Stabilizing a graphene platform toward discrete components

© 2016 Author(s).We report on statistical analysis and consistency of electrical performances of devices based on a large scale passivated graphene platform. More than 500 graphene field effect transistors (GFETs) based on graphene grown by chemical vapor deposition and transferred on 4 in. SiO2/Si substrates were fabricated and tested. We characterized the potential of a two-step encapsulation process including an Al2O3 protection layer to avoid graphene contamination during the lithographic process followed by a final Al2O3 passivation layer subsequent to the GFET fabrication. Devices were investigated for occurrence and reproducibility of conductance minimum related to the Dirac point. While no conductance minimum was observed in unpassivated devices, 75% of the passivated transistors exhibited a clear conductance minimum and low hysteresis. The maximum of the device number distribution corresponds to a residual doping below 5 × 1011 cm−2 (0.023 V/nm). This yield shows that GFETs integrating low-doped graphene and exhibiting small hysteresis in the transfer characteristics can be envisaged for discrete components, with even further potential for low power driven electronics.This study was partly funded by the European Union through the projects Grafol (No. 285275) and Graphene Flagship (No. 604391 and Core1 No. 696656)

APCcdh1 Mediates Degradation of the Oncogenic Rho-GEF Ect2 after Mitosis

Background: Besides regulation of actin cytoskeleton-dependent functions, Rho GTPase pathways are essential to cell cycle progression and cell division. Rho, Rac and Cdc42 regulate G1 to S phase progression and are involved in cytokinesis. RhoA GDP/GTP cycling is required for normal cytokinesis and recent reports have shown that the exchange factor Ect2 and the GTPase activating protein MgcRacGAP regulate RhoA activity during mitosis. We previously showed that the transcription factors E2F1 and CUX1 regulate expression of MgcRacGAP and Ect2 as cells enter S-phase. Methodology/Principal Findings: We now report that Ect2 is subject to proteasomal degradation after mitosis, following ubiquitination by the APC/C complex and its co-activator Cdh1. A proper nuclear localization of Ect2 is necessary for its degradation. APC-Cdh1 assembles K11-linked poly-ubiquitin chains on Ect2, depending upon a stretch of,25 amino acid residues that contain a bi-partite NLS, a conventional D-box and two TEK-like boxes. Site-directed mutagenesis of target sequences generated stabilized Ect2 proteins. Furthermore, such degradation-resistant mutants of Ect2 were found to activate RhoA and subsequent signalling pathways and are able to transform NIH3T3 cells. Conclusions/Significance: Our results identify Ect2 as a bona fide cell cycle-regulated protein and suggest that its ubiquitination-dependent degradation may play an important role in RhoA regulation at the time of mitosis. Our findings raise the possibility that the overexpression of Ect2 that has been reported in some human tumors might result not only from deregulated transcription, but also from impaired degradation

Focused Examination of the Intestinal lamina Propria Yields Greater Molecular Insight into Mechanisms Underlying SIV Induced Immune Dysfunction

Background: The Gastrointestinal (GI) tract is critical to AIDS pathogenesis as it is the primary site for viral transmission and a major site of viral replication and CD4 + T cell destruction. Consequently GI disease, a major complication of HIV/SIV infection can facilitate translocation of lumenal bacterial products causing localized/systemic immune activation leading to AIDS progression. Methodology/Principal Findings: To better understand the molecular mechanisms underlying GI disease we analyzed global gene expression profiles sequentially in the intestine of the same animals prior to and at 21 and 90d post SIV infection (PI). More importantly we maximized information gathering by examining distinct mucosal components (intraepithelial lymphocytes, lamina propria leukocytes [LPL], epithelium and fibrovascular stroma) separately. The use of sequential intestinal resections combined with focused examination of distinct mucosal compartments represents novel approaches not previously attempted. Here we report data pertaining to the LPL. A significant increase (61.7-fold) in immune defense/inflammation, cell adhesion/migration, cell signaling, transcription and cell division/differentiation genes were observed at 21 and 90d PI. Genes associated with the JAK-STAT pathway (IL21, IL12R, STAT5A, IL10, SOCS1) and T-cell activation (NFATc1, CDK6, Gelsolin, Moesin) were notably upregulated at 21d PI. Markedly downregulated genes at 21d PI included IL17D/IL27 and IL28B/IFNc3 (anti-HIV/viral), activation induced cytidine deaminase (B-cell function) an

