Investigation of immune and haematopoietic disorders View Homepage


Ontology type: schema:MonetaryGrant     


Grant Info

YEARS

2005-

FUNDING AMOUNT

18006920 GBP

ABSTRACT

The World Health Organisation estimates that in the region of 300 million people worldwide now suffer from asthma. Allergic asthma is caused by an abnormal reaction to a variety of environmental agents, called allergens. This leads to long-term lung inflammation and an over-responsiveness of the airways. As the airways become narrowed and irritated, coughing, wheezing and shortness of breath occur. The body is normally protected by its immune system, but during asthma it becomes inappropriately activated by allergens such as pollen and dust. We are trying to understand how the immune system is being controlled and identify points at which we may be able to block it and thereby improve asthma symptoms. Cells of the immune system communicate by sending out protein messengers (called interleukins ) that are received by other cells and cause them to switch on specific functions – for example to start producing mucus in the lung in response to irritation. We have discovered a new immune cell (ILC2) that plays a key role in receiving and sending out messages during asthma-like disease. Recently using mouse asthma models we have shown that blocking the action of Interleukin-25 (IL-25), asthma-like responses. We are now investigating the therapeutic potential of this approach for treating asthma. Technical Summary Allergic asthma is characterised by uncontrollable airways hyperresponsiveness (AHR) induced by a variety of provocative stimuli and is associated with type-2 inflammatory infiltrates into the lungs. The number of sufferers has increased dramatically over recent decades and the World Health Organisation estimates that in the region of 300 million people worldwide suffer from this disorder. Genes residing on human chromosome 5q31-34 have been implicated in the induction and progression of several immune and haematopoietic disorders including asthma and allergy, autoimmunity, parasite susceptibility, and myelodysplasia. We combine information derived from the human and mouse genomes, with techniques to modify the mouse genome to identify and define the functions of disease susceptibility genes. Using transgenic mouse models we have characterised fundamental inter-dependent roles for the type-2 cytokines interleukin-4 (IL-4), IL-5, IL-9 and IL-13 as mediators of asthma and allergy. More recently we have focussed on characterising critical molecules that initiate the type-2 response. These include IL-25 and IL-33. IL-25 is a member of the IL-17 family of cytokines and we have demonstrated an important role for IL-25 in protective immunity to infection and uncovered a critical role for IL-25 in airways hyperresponsiveness and inflammation. We developed a unique monoclonal antibody that blocks the interaction of IL-25 with its receptor, and administration of this antibody prevents airways hyperresponsiveness in a mouse model of allergic asthma. Importantly, since the anti-IL-25 antibody cross-reacts with human IL-25, blocking its interaction with the human IL-25 receptor, we have humanised this antibody in collaboration with MRC Technology, and are continuiing to validate this molecule in asthma models. It is becoming increasingly clear that innate immune cell types, in addition to the classical Th2 cells, can produce type-2 cytokines and that they may play critical roles in the initiation of the type-2 response. Using Il13-eGFP reporter mice, we discovered type-2 innate lymphoid cells (ILC2) and demonstrated that they are the predominant early source of the IL-13 critical for inducing expulsion of the helminth parasite, Nippostrongylus brasiliensis, following infection. ILC2 also expand in experimental models of asthma, where they represent an important source of type-2 cytokines. Our recent studies have indicated that ILC2 interact with dendritic cells and Th2 cells to potentiate type-2 immunity. We have shown that these type-2 ILCs develop from common lymphoid progenitors under signals from IL-7 and IL-33 and Notch. We have gone on to show that the transcription factors ROR, a relative of ROR t, and Bcl11b play important roles in ILC2 development. More... »

