatin-induced DNA damage. Mad2B/Rev7 depletion causes the accumulation of damaged nuclei, thereby accelerating apoptosis in human cancer cells in response to cisplatin-induced DNA damage. Therefore, our results suggest that Mad2B may be a critical modulator of DNA damage response.

• Journal of the Korean Mathematical Society
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• v.41 no.3
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• pp.423-433
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• 2004

In this paper we obtained the following: Let H. be a Hilbert space and (equation omitted) be a subspace lattice on H. Let X and Y be operators acting on H. If the range of X is dense in H, then the following are equivalent: (1) there exists an operator A in Alg(equation omitted) such that AX = Y, (2) sup (equation omitted) Moreover, if condition (2) holds, we may choose the operator A such that ∥A∥ = K.

• Kyungpook Mathematical Journal
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• v.48 no.2
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• pp.281-286
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• 2008

In this note we prove that if A and $B^*$ are subnormal operators and is a bounded linear operator such that AX - XB is a Hilbert-Schmidt operator, then f(A)X - Xf(B) is also a Hilbert-Schmidt operator and $${\parallel}f(A)X\;-\;Xf(B){\parallel}_2\;\leq\;L{\parallel}AX\;-\;XB{\parallel}_2$$, for f belonging to a certain class of functions. Furthermore, we investigate the similar problem in the case that S, T are hyponormal operators and $X\;{\in}\;\cal{L}(\cal{H})$ is such that SX - XT belongs to a norm ideal (J, ${\parallel}\;{\cdot}\;{\parallel}_J$) and prove that f(S)X - Xf(T) $\in$ J and ${\parallel}f(S)X\;-\;Xf(T){\parallel}_J\;\leq\;C{\parallel}SX\;-\;XT{\parallel}_J$, for f in a certain class of functions.

• Journal of applied mathematics & informatics
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• v.29 no.3_4
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• pp.981-986
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• 2011

Given vectors x and y in a Hilbert space $\cal{H}$, an interpolating operator is a bounded operator T such that Tx = y. An interpolating operator for n vectors satisfies the equations $Tx_i=y_i$, for i = 1, 2, ${\cdots}$, n. In this paper the following is proved : Let $\cal{L}$ be a subspace lattice on a Hilbert space $\cal{H}$. Let x and y be vectors in $\cal{H}$ and let $P_x$ be the projection onto sp(x). If $P_xE=EP_x$ for each $E{\in}\cal{L}$, then the following are equivalent. (1) There exists an operator A in Alg$\cal{L}$ such that Ax = y, Af = 0 for all f in $sp(x)^{\perp}$ and $A=A^*$. (2) sup $sup\;\{\frac{{\parallel}E^{\perp}y{\parallel}}{{\parallel}E^{\perp}x{\parallel}}\;:\;E\;{\in}\;{\cal{L}}\}$ < ${\infty}$, $y\;{\in}\;sp(x)$ and < x, y >=< y, x >.

• The Journal of Korean Medicine
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• v.23 no.3
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• pp.145-163
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• 2002

Objectives: The purpose of this investigation was to evaluate the effects of Woohwangcheongsim-won and to study the mechanism for neuronal death protection in hypoxia with Embryonic day 20 (E20) cortical cells of a rat (Sprague Dawley). Methods: E20 cortical cells were dissociated in neurobasal media and grown for 14 days in vitro (DIV). On 14 DIV, Woohwangcheongsim-won was added to the culture media for 24 hrs or 72 hrs. On 17 DIV, cells were given a hypoxic shock and further incubated in normoxia for another three days. On 20 DIV, Woohwangcheongsim-won's effects for neuronal death protection were evaluated by LDH assay, propidium iodide stain and phospho-H2AX immunostain and the mechanisms were studied by Bcl-2, Bak, Bax, caspase family, PKCα, ca1pain I. Results & Conclusions : 1. This study indicated that Woohwangcheongsim-won's effects for neuronal death protection in hypoxia were confirmed by LDH assay, propidium iodide stain and phospho-H2AX immunostain in culture method of Embryonic day 20(E20) cortical neuroblasts. 2. Woohwangcheongsim-won's mechanisms for neuronal death protection in hypoxia are to reduce the membrane damage fraction, to restrain DNA truncate, to restrain inflow of cytochrome c into cellularity caused by Bak diminution, to reduce the caspase cascade intiator caspase-8 and the effector caspase-3, to reduce the calpain I activity and to increase PKCand its activity in the membrane fraction. (J Korean Oriental Moo 2002;23(3):145～163)

• Korean Chemical Engineering Research
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• v.54 no.4
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• pp.487-493
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• 2016

The moment analysis of lysozyme was implemented using chromatograms that were obtained from weak cation exchange column in high performance liquid chromatography system. Three elution sodium phosphate buffers containing 1.0, 0.75, 0.5M sodium chloride were used. Experiments were conducted by varying flow rate, elution sodium chloride concentration, and lysozyme solute concentration. The general rate (GR) model was employed to calculate the first moment and the second moment. By plotting $L/u_0$ vs. $({\mu}_1-t_0)/(1-{\varepsilon}_e)(1-{\varepsilon}_i)$] equilibrium constants (K) were obtained from first moment analysis. Intra-particle diffusivity was obtained from theoretical plate number data. Based on the results of moment analysis, van Deemter plots were drawn in order to investigate the contributions of $H_{ax}$, $H_f$, and $H_d$ to total Height Equivalent to a Theoretical Plate (HETP, $H_{total}$). The effect of intra-particle diffusion ($H_d$) was the most dominant factor contributing to HETP while external mass transfer ($H_f$) was negligible factor.

