The 25 percent-efficient GaAs Cassegrainian concentrator cell

Very high-efficiency GaAs Cassegrainian solar cells have been fabricated in both the n-p and p-n configurations. The n-p configuration exhibits the highest efficiency at concentration, the best cells having an efficiency eta of 24.5 percent (100X, AM0, temperature T = 28 C). Although the cells are designed for operation at this concentration, peak efficiency is observed near 300 suns (eta = 25.1 percent). To our knowledge, this is the highest reported solar cell efficiency for space applications. The improvement in efficiency over that reported at the previous SPRAT conference is attributed primarily to lower series resistance and improved grid-line plating procedures. Using previously measured temperature coefficients, researchers estimate that the n-p GaAs cells should deliver approximately 22.5 percent efficiency at the operating conditions of 100 suns and T = 80 C. This performance exceeds the NASA program goal of 22 percent for the Cassegrainian cell. One hundred Cassegrainian cells have been sent to NASA as deliverables, sixty-eight in the n-p configuration and thirty-two in the p-n configuration

Progress toward a 30 percent-efficient, monolithic, three-junction, two-terminal concentrator solar cell for space applications

Component efficiencies of 0.2/sq cm cells at approximately 100x AMO light concentration and 80 C temperatures are not at 15.3 percent for a 1.9 eV AlGaAs top cell, 9.9 percent for a 1.4 eV GaAs middle cell under a 1.9 eV AlGaAs filter, and 2.4 percent for a bottom 1.0 eV InGaAs cell under a GaAs substrate. The goal is to continue improvement in these performance levels and to sequentially grow these devices on a single substrate to give 30 percent efficient, monolithic, two-terminal, three-junction space concentrator cells. The broad objective is a 30 percent efficient monolithic two-terminal cell that can operate under 25 to 100x AMO light concentrations and at 75 to 100 C cell temperatures. Detailed modeling predicts that this requires three junctions. Two options are being pursued, and both use a 1.9 eV AlGaAs top junction and a 1.4 eV GaAs middle junction grown by a 1 atm OMVPE on a lattice matched substrate. Option 1 uses a low-doped GaAs substrate with a lattice mismatched 1.0 eV InGaAs cell formed on the back of the substrate. Option 2 uses a Ge substrate to which the AlGaAs and GaAs top junctions are lattice matched, with a bottom 0.7 eV Ge junction formed near the substrate interface with the GaAs growth. The projected efficiency contributions are near 16, 11, and 3 percent, respectively, from the top, middle, and bottom junctions

Hydrogen Bonding Controls Excited-State Decay of the Photoactive Yellow Protein Chromophore

International audienceWe have performed excited-state dynamics simulations of a Photoactive Yellow Protein chromophore analogue in water. The results of the simulations demonstrate that in water the chromophore predominantly undergoes single-bond photoisomerization, rather than double-bond photoisomerization. Despite opposite charge distributions in the chromophore, excited-state decay takes place very efficiently from both single- and double-bond twisted minima in water. Radiationless decay is facilitated by ultrafast solvent reorganization, which stabilizes both minima by specific hydrogen bond interactions. Changing the solvent to the slightly more viscous D(2)O leads to an increase of the excited-state lifetime. Together with previous simulations, the present results provide a complete picture of the effect of the protein on the photoisomerization of the chromophore in PYP: the positive guanidinium group of Arg52 favors double-bond isomerization over single-bond isomerization by lowering the barrier for double-bond isomerization, while the hydrogen bonds with Tyr42 and Glu46 enhance deactivation from the double-bond twisted minimum

Two Ck1δ transcripts regulated by m6A methylation code for two antagonistic kinases in the control of the circadian clock.