URL

http://gtr.rcuk.ac.uk/project/D31EBCA2-A303-40E7-A9CD-FD23260BBC69

Related SciGraph Publications

  • 2019-03. Pulmonary group 2 innate lymphoid cells: surprises and challenges in MUCOSAL IMMUNOLOGY
  • 2018-12. Genome-wide analyses reveal the IRE1a-XBP1 pathway promotes T helper cell differentiation by resolving secretory stress and accelerating proliferation in GENOME MEDICINE
  • 2018-09. FBP17 and CIP4 recruit SHIP2 and lamellipodin to prime the plasma membrane for fast endophilin-mediated endocytosis in NATURE CELL BIOLOGY
  • 2018-01. IFN-γ increases susceptibility to influenza A infection through suppression of group II innate lymphoid cells in MUCOSAL IMMUNOLOGY
  • 2017-12. Tumour-derived PGD2 and NKp30-B7H6 engagement drives an immunosuppressive ILC2-MDSC axis in NATURE COMMUNICATIONS
  • 2017-10-30. TH2 cell development and function in NATURE REVIEWS IMMUNOLOGY
  • 2017-08. Resolution of inflammation by interleukin-9-producing type 2 innate lymphoid cells in NATURE MEDICINE
  • 2017-06-07. Type-2 innate lymphoid cells control the development of atherosclerosis in mice in NATURE COMMUNICATIONS
  • 2016-12. Single-cell analysis of CD4+ T-cell differentiation reveals three major cell states and progressive acceleration of proliferation in GENOME BIOLOGY
  • 2016-12. Erratum to: Single cell analysis of CD4+ T cell differentiation reveals three major cell states and progressive acceleration of proliferation in GENOME BIOLOGY
  • 2016-11. Single-cell RNA-seq identifies a PD-1hi ILC progenitor and defines its development pathway in NATURE
  • 2016-11. IL-4-producing ILC2s are required for the differentiation of TH2 cells following Heligmosomoides polygyrus infection in MUCOSAL IMMUNOLOGY
  • 2016-05-02. The topography of mutational processes in breast cancer genomes in NATURE COMMUNICATIONS
  • 2016-01. Group 2 innate lymphoid cells license dendritic cells to potentiate memory TH2 cell responses in NATURE IMMUNOLOGY
  • 2015-12. A dominant role for the methyl-CpG-binding protein Mbd2 in controlling Th2 induction by dendritic cells in NATURE COMMUNICATIONS
  • 2015-08. Inflammation-induced formation of fat-associated lymphoid clusters in NATURE IMMUNOLOGY
  • 2015-04. Deciphering the transcriptional switches of innate lymphoid cell programming: the right factors at the right time in GENES & IMMUNITY
  • 2015-01. Endophilin marks and controls a clathrin-independent endocytic pathway in NATURE
  • 2014-09. Blockade of IL-33 release and suppression of type 2 innate lymphoid cell responses by helminth secreted products in airway allergy in MUCOSAL IMMUNOLOGY
  • 2014-07. TH9 cells that express the transcription factor PU.1 drive T cell-mediated colitis via IL-9 receptor signaling in intestinal epithelial cells in NATURE IMMUNOLOGY
  • 2014-07. The TNF-family cytokine TL1A promotes allergic immunopathology through group 2 innate lymphoid cells in MUCOSAL IMMUNOLOGY
  • 2013-04. The transcription factor T-bet is essential for the development of NKp46+ innate lymphocytes via the Notch pathway in NATURE IMMUNOLOGY
  • 2013-02. Innate lymphoid cells — a proposal for uniform nomenclature in NATURE REVIEWS IMMUNOLOGY
  • 2013-02. Innate lymphoid cells — how did we miss them? in NATURE REVIEWS IMMUNOLOGY
  • 2013. Innate Lymphoid Cells in Immunity and Disease in CROSSROADS BETWEEN INNATE AND ADAPTIVE IMMUNITY IV
  • 2012-11. Blocking IL-25 signalling protects against gut inflammation in a type-2 model of colitis by suppressing nuocyte and NKT derived IL-13 in JOURNAL OF GASTROENTEROLOGY
  • 2012-03. Transcription factor RORα is critical for nuocyte development in NATURE IMMUNOLOGY
  • 2011-07. Innate lymphoid cells mediate influenza-induced airway hyper-reactivity independently of adaptive immunity in NATURE IMMUNOLOGY
  • 2010-07. T<sub>H</sub>9: the latest addition to the expanding repertoire of IL-25 targets in IMMUNOLOGY AND CELL BIOLOGY
  • 2010-06. Interleukin-33 attenuates sepsis by enhancing neutrophil influx to the site of infection in NATURE MEDICINE
  • 2010-04. Nuocytes represent a new innate effector leukocyte that mediates type-2 immunity in NATURE
  • 2010-01. A p53-dependent mechanism underlies macrocytic anemia in a mouse model of human 5q– syndrome in NATURE MEDICINE
  • JSON-LD is the canonical representation for SciGraph data.

    TIP: You can open this SciGraph record using an external JSON-LD service: JSON-LD Playground Google SDTT

