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Current Filters

Amounts:
£1,000,000 - £10,000,000
Award Year:
2017

Results

NGB Funding 2017-21 02 May 2017

Funding under Sport England's NGB Funding 2017-21 funding programme for a Revenue project titled 'NGB Funding 2017-21'. This project lists its main activity as Judo.

Amount: £3,131,000
Funder: Sport England
Recipient: British Judo Association
Region: East Midlands
District: Charnwood District

NGB Funding 2017-21 04 May 2017

Funding under Sport England's NGB Funding 2017-21 funding programme for a Revenue project titled 'NGB Funding 2017-21'. This project lists its main activity as Triathlon.

Amount: £3,144,397
Funder: Sport England
Recipient: British Triathlon Federation
Region: East Midlands
District: Charnwood District

NGB Funding 2017-21 04 May 2017

Funding under Sport England's NGB Funding 2017-21 funding programme for a Revenue project titled 'NGB Funding 2017-21'. This project lists its main activity as Basketball.

Amount: £4,730,000
Funder: Sport England
Recipient: Basketball England
Region: Yorkshire and the Humber
District: Sheffield District

NGB Funding 2017-21 08 May 2017

Funding under Sport England's NGB Funding 2017-21 funding programme for a Revenue project titled 'NGB Funding 2017-21'. This project lists its main activity as Exercise & Fitness.

Amount: £1,493,241
Funder: Sport England
Recipient: Exercise, Movement and Dance Partners...
Region: South East Coast
District: Horsham District

Revenue Funding 2016-19 25 May 2017

Funding under Sport England's Commonwealth Games funding programme for a Revenue project titled 'Revenue Funding 2016-19'. This project lists its main activity as Sports Development.

Amount: £4,001,487
Funder: Sport England
Recipient: Commonwealth Games England
Region: London
District: Camden London Boro

NGB Funding 2017-21 20 Jun 2017

Funding under Sport England's NGB Funding 2017-21 funding programme for a Revenue project titled 'NGB Funding 2017-21'. This project lists its main activity as Rugby League.

Amount: £4,275,200
Funder: Sport England
Recipient: Rugby Football League Limited
Region: Yorkshire and the Humber
District: Leeds District

Women’s Marketing Campaign Phase 2 17 Jan 2017

Funding under Sport England's National Programme funding programme for a Revenue project titled 'Women’s Marketing Campaign Phase 2'. This project lists its main activity as Sport participation and capacity building.

Amount: £7,200,000
Funder: Sport England
Recipient: English Sports Development Trust Ltd

Leisure Transformation Project - Stechford Leisure Centre 28 Nov 2017

Funding under Sport England's Strategic Facilities funding programme for a Capital project titled 'Leisure Transformation Project - Stechford Leisure Centre'. This project lists its main activity as Multi Sports. This funding has contributed towards a Multi Facility - Swimming Pool (Training),Swimming Pool (Learner),Fitness Facility (Indoor),Sports Hall (Main (4 or more courts))

Amount: £1,000,000
Funder: Sport England
Recipient: Birmingham City Council
Region: West Midlands
District: Birmingham District

NGB Funding 2017-21 24 Apr 2017

Funding under Sport England's NGB Funding 2017-21 funding programme for a Revenue project titled 'NGB Funding 2017-21'. This project lists its main activity as Squash.

Amount: £1,525,015
Funder: Sport England
Recipient: England Squash Limited
Region: North West
District: Manchester District

Revenue Funding 2017-19 24 Apr 2017

Funding under Sport England's Funded Partners funding programme for a Revenue project titled 'Revenue Funding 2017-19'. This project lists its main activity as Sports Development.

Amount: £2,200,000
Funder: Sport England
Recipient: National Coaching Foundation
Region: Yorkshire and the Humber
District: Leeds District

NGB Funding 2017-21 26 Apr 2017

Funding under Sport England's NGB Funding 2017-21 funding programme for a Revenue project titled 'NGB Funding 2017-21'. This project lists its main activity as Basketball.

Amount: £1,000,000
Funder: Sport England
Recipient: British Basketball Federation
Region: London
District: Newham London Boro

Challenging trypanosome antigenic variation paradigms using natural systems 11 Jul 2017

Antigenic variation (AV) is a common mechanism used by pathogens to evade host immunity and ensure infection chronicity. Recently the capacity to study AV at a molecular and population-level has expanded through systems level approaches. However, there is urgent need to challenge existing paradigms by assessing temporal (early vs. chronic infection) and spatial (tissue compartment) influences on the pathogen antigen repertoire, as well as pathogen genotype and host context. Here, we will quantitate and derive models to parameterize antigen diversity and infection chronicity in African trypanosomes. These are an exemplar of AV where population-scale antigen mRNA sequencing is tractable and underlying molecular regulators of infection are identified and manipulable. Critically, we will extend the trypanosome AV paradigm beyond the limited infection model commonly used to date, i.e. Trypanosoma brucei in mice. Thus, we will (i) quantitate the contributors to AV in chronic bovine infections for the clinically-relevant pathogens T. congolense and T. vivax, relating this to conventional infections in mice (ii) determine the contribution of identified molecular regulators of AV, parasite development and tissue compartmentation, and (iii) use the derived information to build mathematical models to interpret and unify molecular and population-level understanding of AV in these clinically-relevant infections.

