Design of Star-Shaped Trimer Acceptors for High-Performance (Efficiency > 19%), Photostable,and Mechanically Robust Organic Solar Cells

High power conversion efficiency (PCE), long-term stability, and mechanical robustness are prerequisites for the commercial applications of organic solar cells (OSCs). In this study, a new star-shaped trimer acceptor (TYT-S) is developed and high-performance OSCs with a PCE of 19.0%, high photo-stability (t_80% lifetime = 2600 h under 1-sun illumination), and mechanical robustness with a crack-onset strain (COS) of 21.6% are achieved. The isotropic molecular structure of TYT-S affords efficient multi-directional charge transport and high electron mobility. Furthermore, its amorphous structure prevents the formation of brittle crystal-to-crystal interfaces, significantly enhancing the mechanical properties of the OSC. As a result, the TYT-S-based OSCs demonstrate a significantly higher PCE (19.0%) and stretchability (COS = 21.6%) than the linear-shaped trimer acceptor (TYT-L)-based OSCs (PCE = 17.5% and COS = 6.4%) and the small-molecule acceptor (MYT)-based OSCs (PCE = 16.5% and COS = 1.3%). In addition, the increased molecular size of TYT-S, relative to that of MYT and dimer (DYT), suppresses the diffusion kinetics of the acceptor molecules, substantially improving the photostability of the OSCs. Finally, to effectively demonstrate the potential of TYT-S, intrinsically stretchable (IS)-OSCs are constructed. The TYT-S-based IS-OSCs exhibit high device stretchability (strain at PCE_80% = 31%) and PCE of 14.4%.     

Capsicum annuum tobacco mosaic virus-induced clone 1 expression perturbation alters the plant's response to ethylene and interferes with the redox homeostasis

Capsicum annuum tobacco mosaic virus (TMV)-induced clone 1 (CaTin1) gene was expressed early during incompatible interaction of hot pepper (Caspsicum annuum) plants with TMV and Xanthomonas campestris. RNA-blot analysis showed that CaTin1 gene was expressed only in roots in untreated plants and induced mainly in leaf in response to ethylene, NaCl, and methyl viologen but not by salicylic acid and methyl jasmonate. The ethylene dependence of CaTin1 induction upon TMV inoculation was demonstrated by the decrease of CaTin1 expression in response to several inhibitors of ethylene biosynthesis or its action. Transgenic tobacco (Nicotiana tabacum) plants expressing CaTin1 gene in sense- or antisense-orientation showed interesting characteristics such as the accelerated growth and the enhanced resistance to biotic as well as abiotic stresses. Such characteristics appear to be caused by the elevated level of ethylene and H2O2. Moreover, in transgenic plants expressing antisense CaTin1 gene, the expression of some pathogenesis-related genes was enhanced constitutively, which may be mainly due to the increased ethylene level. The promoter of CaTin1 has four GCC-boxes, two AT-rich regions, and an elicitor-inducible W-box. The induction of the promoter activity by ethylene depends on GCC-boxes and by TMV on W-box. Taken together, we propose that the CaTin1 up-regulation or down-regulation interferes with the redox balance of plants leading to the altered response to ethylene and biotic as well as abiotic stresses.     

Specific modulation of the anti-DNA autoantibody-nucleic acids interaction by the high affinity RNA aptamer

Anti-DNA autoantibodies are one of the frequently found autoantibodies in systemic lupus erythematosus patient sera. RNA aptamers for the monoclonal G6-9 anti-DNA autoantibody were selected from a random pool of RNA library. Binding affinity of the best aptamer is around 2nM, which is at least 100-fold higher than that of cognate DNA antigen to the autoantibody. Aptamer binds specifically to the G6-9 autoantibody but not to other similar autoantibodies. Minimal binding motif of the aptamer was mapped, providing a hint for a natural epitope of the autoantibody. DNA binding to the G6-9 autoantibody is shown to be efficiently inhibited by the aptamer. Such binding property of the RNA aptamer could be used not only as a modulator for the pathogenic anti-DNA autoantibody, but also as a useful biochemical reagent for elucidating a fine specificity of the autoantibody-nucleic acid interaction.     

Activity assay of mammalian 2-cys peroxiredoxins using yeast thioredoxin reductase system

2-Cys peroxiredoxin (Prx) is a novel cellular peroxidase that reduces peroxides in the presence of thioredoxin, thioredoxin reductase, and nicotinamide adenine dinucleotide phosphate (NADPH) and that functions in H(2)O(2)-mediated signal transduction. Recent studies have shown that 2-cys Prx can be inactivated by cysteine overoxidation in conditions of oxidative stress. Therefore, peroxidase activity, rather than the protein level, of 2-cys Prx is the more important measure to predict its cellular function. Here, we introduce a modified activity assay method for mammalian 2-cys Prx based on yeast nonselenium thioredoxin reductase. Yeast thioredoxin reductase is expressed in Escherichia coli cells and purified at high yield (40 mg/L of culture broth) as an active flavoprotein by combined diethyl aminoethyl (DEAE) and phenyl hydrophobic chromatography. The optimal concentrations of yeast thioredoxin and thioredoxin reductase required to achieve maximum mammalian 2-cys Prx activity are 3.0 and 1.5 microM, respectively. This modified assay method is useful for measuring 2-cys Prx activity in cell lysates and can also be adapted for a 96-well plate reader for high-throughput screening of chemical compounds that target 2-cys Prx.     