    [
      {
        "@context": "https://springernature.github.io/scigraph/jsonld/sgcontext.json", 
        "about": [
          {
            "id": "http://purl.org/au-research/vocabulary/anzsrc-for/2008/2211", 
            "inDefinedTermSet": "http://purl.org/au-research/vocabulary/anzsrc-for/2008/", 
            "type": "DefinedTerm"
          }, 
          {
            "id": "http://purl.org/au-research/vocabulary/anzsrc-for/2008/2211", 
            "inDefinedTermSet": "http://purl.org/au-research/vocabulary/anzsrc-for/2008/", 
            "type": "DefinedTerm"
          }
        ], 
        "amount": {
          "currency": "GBP", 
          "type": "MonetaryAmount", 
          "value": "18006920"
        }, 
        "description": "The World Health Organisation estimates that in the region of 300 million people worldwide now suffer from asthma.\nAllergic asthma is caused by an abnormal reaction to a variety of environmental agents, called allergens. This leads to long-term lung inflammation and an over-responsiveness of the airways. As the airways become narrowed and irritated, coughing, wheezing and shortness of breath occur.\nThe body is normally protected by its immune system, but during asthma it becomes inappropriately activated by allergens such as pollen and dust. We are trying to understand how the immune system is being controlled and identify points at which we may be able to block it and thereby improve asthma symptoms.\nCells of the immune system communicate by sending out protein messengers (called interleukins ) that are received by other cells and cause them to switch on specific functions \u2013 for example to start producing mucus in the lung in response to irritation. We have discovered a new immune cell (ILC2) that plays a key role in receiving and sending out messages during asthma-like disease. \nRecently using mouse asthma models we have shown that blocking the action of Interleukin-25 (IL-25), asthma-like responses. We are now investigating the therapeutic potential of this approach for treating asthma.\n\nTechnical Summary\nAllergic asthma is characterised by uncontrollable airways hyperresponsiveness (AHR) induced by a variety of provocative stimuli and is associated with type-2 inflammatory infiltrates into the lungs. The number of sufferers has increased dramatically over recent decades and the World Health Organisation estimates that in the region of 300 million people worldwide suffer from this disorder. Genes residing on human chromosome 5q31-34 have been implicated in the induction and progression of several immune and haematopoietic disorders including asthma and allergy, autoimmunity, parasite susceptibility, and myelodysplasia. We combine information derived from the human and mouse genomes, with techniques to modify the mouse genome to identify and define the functions of disease susceptibility genes.\nUsing transgenic mouse models we have characterised fundamental inter-dependent roles for the type-2 cytokines interleukin-4 (IL-4), IL-5, IL-9 and IL-13 as mediators of asthma and allergy. More recently we have focussed on characterising critical molecules that initiate the type-2 response. These include IL-25 and IL-33. IL-25 is a member of the IL-17 family of cytokines and we have demonstrated an important role for IL-25 in protective immunity to infection and uncovered a critical role for IL-25 in airways hyperresponsiveness and inflammation. We developed a unique monoclonal antibody that blocks the interaction of IL-25 with its receptor, and administration of this antibody prevents airways hyperresponsiveness in a mouse model of allergic asthma. Importantly, since the anti-IL-25 antibody cross-reacts with human IL-25, blocking its interaction with the human IL-25 receptor, we have humanised this antibody in collaboration with MRC Technology, and are continuiing to validate this molecule in asthma models. \nIt is becoming increasingly clear that innate immune cell types, in addition to the classical Th2 cells, can produce type-2 cytokines and that they may play critical roles in the initiation of the type-2 response. Using Il13-eGFP reporter mice, we discovered type-2 innate lymphoid cells (ILC2) and demonstrated that they are the predominant early source of the IL-13 critical for inducing expulsion of the helminth parasite, Nippostrongylus brasiliensis, following infection. ILC2 also expand in experimental models of asthma, where they represent an important source of type-2 cytokines. Our recent studies have indicated that ILC2 interact with dendritic cells and Th2 cells to potentiate type-2 immunity. We have shown that these type-2 ILCs develop from common lymphoid progenitors under signals from IL-7 and IL-33 and Notch. We have gone on to show that the transcription factors ROR, a relative of ROR t, and Bcl11b play important roles in ILC2 development.", 
        "funder": {
          "id": "https://www.grid.ac/institutes/grid.14105.31", 
          "type": "Organization"
        }, 
        "id": "sg:grant.2779972", 
        "identifier": [
          {
            "name": "dimensions_id", 
            "type": "PropertyValue", 
            "value": [
              "2779972"
            ]
          }, 
          {
            "name": "gtr_id", 
            "type": "PropertyValue", 
            "value": [
              "D31EBCA2-A303-40E7-A9CD-FD23260BBC69"
            ]
          }
        ], 
        "inLanguage": [
          "en"
        ], 
        "keywords": [
          "classical Th2 cells", 
          "Nippostrongylus brasiliensis", 
          "asthma symptoms", 
          "important source", 
          "expulsion", 