Amount: £2,070,288
Funder: The Wellcome Trust
Recipient: University of Edinburgh

Putting genomic surveillance at the heart of viral epidemic response. 05 Apr 2017

This proposal is to develop an end-to-end system for processing samples from viral outbreaks to generate real-time epidemiological information that is interpretable and actionable by public health bodies. Fast evolving RNA viruses (such as Ebola, MERS, SARS, influenza etc) continually accumulate changes in their genomes that can be used to reconstruct the epidemiological processes that drive the epidemic. Based around a recently developed, single-molecule portable sequencing instrument, the MinION, we will create a 'lab-in-a-suitcase' that will be deployed to remote and resource-limited locations. These will be used to sequence viral genomes from infected patients which will then be uploaded to a central database for rapid analysis. We will develop methods for a wide-range of emerging viral diseases. Novel molecular biology methods will allow us to sequence individual viruses within a patient. Bioinformatics tools will be developed simple enough for non-bioinformaticians to use, without reliance on Internet connectivity. We will develop software to integrate these data and associated epidemiological knowledge to reveal the processes of transmission, virus evolution and epidemiological linkage. Finally we will develop a web-based visualization platform where the outputs of the statistical analyses can be interrogated for epidemiological insights within days of samples being taken from patients.

Amount: £1,721,712
Funder: The Wellcome Trust
Recipient: University of Edinburgh

Understanding mammalian interphase genome structure in mouse ES cells 05 Apr 2017

The folding of genomic DNA from the beads-on-a-string like structure of nucleosomes into higher order assemblies is critically linked to nuclear processes, but it is unclear to what degree it is a cause or consequence of function. We aim to understand whether the Nucleosome Remodeling and Deacetylation (NuRD) complex regulates chromatin structure to control transcription, or whether it is NuRD’s regulation of transcription that results in global changes in chromosome structure. We have calculated the first 3D structures of entire mammalian genomes using a new chromosome conformation capture procedure, which combines imaging with Hi-C processing of the same single cell. Our objectives are now: To study: 1) how interphase mammalian genome structure is established in G1; 2) the factors that drive this formation and; 3) how this organisation is regulated by chromatin remodellers (such as the NuRD complex) as mESC’s differentiate. To build a dedicated bespoke microscope for 3D double helix point spread function detection with light sheet activation, optimised for 3D single-molecule/super-resolution imaging of proteins such as the NuRD complex. To combine 3D super-resolution imaging and the biochemical processing steps of single cell Hi-C to directly correlate binding of protein complexes to regions of the structures.

Amount: £2,031,409
Funder: The Wellcome Trust
Recipient: University of Cambridge

Institutional Translation Partnership Award: Robotic Surgery 30 Sep 2017

Surgical robotics is an ever-expanding area of innovation and development internationally, spearheading evolution in precision medicine. Access to increasingly small and remote anatomies, characterisation of cellular and molecular information in-situ, in-vivo, and targeted therapy with increased precision are major drivers of the future generation of surgical robots. The purpose of this partnership is to capitalise on the timely evolution in the imaging, sensing and robotics research programmes currently being conducted within the Hamlyn Centre for Robotic Surgery and to address research and clinical translational challenges of precision surgery, focusing on knowledge transfer between academic research, industry, and clinical practice. Through a pioneering new model of academic translation, this partnership will stimulate Imperial's multidisciplinary academic community in surgical robotics, driving the progression of a portfolio of new medical engineering products

Amount: £1,000,000
Funder: The Wellcome Trust
Recipient: Imperial College London

In vivo mechanisms of epithelial tissue morphogenesis 11 Jul 2017

Understanding how a tri-dimensional tissue is built from the genetic blueprint is a key frontier in biology. In addition to genes known to be important in specific aspects of morphogenesis, physical constraints and properties play a major role in building tissues. In this proposal, I aim to understand how the genetic inputs integrate with the mechanical properties of the cells and tissues to produce form. To investigate this, we study the early development of the Drosophila embryo. We have found previously that actomyosin-rich boundaries play an important role in two fundamental and conserved morphogenetic phenomena, axis extension and compartmental boundary formation. We have also found that an extrinsic force contributes to axis extension. We will build on these findings by first investigating how the actomyosin-rich boundaries form and how they might repair genetic patterns during axis extension. Second, we will ask how, during compartmentalisation, they control the planar orientation of cell division and also epithelial folding. Finally, we will examine the impact of actomyosin-rich boundaries and extrinsic forces on epithelial tissue mechanics. Our approaches will be interdisciplinary, combining genetic, quantitative and in silico analyses to find novel and universal morphogenetic rules.

