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Jung, K. J.,Lee, E. K.,Kim, S. J.,Song, C. W.,Maruyama, N.,Ishigami, A.,Kim, N. D.,Im, D. S.,Yu, B. P.,Chung, H. Y. Springer Science + Business Media 2015 Journal of molecular medicine Vol.93 No.3
<P>Recent studies on senescence marker protein-30 (SMP30) have shown that it has an important functional role in the aging process, but its precise participation in cellular works has not been fully determined. We hypothesize that SMP30 plays crucial roles in signaling processes by modulating the balance of protein tyrosine kinase (PTK)/protein tyrosine phosphatase (PTP) and in activating proinflammatory NF-kappa B. An experimental paradigm of gain and loss of SMP30 function was established using SMP30-overexpressed YPEN-1 cells (herein referred to as 'SMP30(+) cells') and SMP30 (Y/-) knockout mouse kidneys. The resulting data show that SMP30 expression suppressed oxidative stress-induced PTK/PTP dysregulation and PP1/2A inactivation in SMP30(+) cells, leading to the suppression of NF-kappa B activation. In the kidneys of SMP30 (Y/-) mice, SMP30 deficiency was found to induce NF-kappa B activation via the upstream signaling of NIK/IKK and MAPKs and to upregulate downstream NF-kappa B-responsive gene expression. In this study, we also demonstrate for the first time that SMP30 deficiency induced PTK activity in SMP30 (Y/-) kidneys, thereby significantly increasing the tyrosine phosphorylation of a catalytic subunit of PP2A (PP2Ac-Tyr307). Based on these findings, we propose that SMP30 involves NF-kappa B regulation through the PTK/PTP balance and that the age-related decrease of SMP30 causes NF-kappa B activation, which contributes to an exacerbation of the inflammatory process during aging. Key message SMP30-deficient mice induced a shorter lifespan and redox changes. Overexpression of SMP30 prevented oxidative stress insults. The depletion of SMP30 increased redox-related PTK/PTP imbalance and PP1/PP2A inactivation. The depletion of SMP30 caused an elevation of NF-kappa B-responsive inflammatory markers. SMP30 may be a potent inhibitory protein against oxidative stress and chronic inflammation.</P>
Diamond 박막 성장에 미치는 Si 표면 영향의 AES에 의한 연구
이철로(C. R. Lee),신용현(Y. H. Shin),임재영(J. Y. Leem),정광화(K. H. Chung),천병선(B. S. Chun) 한국진공학회(ASCT) 1993 Applied Science and Convergence Technology Vol.2 No.2
Si 기판 표면상태 변화와 관련된 핵생성 자유에너지 증가에 따른 다이아몬드 박막성장 거동을 관찰하였다. 표면 연마조건 변화에 따른 3가지 기판(A-Si, B-Si, C-Si) 위에 동일한 성장조건으로 다이아몬드를 성장하였으며, 이때 형상인자와 관련된 자유에너지 관계는 ΔG_(A-Si)<ΔG_(B-Si)<ΔG_(C-Si)이다. AES, SEM, XRD, RHEED에 의해 각각의 박막 A, B, C를 조사한 결과, 핵생성 자유에너지가 가장 적은 A 박막은 (100) (110) 면이 지배적인 고품위 다이아몬드 박막이다. 자유에너지가 A에 비해 다소 적은 B 박막은 (111) 면이 지배적인 8면체 다이아몬드 박막이고, 자유에너지가 가장 적은 C 박막은 흑연이 많이 함유된 구상의 다이아몬드이다. The effect of nucleation free energy related to Si surface states on diamond film growth behavior has been studied. At first, the three kinds of diamond thin films (A, B, C) were deposited on various Si substrates (A-Si, B-Si, C-Si) whose surfaces were polished with 1 ㎛ diamond paste, 6 ㎛ Al₂O₃ powder and 12 ㎛ Al₂O₃ powder respectively. And then, relative nucleation free energy calculated is ΔG_(A-Si)<ΔG_(B-Si)<ΔG_(c-Si) Although there are some difference in grain size, shape and nucleation site, the thin films on A-Si and B-Si were diamond including a small amount of DLC which was confirmed by AES, SEM, XRD and RHEED. Namely, the diamonds of films (B) were not nucleated in scratches but in dents and larger in grain size compare with the film (C) of which diamond were nucleated not only scratches but also dents. And, the sphere diamond which is not general shape was grown on C-Si. After all, the sphere was turned out to be the diamond including much graphite as a result of the AES in situ depth profiling. Consequently, the diamond shape and quality grown on Si were changed from the crystal which the (100) and (110) planes were predominent to the crystal in which (111) plane was predominent, and next to sphere shape diamond including much graphite according as the nucleation free energy increases.