Fustin, J.-M., Kojima, R., Itoh, K., Chang, H.-Y., Shiqi, Y., Zhuang, B., . . . Okamura, H. (2018). Two Ck1δ transcripts regulated by m6A methylation code for two antagonistic kinases in the control of the circadian clock. Proceedings of the National Academy of Sciences of the United States of America, 115(23), 5980-5985. doi:10.1073/pnas.172137111

USP6 oncogene promotes Wnt signaling by deubiquitylating Frizzleds

Ubiquitin-specific protease 6 (USP6) is a deubiquitylase that is overexpressed by chromosome translocation in two human neoplasms, aneurysmal bone cyst and nodular fasciitis. The relevant substrates of this ubiquitin-specific protease are not clear. Here, we identify the Wnt receptor Frizzled (Fzd) as a key target of the USP6 oncogene. Increased expression of USP6 increases the membrane abundance of Fzd, and hence increases cellular sensitivity to Wnts. USP6 opposes the activity of the ubiquitin ligase and tumor suppressor ring finger protein 43 (RNF43). This study identifies a new mechanism for pathological Wnt pathway activation in human disease and suggests a new approach to regulate Wnt activity therapeutically

Wnt addiction of genetically defined cancers reversed by PORCN inhibition

Enhanced sensitivity to Wnts is an emerging hallmark of a subset of cancers, defined in part by mutations regulating the abundance of their receptors. Whether these mutations identify a clinical opportunity is an important question. Inhibition of Wnt secretion by blocking an essential post-translational modification, palmitoleation, provides a useful therapeutic intervention. We developed a novel potent, orally available PORCN inhibitor, ETC-1922159 (henceforth called ETC-159) that blocks the secretion and activity of all Wnts. ETC-159 is remarkably effective in treating RSPO-translocation bearing colorectal cancer (CRC) patient-derived xenografts. This is the first example of effective targeted therapy for this subset of CRC. Consistent with a central role of Wnt signaling in regulation of gene expression, inhibition of PORCN in RSPO3-translocated cancers causes a marked remodeling of the transcriptome, with loss of cell cycle, stem cell and proliferation genes, and an increase in differentiation markers. Inhibition of Wnt signaling by PORCN inhibition holds promise as differentiation therapy in genetically defined human cancers

Essential Roles of the Tap42-Regulated Protein Phosphatase 2A (PP2A) Family in Wing Imaginal Disc Development of Drosophila melanogaster

Protein ser/thr phosphatase 2A family members (PP2A, PP4, and PP6) are implicated in the control of numerous biological processes, but our understanding of the in vivo function and regulation of these enzymes is limited. In this study, we investigated the role of Tap42, a common regulatory subunit for all three PP2A family members, in the development of Drosophila melanogaster wing imaginal discs. RNAi-mediated silencing of Tap42 using the binary Gal4/UAS system and two disc drivers, pnr- and ap-Gal4, not only decreased survival rates but also hampered the development of wing discs, resulting in a remarkable thorax cleft and defective wings in adults. Silencing of Tap42 also altered multiple signaling pathways (HH, JNK and DPP) and triggered apoptosis in wing imaginal discs. The Tap42RNAi-induced defects were the direct result of loss of regulation of Drosophila PP2A family members (MTS, PP4, and PPV), as enforced expression of wild type Tap42, but not a phosphatase binding defective Tap42 mutant, rescued fly survivorship and defects. The experimental platform described herein identifies crucial roles for Tap42•phosphatase complexes in governing imaginal disc and fly development

PORCN moonlights in a wnt-independent pathway that regulates cancer cell proliferation

10.1371/journal.pone.0034532PLoS ONE74

Modulation of Wnt/β-catenin signaling and proliferation by a ferrous iron chelator with therapeutic efficacy in genetically engineered mouse models of cancer

Using a screen for Wnt/β-catenin inhibitors, a family of 8-hydroxyquinolone derivatives with in vivo anti-cancer properties was identified. Analysis of microarray data for the lead compound N-((8-hydroxy-7-quinolinyl) (4-methylphenyl)methyl)benzamide (HQBA) using the Connectivity Map database suggested that it is an iron chelator that mimics the hypoxic response. HQBA chelates Fe2+ with a dissociation constant of ∼10−19 , with much weaker binding to Fe3+ and other transition metals. HQBA inhibited proliferation of multiple cell lines in culture, and blocked the progression of established spontaneous cancers in two distinct genetically engineered mouse models of mammary cancer, MMTV-Wnt1 and MMTV-PyMT mice, without overt toxicity. HQBA may inhibit an iron-dependent factor that regulates cell-type-specific β-catenin-driven transcription. It inhibits cancer cell proliferation independently of its effect on β-catenin signaling, as it works equally well in MMTV-PyMT tumors and diverse β-catenin-independent cell lines. HQBA is a promising specific intracellular Fe2+ chelator with activity against spontaneous mouse mammary cancers