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ABSTRACT: Ataxin-1 is a polyglutamine protein of unknown function that is encoded by the ATXN1 gene in humans. To gain insight into the function of ataxin-1, we sought to identify proteins that interact with ataxin-1 through yeast two-hybrid screening. In this study, transcriptional corepressor CtBP2 was identified as a protein that interacted with ataxin-1. CtBP2 and ataxin-1 colocalized in the nucleus of mammalian cells. Since the E-cadherin promoter is a target of CtBP-mediated repression, the relationship between ataxin-1 and the E-cadherin promoter was investigated. Chromatin immunoprecipitation assays showed that CtBP2 and ataxin-1 were recruited to the E-cadherin promoter in mammalian cells. Luciferase assays using E-cadherin promoter reporter constructs revealed that the luciferase activity was enhanced as the level of ataxin-1 protein expression increased. CtBP2 overexpression decreased E-cadherin expression, but expression of ataxin-1 inversely increased the mRNA and protein levels of endogenous E-cadherin. Interestingly, siRNA experiments showed that the transcriptional activation of ataxin-1 was associated with the presence of CtBP2. This study demonstrates that ataxin-1 occupies the promoter region of E-cadherin in vivo and that ataxin-1 activates the promoter in a CtBP2-mediated transcriptional regulation manner. This article is part of a Special Issue entitled: 11th European Symposium on Calcium.
Biochimica et Biophysica Acta 02/2011; 1813(5):713-22. · 4.66 Impact Factor
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ABSTRACT: Abstract Nano-floating gate memory devices were fabricated on a flexible plastic substrate by a low-temperature fabrication process. The memory characteristics of ZnO-based thin-film transistors with Al nanoparticles embedded in the gate oxides were investigated in this study. Their electron mobility was found to be 0.18 cm2/V·s and their on/off ratio was in the range of 104–105. The threshold voltages of the programmed and erased states were negligibly changed up to 103 cycles. The flexibility, memory properties, and low-temperature fabrication of the nano-floating gate memory devices described herein suggest that they have potential applications for future flexible integrated electronics.
Nanoscale Research Letters. 01/2011;
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ABSTRACT: We construct fully transparent nano-floating gate memory devices on a glass substrate. These memory thin-film transistors consist of channel layers of ZnO films, electrodes of Al/ITO, and floating gate nodes of Al nanoparticles, exhibiting a transmittance of approximately 71% in the visible region. Their electron mobility, on/off ratio, and threshold voltage shift are estimated to be 0.92 cm(2) V( - 1) s( - 1), about 10(4), and 3.1 V, respectively. Moreover, their programming/erasing, endurance and retention are characterized in this study. Our study suggests that our memory devices have great potential for realizing transparent systems-on-glass.
Nanotechnology 08/2010; 21(33):335201. · 3.98 Impact Factor
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ABSTRACT: Double-strand breaks (DSBs) of chromosomal DNA trigger the cellular response that activates the pathways for DNA repair and cell-cycle checkpoints, and sometimes the pathways leading to cell death if the damage is too severe to be tolerated. Evidence indicates that, upon generation of DNA DSBs, many nuclear proteins that are involved in DNA repair and checkpoints are recruited to chromatin around the DNA lesions. In the present study we used a proteomics approach to identify DNA-damage-induced chromatin-binding proteins in a systematic way. Two-dimensional gel analysis for protein extracts of chromatin from DNA-damage-induced and control HeLa cells identified four proteins as the candidates for DNA-damage-induced chromatin-binding proteins. MALDI-TOF (matrix-assisted laser-desorption ionization-time-of-flight) MS analysis identified these proteins to be NPM (nucleophosmin), hnRNP (heterogeneous nuclear ribonucleoprotein) C1, hnRNP C2 and 37-kDa laminin-receptor precursor, and the identity of these proteins was further confirmed by immunoblot analysis with specific antibodies. We then demonstrated with chromatin-binding assays that NPM and hnRNP C1/C2, the abundant nuclear proteins with pleiotropic functions, indeed bind to chromatin in a DNA-damage-dependent manner, implicating these proteins in DNA repair and/or damage response. Immunofluorescence experiments showed that NPM, normally present in the nucleoli, is mobilized into the nucleoplasm after DNA damage, and that neither NPM nor hnRNP C1/C2 is actively recruited to the sites of DNA breaks. These results suggest that NPM and hnRNP C1/C2 may function at the levels of the global context of chromatin, rather than by specifically targeting the broken DNA.
Biochemical Journal 06/2005; 388(Pt 1):7-15. · 4.90 Impact Factor
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ABSTRACT: The performance of dual floating gate memory devices constructed on glass is examined in this study. The dual floating gate memory device is composed of a ZnO transistor with a bottom-gate oxide layer whose two laterally separated regions are embedded with Al nanoparticles. For the memory device, four different states are achieved through Fowler–Nordheim (F–N) tunneling and channel hot electron (CHE) injection. Each of these four different states is distinguished by a difference of about 0.5 V in the threshold voltage shift. A detailed description on the four-state operation is given in this paper.Research highlights► The dual floating gate memory device shows a successful multi-state operation. ► Laterally separated regions are used embedded with Al nanoparticles as charge nodes. ► The memory device is programmed by the F–N tunneling and CHE injection method. ► Four different states are achieved through operating the memory.
Solid State Communications 151(2):151-154. · 1.65 Impact Factor
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ABSTRACT: In this study, nonvolatile nano-floating gate memory devices were fabricated based on ZnO films and Al nanoparticles and their electrical properties were investigated. Al nanoparticles were embedded in between SiO2 tunneling and control oxide layers deposited on ZnO channels, and these nanoparticles acted as floating gate nodes in the devices. Their electron mobility, on/off ratio, and threshold voltage shift were estimated to be 9.42 cm2/V s, about 106, and 4.2 V, respectively. Their programming/erasing, endurance and retention were also characterized. Especially, the low-temperature processes applied in this work indicate that integrated electronic devices can be fabricated on temperature-sensitive substrates.Graphical abstract
Solid State Sciences. 12(12):1966-1969.
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ABSTRACT: Although SWI/SNF chromatin remodeling complexes play important roles in transcription, recent studies suggest that they also participate directly in DNA repair. In yeast, SWI/SNF and related RSC complexes have been shown to be recruited to the sites of DNA double strand breaks (DSBs) to facilitate DNA repair. We recently have shown that mammalian SWI/SNF complexes contribute to DBS repair by direct mechanisms of stimulating the phosphorylation of histone H2AX at DSB-surrounding chromatin. Here we investigated the role of mammalian SWI/SNF complexes in cell survival after DNA damage. When SWI/SNF was inactivated by means of dominant negativity or its catalytic subunit BRG1 was knockdowned by small interfering RNA, cells became highly susceptible to DNA damage-induced apoptosis. SWI/SNF inactivation had no effect on the activation and establishment of G2/M DNA damage checkpoint. However, SWI/SNF-defective cells could not sustain the G2/M checkpoint long enough to survive DNA damage, and rather underwent apoptosis before entering mitosis. We also found that, although the basal state and DNA damage-triggered activation of p53 were normal, the kinetics of p53 downregulation was significantly delayed in SWI/SNF-defective cells. Finally, the sustained p53 activation in SWI/SNF-defective cells was accompanied by accumulation of unrepaired DSBs owing to inefficient DNA repair. These results suggest that mammalian SWI/SNF complexes prevent DNA damage-induced apoptosis in part by facilitating efficient repair and thereby ensuring timely elimination of unrepaired DSBs that could otherwise lead to excessive prolongation of p53 activation.
DNA Repair.