Amount: £1,440,082
Funder: The Wellcome Trust
Recipient: University of Cambridge

Human retroviral latency: regulation and dynamics at the single-cell level 11 Jul 2017

Latent persistence of retroviruses, including HIV-1 and the human leukaemia virus HTLV-1, remains a major barrier to their eradication from the host. HTLV-1 appears to be latent in circulating lymphocytes, but the strong, persistently activated immune response indicates that the virus is not latent in vivo. We infer that HTLV-1 undergoes intermittent bursts of gene expression. We have now obtained direct evidence of HTLV-1 gene bursts in naturally-infected cells in vitro. The central question "What regulates HTLV-1 latency?" therefore becomes "What regulates the gene expression bursts of HTLV-1?" We have developed a powerful set of materials and techniques to identify the causes and quantify the kinetics of this gene bursting at the single-cell level. A major regulator of mammalian gene expression is the key chromatin architectural protein CTCF. We recently discovered that the HTLV-1 provirus binds CTCF and alters the higher-order structure of host chromatin. In this programme we will investigate the consequences for both the virus and the host cell of this remarkable experiment of nature. The results of this work will answer fundamental questions on the persistence and pathogenesis of HTLV-1, and contribute to the growing understanding of mammalian gene bursting.

Amount: £1,927,877
Funder: The Wellcome Trust
Recipient: Imperial College London

Mechanisms and Regulation of RNAP transcription 11 Jul 2017

This grant focuses on four lines of scientific enquiry converging on RNAP function Characterisation of the molecular mechanisms underlying RNA polymerase and basal factors that facilitate transcription initiation, elongation and termination by using multidisciplinary approaches in vivo and in vitro. This includes using bespoke transcription assays, structure elucidation and a global characterization of the occupancy and transcriptomes. Identification of novel gene-specific factors and characterization of the proteomes of transcription preinitiation- and elongation complexes in vivo. Identification and characterization of RNAP-associated proteinaceous- and RNA regulators. Characterisation of the structure and function of archaeal chromatin formed by A3 and 1647 histone variants. A biophysical characterization of protein-DNA interactions and a whole-genome view of histone occupancy. Focus on the impact of chromatin on RNAP as it progresses through the transcription cycle, and the role of elongation factors to overcome the inhibitory effect of chromatin. Characterisation of factors that modulate RNAP during virus-host interactions. Virus (RIP)- and host (TFS4)-encoded RNAP-binding factors function as global inhibitors of transcription and their mechanism is reminiscent of antibiotics. Using two virus libraries of we want to screen for novel RNAP-binding regulators and use them as molecular probes to dissect RNAP function.

Amount: £2,029,869
Funder: The Wellcome Trust
Recipient: University College London

Molecular mechanisms of HIV-1 restriction by capsid-sensing host cell proteins 05 Apr 2017

Infections by retroviruses, such as HIV-1, critically depend on the viral capsid. Many host cell defence proteins, including restriction factors Trim5alpha, TrimCyp and MxB, target the viral capsid at the early stages of infection and potently inhibit virus replication. These restriction factors appear to function through a remarkable capsid pattern sensing ability that specifically recognizes the assembled capsid, but not the individual capsid protein. Using an integrative and multidisciplinary approach, I aim to determine the molecular interactions between the viral capsid and host restriction factors, TrimCyp and MxB, that underpin their capsid pattern-sensing capability and ability to inhibit HIV-1 replication. Specifically, I will combine cryoEM and cryoET with all-atom molecular-dynamics simulations to obtain high-resolution structures and atomic models of the capsid and host protein complexes (in vitro), together with mutational and functional analysis as well as correlative light and cryoET imaging of viral infection process (in vivo and in situ), to reveal the essential interfaces in their 3D organization for HIV-1 capsid recognition and inhibition of HIV-1 infection. Information derived from our studies will allow to design more robust therapeutic agents to block HIV-1 replication by strengthening the pattern recognition feature.

Amount: £1,476,229
Funder: The Wellcome Trust
Recipient: University of Oxford

Defining the Fc receptor-mediated trafficking of IgG-antigen complexes in macrophages 05 Apr 2017

Macrophages represent the most abundant antigen presenting cells in inflammatory infiltrates and tumors. An important immunoregulatory function of macrophages is to present antigen to cognate T cells. Antibody (IgG)-antigen complexes are internalized into macrophages through potential interactions with multiple different Fc receptors and are subsequently delivered to subcellular compartments where peptides derived from the proteolyzed antigen can be loaded onto MHC molecules. However, the multitude of possible Fc receptor interactions with the antibody-antigen complexes influences the spatial and temporal behavior of antigen and consequent peptide-MHC repertoire through a complex, and poorly understood, network of subcellular trafficking pathways. We have developed advanced microscopy tools to enable the analysis of three-dimensional, dynamic cellular processes at unprecedented levels of spatiotemporal resolution. We will combine these approaches with antibody engineering and analyses in mouse models of cancer and autoimmunity to elucidate how the combination of antigen delivery vehicle, microenvironmental factors and macrophage phenotype interplay to result in specific antigen presentation outcomes. The two long term goals of these studies are: one, to develop novel mechanistic insights into the fundamental cell biological processes determining the repertoire of presented antigens; two, to define how to deliver antigen to macrophages to orchestrate a predictable immune response.

Amount: £2,700,000
Funder: The Wellcome Trust
Recipient: University of Southampton