• Journal of applied mathematics & informatics
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• v.18 no.1_2
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• pp.513-524
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• 2005

Given operators X and Y acting on a Hilbert space H, an interpolating operator is a bounded operator A such that AX = Y. Let L be a subspace lattice on H. We obtained a necessary and sufficient condition for the existence of an interpolating operator A which is in AlgL.

• Korean Journal of Plant Resources
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• v.24 no.2
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• pp.130-138
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• 2011

In this study, we evaluated the protective effects of the hot water extract from red bean (Phaseolus angularis) against oxidative DNA and cell damage induced by hydroxyl radical. The antioxidant activities were evaluated by hydroxyl radical and hydrogen peroxide scavenging assay, and $Fe^{2+}$-chelating assay. Although the extract with hot water didn't scavenge the hydroxyl radical, it removed and chelated hydrogen peroxide and ferrous iron necessary for the induction of hydroxyl radical by 71% and 64% at 200 ${\mu}g/ml$, respectively. Its protective effect on oxidative DNA damage was carried using ${\Psi}$X-174 RF I plasmid DNA comparing the conversion level of supercoiled form of the plasmid DNA into open-circular form and linear form and the expression level of phospho-H2AX in NIH 3T3 cells. In ${\Psi}$X-174 RF I plasmid DNA cleavage assay, it inhibited oxidative DNA damage by 96% at 200 ${\mu}g/ml$. Also, it decreased the expression of phospho-H2AX by 50.1% at 200 ${\mu}g/ml$. Its protective effect against oxidative cell damage was measured by MTT assay and the expression level of p21 protein in NIH 3T3 cells. In MTT assay for the protective effect against the oxidative cell damage, it inhibited the oxidative cell death and the abnormal cell growth induced by hydroxyl radical. Also, it inhibited p21 protein expression by 98% at 200 ${\mu}g/ml$. In conclusion, the results of the present studies indicate that hot water extract from red bean exhibits antioxidant properties and inhibit oxidative DNA damage and the cell death caused by hydroxyl radical.

• Journal of Pharmacopuncture
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• v.19 no.1
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• pp.59-69
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• 2016

Objectives: The mushroom Ganoderma lucidum has been widely used as a traditional herbal medicine for many years. Although several studies have focused on the anti-oxidative activity of this mushroom, the molecular mechanisms underlying its activity have not yet been clearly established. The present study investigated the cytoprotective effect of ethanol extract of Ganoderma lucidum (EGL) against oxidative stress (hydrogen peroxide, $H_2O_2$) and elucidated the underlying mechanisms in a C2C12 myoblast cell line. Methods: Oxidative stress markers were determined by using the comet assay to measure reactive oxygen species (ROS) generation and deoxyribonucleic acid (DNA) damage. Cell viability and Western blotting analyses were employed to evaluate the cellular response to EGL and $H_2O_2$ in C2C12 cells. Transfection with nuclear factor erythroid 2-related factor 2 (Nrf2)-specific small interfering ribonucleic acid (siRNA) was conducted to understand the relationship between Nrf2 expression and $H_2O_2$-induced growth inhibition. Results: The results showed that EGL effectively inhibited $H_2O_2$-induced growth and the generation of ROS. EGL markedly suppressed $H_2O_2$-induced comet-like DNA formation and phosphorylation of histone H2AX at serine 139 ($p-{\gamma}H2AX$), a widely used marker of DNA damage, suggesting that EGL prevented $H_2O_2$-induced DNA damage. Furthermore, the EGL treatment effectively induced the expression of Nrf2, as well as heme oxygenase-1 (HO-1), with parallel phosphorylation and nuclear translocation of Nrf2 in the C2C12 myoblasts. However, zinc protoporphyrin IX, a HO-1 inhibitor, significantly abolished the protective effects of EGL against $H_2O_2$-induced accumulation of ROS and reduced cell growth. Notably, transient transfection with Nrf2-specific siRNA attenuated the cytoprotective effects and HO-1 induction by EGL, indicating that EGL induced the expression of HO-1 in an Nrf2-dependent manner. Conclusion: Collectively, these results demonstrate that EGL augments the cellular anti-oxidant defense capacity through activation of Nrf2/HO-1, thereby protecting C2C12 myoblasts from $H_2O_2$-induced oxidative cytotoxicity.

• Journal of Life Science
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• v.21 no.12
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• pp.1698-1704
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• 2011

In this study, we evaluated the protective effects of ethanol extracts from Dendranthema indicum on cell and DNA damages induced by oxidative stress. Antioxidant activities of D. indicum extracts are higher than scavenging activities of DPPH free radical and hydroxyl radical by 92.8% and 73.8%, respectively, and higher than ferrous iron chelating effects by 59.4%. D. indicum extracts showed a protective effect on oxidative cell damage by inhibiting lipid peroxidation by 90.3% in the control group, and inhibiting expression level of p21 protein by 79.6% for the control group. This means D. indicum extracts have a great protective effect against oxidative stress. DNA fragmentation inhibition in D. indicum extracts were 89.6% for the control group, which makes the movement of DNA tail reduced, and phosphorylation of H2AX was 20.2% of the radical experiment group. This means that D. indicum extracts effectively inhibit DNA fragmentation and H2AX phosphorylation. Taken together, we suggest that ethanol extract from D. indicum has a role as a useful chemopreventor against oxidative damage.