• Title/Summary/Keyword: molecular mechanism

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Two-dimensional Chiral Honeycomb Structures of Unnatural Amino Acids on Au(111)

  • Yang, Sena;Jeon, Aram;Lee, Hee-Seung;Kim, Sehun
    • Proceedings of the Korean Vacuum Society Conference
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    • 2014.02a
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    • pp.191.1-191.1
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    • 2014
  • Crystallization has become the most popular technique for the separation of enantiomers since the Pasteur's discovery. To investigate mechanism of crystallization of chiral molecules, it is necessary to study self-assembled structures on two-dimensional surface. Here, we have studied two-dimensional self-assembled structures of an unnatural amino acid, (S)-${\beta}$-methyl naphthalen-1-${\gamma}$-aminobutyric acid (${\gamma}^2$-1-naphthylalanine) on Au(111) surface at 150 K using scanning tunneling microscopy (STM). At initial stage, we found two chiral honeycomb structures which are counter-clockwise and clockwise configurations in one domain. The molecules are arranged around molecular vacancies, dark hole. By further increasing the amounts of adsorbed ${\gamma}^2$-1-naphthylalanine, a well-ordered square packed structure was observed. In addition, we found the other structure that molecules were trapped in the pore of the hexagonal molecular assembly.

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Understanding of Schizophrenia Based on the Study of Molecular Genetics (분자유전학을 통한 정신분열증의 이해)

  • Lee, Min-Soo;Kim, Pyo-Han
    • Korean Journal of Biological Psychiatry
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    • v.3 no.1
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    • pp.14-21
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    • 1996
  • Molecular genetic approaches contribute to the understanding of the underlying genetic mechanism for schizophrenia. Currently genetic evidence rests on molecular genetic methods. However, the result are contradictory and somewhat confusing due to genetic heterogeneity, incomplete penetrance, misspecification of genetic model. It is expected that molecular genetics could provide key answers to the genetic cause of schizophrenia. The purpose of this article is to call attention of the readers to heterogeneity, linkage, association, basic molecular genetic methods and genetic markers and to the need far further research. It is the author's hope thai continuous research on the molecular genetics con provide clinicians with better understanding of the schizophrenia.

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SYNTHESIS OF HALOGENATED 9-(DIHYDROXYCYCLOPENT -4′-ENYL) ADENINES AND THEIR INHIBITORY ACTIVITIES AGAINST S-ADENOSYLHOMOCYSTEINE HYDROLASE

  • Choi, Won-Jun;Park, Jae-Gyu;Moon, Hyung-Ryong;Gunaga Prashantha;Lee, Kang-Man;Kim, Hea-Ok;Jeong, Lak-Shin
    • Proceedings of the PSK Conference
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    • 2002.10a
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    • pp.365.2-365.2
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    • 2002
  • S-Adenosylhomocysteine hydrolase (SAH) catalyzes the hydrolysis of S-adenosylhomocysteine to adenosine and L -homocysteine and has been an attractive target for the development of broad spectrum antiviral agents. Neplanocin A and 9-(dihydroxycyclopent-4' -enyl)adenine (DHCeA) have been known to inhibit SAH by cofactor (NAD+) depletion mechanism and their inhibition is reversed by the addition of NAD+ or dialysis. (omitted)

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Sodium selenite-induced activation of DAPK promotes autophagy in human leukemia HL60 cells

  • Jiang, Qian;Li, Feng;Shi, Kejian;Yang, Yang;Xu, Caimin
    • BMB Reports
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    • v.45 no.3
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    • pp.194-199
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    • 2012
  • Autophagy has been suggested as a possible mechanism for non-apoptotic death despite evidence from many species that autophagy represents a survival strategy of cells under stress. From our previous findings that supranutritional doses of sodium selenite induced apoptosis in human leukemia cells, now we show autophagic cell death occurred after selenite exposure in HL60, suggested an alternative mechanism for the potential therapeutic properties of selenite. Additionally, Death-associated Protein Kinase (DAPK) performed a significantly increased expression during this process, concomitantly with gradually decreased phosphorylation at $Ser^{308}$. We further reveal that the up-regulation of DAPK which depends on selenite-activated ERK had no effect on autophagy. However, activation of DAPK via PP2A-mediated dephosphorylation at $Ser^{308}$ serves as a new strategy for autophagy induction. In conclusion, these results indicate that PP2A-mediated activated DAPK sensitizes HL60 cells to selenite, ultimately triggers autophagic cell death pathway to commit cell demise.