Inhibition of the angiogenesis by the MCP-1 (monocyte chemoattractant protein-1) binding peptide

The CC chemokine, monocyte chemoattractant protein-1 (MCP-1), plays a crucial role in the initiation of atherosclerosis and has direct effects that promote angiogenesis. To develop a specific inhibitor for MCP-1-induced angiogenesis, we performed in vitro selection employing phage display random peptide libraries. Most of the selected peptides were found to be homologous to the second extracellular loops of CCR2 and CCR3. We synthesized the peptide encoding the homologous sequences of the receptors and tested its effect on the MCP-1 induced angiogenesis. Surface plasmon resonance measurements demonstrated specific binding of the peptide to MCP-1 but not to the other homologous protein, MCP-3. Flow cytometry revealed that the peptide inhibited the MCP-1 binding to THP-1 monocytes. Moreover, CAM and rat aortic ring assays showed that the peptide inhibited MCP-1 induced angiogenesis. Our observations indicate that the MCP-1-binding peptide exerts its anti-angiogenic effect by interfering with the interaction between MCP-1 and its receptor.     

Inhibition of the functions of the nucleocapsid protein of human immunodeficiency virus-1 by an RNA aptamer

The nucleocapsid (NC) protein plays many roles in the life cycle of human immunodeficiency virus type-1 (HIV-1). Previously we selected the NC binding RNA aptamers from diverse forms of RNA libraries. Here we used one of the RNA aptamers to the NC protein, N70-13, and tested its effect on NC protein in vitro and in cells. The high affinity RNA aptamer completely abolished NC binding to the stable transactivation response hairpin and psi RNA stem-loops of HIV-1 RNA. When it was expressed in cells as an intramer it inhibited the packaging of viral genomic RNA and therefore promises to be an effective anti-HIV therapeutic tool.     

Design of Cyanovinylene‐Containing Polymer Acceptors with Large Dipole Moment Change for Efficient Charge Generation in High‐Performance All‐Polymer Solar Cells

Designing polymers that facilitate exciton dissociation and charge transport is critical for the production of highly efficient all‐polymer solar cells (all‐PSCs). Here, the development of a new class of high‐performance naphthalenediimide (NDI)‐based polymers with large dipole moment change (Δµ_ge) and delocalized lowest unoccupied molecular orbital (LUMO) as electron acceptors for all‐PSCs is reported. A series of NDI‐based copolymers incorporating electron‐withdrawing cyanovinylene groups into the backbone (PNDITCVT‐R) is designed and synthesized with 2‐hexyldecyl (R = HD) and 2‐octyldodecyl (R = OD) side chains. Density functional theory calculations reveal an enhancement in Δµ_ge and delocalization of the LUMO upon the incorporation of cyanovinylene groups. All‐PSCs fabricated from these new NDI‐based polymer acceptors exhibit outstanding power conversion efficiencies (7.4%) and high fill factors (65%), which is attributed to efficient exciton dissociation, well‐balanced charge transport, and suppressed monomolecular recombination. Morphological studies by grazing X‐ray scattering and resonant soft X‐ray scattering measurements show the blend films containing polymer donor and PNDITCVT‐R acceptors to exhibit favorable face‐on orientation and well‐mixed morphology with small domain spacing (30–40 nm).     

SR proteins induce alternative exon skipping through their activities on the flanking constitutive exons

SR proteins are well known to promote exon inclusion in regulated splicing through exonic splicing enhancers. SR proteins have also been reported to cause exon skipping, but little is known about the mechanism. We previously characterized SRSF1 (SF2/ASF)-dependent exon skipping of the CaMKIIδ gene during heart remodeling. By using mouse embryo fibroblasts derived from conditional SR protein knockout mice, we now show that SR protein-induced exon skipping depends on their prevalent actions on a flanking constitutive exon and requires collaboration of more than one SR protein. These findings, coupled with other established rules for SR proteins, provide a theoretical framework to understand the complex effect of SR protein-regulated splicing in mammalian cells. We further demonstrate that heart-specific CaMKIIδ splicing can be reconstituted in fibroblasts by downregulating SR proteins and upregulating a RBFOX protein and that SR protein overexpression impairs regulated CaMKIIδ splicing and neuronal differentiation in P19 cells, illustrating that SR protein-dependent exon skipping may constitute a key strategy for synergism with other splicing regulators in establishing tissue-specific alternative splicing critical for cell differentiation programs.