Determination of the polarization distribution in poled ferroelectric polymer by the thermal pulse method

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The effects of prostate cancer-related plexin-B1 mutations on protein function

Semaphorin/Plexin signalling pathways modulate many biological processes such as neuronal axon pathfinding, angiogenesis, organogenesis, immune response, and cell migration. Given the fact that Semaphorins/Plexins have a strong influence on cytoskeleton structure through their interactions with receptor tyrosine kinases (RTKs) and Rho-like small GTPases, it has been suggested that they may also have a role in tumourigenesis. Recently we have identified a number of mutations in the gene PLXNB1 which encodes the Sema4D receptor protein Plexin-Bl that are associated with prostate cancer metastasis. This study aims at elucidating the effects of three of the identified mutations in PLXNB1, A5359G (amino acid change: T1697A), A5653G (T1795A) and T5714C (L1815P). None of the mutations affected the Sema4D and PDZ-RhoGEF binding function of Plexin-Bl in coimmunoprecipitation assays. In addition, no influence on the Rho regulation function of Plexin-Bl from the mutations could be detected. However by GST-pull down assays we found that Plexin-B1LT5714C was defective in binding RacL61, a constitutively active Rac mutant. This Rac binding defect renders Plexin-B1T5714C unresponsive to the cell surface trafficking effect of RacL61. Moreover, Plexin-B1T5714C failed to sequester and inhibit Rac-GTP as evident from the fact that it could neither inhibit RacL61 mediated Pak phosphorylation nor inhibit the cell spreading process mediated by RacL61. Our results suggest that the prostate cancer related PLXNB1 mutation T5714C has important effects on the functioning of Plexin-Bl by disrupting the interaction of Plexin-B 1 with Rac

Downregulation of ASPP2 in choriocarcinoma contributes to increased migratory potential through Src signaling pathway activation

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Downregulation of the Gli Transcription Factors Regulator Kif7 Facilitates Cell Survival and Migration of Choriocarcinoma Cells

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Integrated human papillomavirus analysis as an adjunct for triage of atypical cervical cytology

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Experimental arthritis is dependent on mouse mast cell protease-5

© 2017 by The American Society for Biochemistry and Molecular Biology, Inc. The constitutive heparin+ (HP) mast cells (MCs) in mice express mouseMCprotease (mMCP)-5 and carboxypeptidaseA (mMC-CPA). The amino acid sequence ofmMCP-5is most similar to that of human chymase-1, as are the nucleotide sequences of their genes and transcripts. Using a homologous recombination approach, a C57BL/6 mouse line was created that possessed a disrupted mMCP-5 gene. The resulting mice were fertile and had no obvious developmental abnormality. Lack of mMCP-5 protein did not alter the granulation of the IL-3/IL-9-dependent mMCP-2+ MCs in the jejunal mucosa of Trichinella spiralisinfected mice. In contrast, the constitutive HP+ MCs in the tongues of mMCP-5-null mice were poorly granulated and lacked mMC-CPA protein. Bone marrow-derived MCs were readily developed from the transgenic mice using IL-3. Although these MCs contained high levels of mMC-CPA mRNA, they also lacked the latter exopeptidase. mMCP-5 protein is therefore needed to target translated mMC-CPA to the secretory granule along with HP-containing serglycin proteoglycans. Alternately, mMCP-5 is needed to protect mMC-CPA from autolysis in the cell's granules. Fibronectin was identified as a target of mMCP-5, and the exocytosis ofmMCP-5from theMCs in the mouse's peritoneal cavity resulted in the expression of metalloproteinase protease-9, which has been implicated in arthritis. In support of the latter finding, experimental arthritis was markedly reduced in mMCP-5-null mice relative to wildtype mice in two disease models

AMPK Activators Suppress Cervical Cancer Cell Growth through Inhibition of DVL3 Mediated Wnt/β-Catenin Signaling Activity

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Overexpression of Forkhead Box Protein M1 (FOXM1) in Ovarian Cancer Correlates with Poor Patient Survival and Contributes to Paclitaxel Resistance

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AMPK Activators Suppress Cervical Cancer Cell Growth through Inhibition of DVL3 Mediated Wnt/β-Catenin Signaling Activity

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Using satellites to monitor Severn Bridge structure, UK

The Severn Bridge is a large UK suspension bridge. In 2010, a series of field surveys was commissioned to monitor the magnitude and frequencies of the bridge’s movements, through attaching nine dual-frequency survey grade global navigation satellite system receivers on the bridge and two reference satellite receivers adjacent to the structure. The satellite antenna locations and configuration allow the movements of the north cable to be analysed at four locations, as well as the differential movements of the two suspension cables to each other. In addition, this configuration allows the movements of the tops of the towers to be compared to the cables’ movements, as well as with each other. All in all, this allowed the relative movements of the various locations on the bridge’s suspension cables and tower tops to be compared to each other, at a rate of up to 20 Hz. Overall, some 3 days of raw code and carrier phase satellite data were gathered. During these sessions, normal traffic loading was experienced. This paper describes the survey, presents a selection of the key results and draws conclusions about the effective use of satellite positioning systems to enhance structural health monitoring.The Highways Agency, Severn River Crossing plc and Mott MacDonal