Thirty Gigahertz Optoelectronic Mixing in Chemical Vapor Deposited Graphene

© 2016 American Chemical Society. The remarkable properties of graphene, such as broadband optical absorption, high carrier mobility, and short photogenerated carrier lifetime, are particularly attractive for high-frequency optoelectronic devices operating at 1.55 μm telecom wavelength. Moreover, the possibility to transfer graphene on a silicon substrate using a complementary metal-oxide-semiconductor-compatible process opens the ability to integrate electronics and optics on a single cost-effective chip. Here, we report an optoelectronic mixer based on chemical vapor-deposited graphene transferred on an oxidized silicon substrate. Our device consists in a coplanar waveguide that integrates a graphene channel, passivated with an atomic layer-deposited Al2O3 film. With this new structure, 30 GHz optoelectronic mixing in commercially available graphene is demonstrated for the first time. In particular, using a 30 GHz intensity-modulated optical signal and a 29.9 GHz electrical signal, we show frequency downconversion to 100 MHz. These results open promising perspectives in the domain of optoelectronics for radar and radio-communication systems

Grhl3 and GEF19 in the front rho

Directional migration is a critical component of cell motility is observed in many diverse processes including embryogenesis, immune surveillance and wound repair. A central aspect of directional migration is cellular polarity, which is established through several signaling pathways that converge on the small GTPases. These factors orchestrate precise spatial and temporal organization of the actin cytoskeleton at the leading edge of the cell, and induce polarized capture and stabilization of microtubules and their associated microtubule organizing center (MTOC). Studies of the regulation of the GTPases have predominantly focused on post-translational mechanisms involving guanine nucleotide exchange factors (GEFs), GTPase activating proteins (GAPs), and guanine nucleotide dissociation inhibitors (GDIs). In this commentary, we examine the transcriptional regulation of these factors, focusing on the recently described regulation of RhoGEF19, an activator of RhoA, by the epidermal-specific transcription factor GRHL3, and the importance of this regulatory mechanism in wound repair. Our findings establish novel links between epidermal cell migration in wound healing and the planar cell polarity (PCP) signaling pathway, and establish a paradigm for tissue-specific regulation of Rho GTPase activity

Real-Time PCR and Melting Curve Analysis for Reliable and Rapid Detection of SHV Extended-Spectrum β-Lactamases

Extended-spectrum β-lactamases (ESBLs), e.g., ESBLs of the TEM or SHV type, compromise the efficacies of expanded-spectrum cephalosporins. An SHV non-ESBL that hydrolyzes only narrow-spectrum cephalosporins can be converted into an SHV ESBL through substitutions at three amino acid positions, 179, 238, or 238–240. In order to improve detection of SHV ESBLs, a novel method, based on real-time PCR monitored with fluorescently labeled hybridization probes and followed by melting curve analysis, was developed. It is able to (i) detect bla(SHV) genes with high degrees of sensitivity and specificity, (ii) discriminate between bla(SHV non-ESBL) and bla(SHV ESBL), and (iii) categorize the SHV ESBL producers into three phenotypically relevant subgroups. This method, termed the SHV melting curve mutation detection method, represents a powerful tool for epidemiological studies with SHV ESBLs. It even has the potential to be used in the diagnostic microbiology laboratory, because up to 32 clinical isolates can be processed in less than 1 h by starting with just a few bacterial colonies