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University of Portsmouth

Country: United Kingdom
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352 Projects, page 1 of 71
  • Project . 2017 - 2022
    Funder: UKRI Project Code: 2708331
    Partners: University of Portsmouth

    Covid Extension

  • Funder: UKRI Project Code: 509721
    Funder Contribution: 94,449 GBP
    Partners: University of Portsmouth

    To develop innovative manufacturing capability to enable the production of current and future products in the UK. Allowing flexible manufacture and reduced importing.

  • Funder: UKRI Project Code: 2596860
    Partners: University of Portsmouth

    Quantifying energy dissipation from Active Galactic Nuclei (AGN) in the

  • Funder: UKRI Project Code: 2116133
    Partners: University of Portsmouth

    Have national and global campaigns made any impact in changing the way in which Somalian family members in the UK view FGM? Are there any generational differences in how members of a Somali families view FGM and if differences exist why? Has the campaigning triggered any unintentional negative consequences? e.g. brought tensions into families? To what extent do campaigners in the end FGM movement view their impact in terms of triggering mind-set change? Is there a disconnect between high profile campaigners and members of the so-called cutting communities?

  • Funder: UKRI Project Code: BB/H00680X/1
    Funder Contribution: 445,030 GBP
    Partners: University of Portsmouth

    Bacteria use the so-called restriction-modification (R-M) system to protect themselves from invasion by foreign DNA (e.g. from bacterial viruses). The R-M system works by producing two enzymes. The first, a so-called methyltransferase (M), marks the bacterium's own DNA by adding methyl groups at strategic positions. The second enzyme, an endonuclease (R), then breaks down DNA that is not correctly marked. The R-M system thus provides a way to destroy foreign DNA selectively. However, if the timing of the production of the two enzymes is disturbed, the endonuclease will destroy the bacterium's own DNA, leading to the bacterial equivalent of an autoimmune disease and to death of the bacterium. To avoid this, so-called controller (C) proteins regulate the synthesis of the two enzymes by binding to the appropriate sites on the DNA that control the individual R-M genes. This leads to a complex regulatory network with positive and negative 'feedback' circuits. Our aim in this proposal is to understand exactly how subtle changes in the DNA sequence influence how strongly the controller protein binds to the control regions of the genes, and how this dictates the order in which they are switched on and off. Also, we want to know how the shape of the DNA is distorted to allow the proteins to interact with the double helix, and how this is involved in the synergy involved when proteins bind to adjacent sites on the DNA. Once we understand these things in molecular detail, it may be possible to design novel anti-bacterial drugs that are specific for different strains of bacteria.