• 제목/요약/키워드: H2AX

검색결과 125건 처리시간 0.03초

SKEW-ADJOINT INTERPOLATION ON Ax-y IN $ALG\mathcal{L}$

  • Jo, Young-Soo;Kang, Joo-Ho
    • 한국수학교육학회지시리즈B:순수및응용수학
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    • 제11권1호
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    • pp.29-36
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    • 2004
  • Given vectors x and y in a Hilbert space, an interpolating operator is a bounded operator T such that Tx=y. 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(equation omitted) such that Ax=y, Af = 0 for all f in ($sp(x)^\perp$) and $A=-A^\ast$. (2) (equation omitted)

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Inactivation of Mad2B Enhances Apoptosis in Human Cervical Cancer Cell Line upon Cisplatin-Induced DNA Damage

  • Ju Hwan Kim;Hak Rim Kim;Rajnikant Patel
    • Biomolecules & Therapeutics
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    • 제31권3호
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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.

ON OPERATOR INTERPOLATION PROBLEMS

  • Jo, Young-Soo;Kang, Joo-Ho;Kim, Ki-Sook
    • 대한수학회지
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    • 제41권3호
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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.

A Note on Subnormal and Hyponormal Derivations

  • Lauric, Vasile
    • Kyungpook Mathematical Journal
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    • 제48권2호
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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.

SELF-ADJOINT INTERPOLATION ON Ax = y IN ALG$\cal{L}$

  • Kwak, Sung-Kon;Kang, Joo-Ho
    • Journal of applied mathematics & informatics
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    • 제29권3_4호
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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 >.

저산소증으로 유발된 지연성 신경세포사에 우황청심원이 미치는 영향 (The Effect of Woohwangcheongsim-won on Delayed Neuronal Death in Hypoxia)

  • 김민석;정승현;신길조;문일수;이원철
    • 대한한의학회지
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    • 제23권3호
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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)

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양이온교환 고성능액체크로마토그래피에서 라이소자임의 모멘트 분석 (Moment Analysis (MA) of Lysozyme in Cation Exchange High Performance Liquid Chromatography (HPLC))

  • 고관영;김인호
    • Korean Chemical Engineering Research
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    • 제54권4호
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    • pp.487-493
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    • 2016
  • 양이온교환 고성능액체크로마토그래피에서 라이소자임을 분석하고, 실험결과인 크로마토그램을 통해 모멘트 분석을 수행하였다. 용리 인산완충용액은 1.0, 0.75, 0.5 M의 소금을 포함하였다. 실험변수는 유량, 용리 완충용액중 소금 농도, 시료의 농도로 하였다. General rate (GR) model을 도입하여 1차와 2차 모멘트를 해석하였다. 1차 모멘트 해석에서 평형상수 K를 구할 수 있으며, 이는 $L/u_0$ vs. $({\mu}_1-t_0)/(1-{\varepsilon}_e)(1-{\varepsilon}_i)$]를 도식화했을 때의 기울기이다. 2차 모멘트 해석에서 입자내 확산계수는 이론단수 실험자료에서 계산하였다. 모멘트 분석결과를 통해 여러 물질전달 현상이 이론단 상당높이(HETP)에 주는 영향을 알아보기 위해 van Deemter plot을 작성하고, 총괄 이론단 상당높이($H_{total}$)에 기여하는 $H_{ax}$, $H_f$, 그리고 $H_d$를 조사하였다. 그 중 입자내 확산계수를 나타내는 $H_d$가 가장 지배적이었고, 외부 물질전달 계수를 나타내는 $H_f$의 영향이 가장 미미했다.

INTERPOLATION PROBLEMS IN ALGL

  • JO YOUNG SOO;KANG JOO HO
    • Journal of applied mathematics & informatics
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    • 제18권1_2호
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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.

팥(Phaseolus angularis) 열수 추출물의 산화적 DNA와 세포 손상 억제 효과 (Inhibitory Effect of Red Bean (Phaseolus angularis) Hot Water Extracts on Oxidative DNA and Cell Damage)

  • 박영미;정진부;서주희;임재환;정형진;서을원
    • 한국자원식물학회지
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    • 제24권2호
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    • pp.130-138
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    • 2011
  • 본 연구에서는 열수 팥 추출물이 hydroxyl 라디칼에 의해 유도되는 산화적 스트레스에 미치는 영향을 알아보기 위하여 항산화활성과 DNA 및 세포의 산화적 손상 억제 효과를 조사하였다. 팥 열수 추출물의 DPPH 라디칼과 hydroxyl 라디칼의 제거능은 다소 낮았으나, $Fe^{2+}$-chelating과 과산화수소 제거효과는 높게 나타나 활성산소의 생성을 억제하는 데 효과적인 것으로 확인되었다. 또한 팥 열수 추출물의 in vitro DNA cleavage, DNA migration 및 H2AX의 인산화비 억제활성은 높은 활성을 보여주고 있어 라디칼에 의한 DNA 손상 억제에 효과적으로 작용하였다. 또한 지질과산화와 p21의 발현율을 통해 세포의 산화적 손상에 미치는 영향을 살펴보면 지질과산화 억제능과 p21의 발현율에 매우 효과적으로 작용하고 있어 라디칼에 의한 산화적 스트레스로부터 세포를 보호할 것으로 생각된다.

Ethanol Extract of Ganoderma lucidum Augments Cellular Anti-oxidant Defense through Activation of Nrf2/HO-1

  • Lee, Yoo-hwan;Kim, Jung-hee;Song, Choon-ho;Jang, Kyung-jeon;kim, Cheol-hong;Kang, Ji-Sook;Choi, Yung-hyun;Yoon, Hyun-Min
    • 대한약침학회지
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    • 제19권1호
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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.