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Babraham Institute

Babraham Institute

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434 Projects, page 1 of 87
  • Funder: UK Research and Innovation Project Code: BBS/E/B/000L0818
    Funder Contribution: 43,715 GBP

    In recent years transcriptome sequencing (RNA Seq) has become a widely used technique in both fundamental and applied biological research. The Turner Lab at the world-class Babraham Institute studies the molecular processes that control development and function of lymphocytes. The lab uses the latest RNA Seq-based methods for exploring transcriptional regulation. This work contributes an important step towards a systems level understanding of immunity. The Turner Lab has partnered with Babraham-based Eagle Genomics Ltd., a leading bioinformatics cloud consultancy business, in an exciting PhD training opportunity due to begin in October 2014 (or potentially later in the 2014/15 academic year).

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  • Funder: UK Research and Innovation Project Code: BBS/E/B/0000C228
    Funder Contribution: 213,920 GBP

    Axons are the long fibres that connect one nerve cell with another and carry electrical communication between them. If these fibres degenerate, nervous function ceases resulting in neurodegenerative diseases such as Alzheimer's disease, motor neuron disease and multiple sclerosis. In many nervous disorders, the degeneration of the fibres precedes death of the cell from which they arise, but in the central nervous system the fibres cannot regenerate even if the cell survives. Thus, it is essential to understand and eventually intervene in axon degeneration mechanisms. We have identified a gene that can delay axon degeneration tenfold in mice, rats and flies, and have now found a chemical treatment that blocks its action. The aim of this project is to understand the basis of this block, and to shed light on how one part of a nerve cell signals to other parts that damage has taken place.

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  • Funder: UK Research and Innovation Project Code: BBS/E/B/0000H183
    Funder Contribution: 124,627 GBP

    When our lungs are invaded by viruses and bacteria, our immune system sends white blood cells to the site, which 'eat' and destroy the invaders. Unfortunately, the weapons that white blood cells use to kill bacteria can sometimes also damage our own lung tissue. This damage can cause diseases like Acute Respiratory Distress Syndrome (ARDS) and Bronchiectasis. At the moment, this process is not well understood and we have no strategies for preventing it. We have been studying a protein in the lungs, known as a small GTPase. We have genetic evidence that this protein has an important role in cells that are a major cause of ARDS. Mice that don't have the protein are perfectly able to fight infections from things like bacteria, but do not experience any associated lung damage. This suggests that this protein is involved in the process that damages lung tissue. This research aims to understand how our immune system attacks the lungs in this way. In so doing the researchers will make advances to prevent such damage. This grant from The British Lung Foundation is to determine whether this signalling mediator is potentially a good target for drugs to fight ARDS. Anti-inflammatory drugs available to treat lung disease are currently very non-specific, affecting many cell types and usually preventing the beneficial effects of white cells in fighting infection. Such drugs (e.g. corticosteroids) thus have many side effects including increased susceptibility to infection. By finding and understanding a new signaling pathway, we hope to identify possible drug targets that may limit inflammation without leading to increased risk of infection. This research may thus lead to novel treatments for ARDS and other inflammatory lung diseases.

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  • Funder: UK Research and Innovation Project Code: G0800013
    Funder Contribution: 904,200 GBP

    We inherit genes from our fathers and mothers and, for most of our genes, the copies we receive from either parent are equally active. An important exception to this general rule occurs in a process called genomic imprinting, whereby one gene copy is deliberately silenced. These imprinted genes are important in determining how the fetus grows and how infants adapt their physiology to life outside the womb. But the fact that these genes have one copy that is preselected to being silent poses a risk and makes them particularly vulnerable to mutation events, such as occurs in cancer. Imprinted genes behave in this manner because they are marked in different ways in the male and female germ cells. How these genes are so marked is not fully known, and it is important to find out, because if the marking process goes wrong problems in fertility or developmental abnormalities may arise. By analysing a single imprinted gene in some detail, we have discovered an important part of the mechanism in the germ cell marking event. In this research, we wish to understand this mechanism in more detail and we need to show that it may apply generally to imprinted genes. This work will be done in a model system, but it will provide important new insights for human studies.

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  • Funder: UK Research and Innovation Project Code: BBS/E/B/000M0823
    Funder Contribution: 12,950 GBP

    Production of pancreatic beta cells is a major objective of regenerative medicine. One promising source of beta cells is through generation from human pluripotent stem cells (hPSC). The non-academic partner of the project, DefiniGEN, are world leaders in producing pancreatic cell types from hPSC. Their technology platform pushes hPSC through sequential cell fate choices that mimic normal developmental processes, ultimately leading to endocrine cells including glucose-responsive insulin-secreting beta cells. Current research challenges include identifying strategies to increase efficiency at each stage of differentiation, and optimise the final steps required to mature the endocrine cells into fully functional hormone-secreting cell types. Trimethylation of histone H3 at lysine 27 (H3K27me3) is catalysed by the Polycomb-protein EZH2, and is associated with the transcriptional repression of genes that encode key developmental regulators. Evidence shows that changes in H3K27me3 are instructive in coordinating cell fate decisions during pancreatic development and beta cell formation in mice. A detailed analysis of the role of EZH2 in human pancreatic development has not been investigated. We will therefore test the hypothesis that EZH2 provides a system of transcriptional repression to control each stage of human pancreatic differentiation. This project will use epigenomic and transcriptomic profiling to define the role of EZH2 in regulating human pancreatic development, and genetic approaches to test whether loss of EZH2 function and associated histone mark at selected stages of differentiation can improve the yield and maturity of beta cell production from hPSC.

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