          "protective immunity", 
          "interaction", 
          "Recent studies", 
          "parasite susceptibility", 
          "inflammatory infiltrate", 
          "antibodies", 
          "cytokines", 
          "infection", 
          "mouse asthma model", 
          "innate immune cell types", 
          "allergic asthma", 
          "recent decades", 
          "environmental agents", 
          "point", 
          "response", 
          "initiation", 
          "lung", 
          "other cells", 
          "IL-25", 
          "autoimmunity", 
          "unique monoclonal antibody", 
          "IL-4", 
          "relatives", 
          "asthma model", 
          "number", 
          "dendritic cells", 
          "Interleukin-25", 
          "specific functions", 
          "messages", 
          "IL-33", 
          "new immune cells", 
          "disease susceptibility genes", 
          "progression", 
          "Bcl11b", 
          "Notch", 
          "variety", 
          "immune system", 
          "fundamental inter-dependent roles", 
          "important role", 
          "mucus", 
          "body", 
          "IL-17 family", 
          "responsiveness", 
          "ILC2", 
          "technique", 
          "protein messengers", 
          "IL-7", 
          "type-2 cytokines", 
          "mediators", 
          "genes", 
          "mouse model", 
          "interleukin", 
          "experimental model", 
          "abnormal reactions", 
          "AHR", 
          "IL-5", 
          "provocative stimuli", 
          "myelodysplasia", 
          "ROR t", 
          "asthma-like responses", 
          "innate lymphoid cells", 
          "anti-IL-25 antibody cross", 
          "administration", 
          "information", 
          "function", 
          "approach", 
          "asthma-like disease", 
          "members", 
          "MRC Technology", 
          "predominant early source", 
          "asthma", 
          "breath", 
          "immunity", 
          "key role", 
          "critical molecules", 
          "example", 
          "transcription factors ROR", 
          "therapeutic potential", 
          "ILC2 development", 
          "transgenic mouse model", 
          "induction", 
          "IL-9", 
          "action", 
          "shortness", 
          "irritation", 
          "human IL-25", 
          "technical summary", 
          "airway", 
          "addition", 
          "disorders", 
          "sufferers", 
          "coughing", 
          "mouse genome", 
          "ILC", 
          "critical role", 
          "receptors", 
          "IL-13", 
          "common lymphoid progenitors", 
          "helminth parasites", 
          "wheezing", 
          "haematopoietic disorders", 
          "molecules", 
          "signal", 
          "allergy", 
          "investigation", 
          "long-term lung inflammation", 
          "allergens", 
          "collaboration", 
          "human chromosome 5q31", 
          "type-2 response", 
          "airway hyperresponsiveness", 
          "World Health Organization", 
          "region", 
          "dust", 
          "pollen", 
          "people", 
          "cells", 
          "inflammation", 
          "reporter mice", 
          "human IL-25 receptor"
        ], 
        "name": "Investigation of immune and haematopoietic disorders", 
        "recipient": [
          {
            "id": "https://www.grid.ac/institutes/grid.42475.30", 
            "type": "Organization"
          }, 
          {
            "affiliation": {
              "id": "https://www.grid.ac/institutes/grid.42475.30", 
              "name": "MRC Laboratory of Molecular Biology", 
              "type": "Organization"
            }, 
            "familyName": "McKenzie", 
            "givenName": "Andrew", 
            "id": "sg:person.0603056221.77", 
            "type": "Person"
          }, 
          {
            "member": "sg:person.0603056221.77", 
            "roleName": "PI", 
            "type": "Role"
          }
        ], 
        "sameAs": [
          "https://app.dimensions.ai/details/grant/grant.2779972"
        ], 
        "sdDataset": "grants", 
        "sdDatePublished": "2019-03-07T11:34", 
        "sdLicense": "https://scigraph.springernature.com/explorer/license/", 
        "sdPublisher": {
          "name": "Springer Nature - SN SciGraph project", 
          "type": "Organization"
        }, 
        "sdSource": "s3://com.uberresearch.data.processor/core_data/20181219_192338/projects/base/gtr_projects_2.xml.gz", 
        "startDate": "2005-01-01T00:00:00Z", 
        "type": "MonetaryGrant", 
        "url": "http://gtr.rcuk.ac.uk/project/D31EBCA2-A303-40E7-A9CD-FD23260BBC69"
      }
    ]
     

    Download the RDF metadata as:  json-ld nt turtle xml License info

    HOW TO GET THIS DATA PROGRAMMATICALLY:

    JSON-LD is a popular format for linked data which is fully compatible with JSON.

    curl -H 'Accept: application/ld+json' 'https://scigraph.springernature.com/grant.2779972'

    N-Triples is a line-based linked data format ideal for batch operations.

    curl -H 'Accept: application/n-triples' 'https://scigraph.springernature.com/grant.2779972'

    Turtle is a human-readable linked data format.

    curl -H 'Accept: text/turtle' 'https://scigraph.springernature.com/grant.2779972'

    RDF/XML is a standard XML format for linked data.

    curl -H 'Accept: application/rdf+xml' 'https://scigraph.springernature.com/grant.2779972'


     

    This table displays all metadata directly associated to this object as RDF triples.

    168 TRIPLES      18 PREDICATES      146 URIs      138 LITERALS      5 BLANK NODES

    Subject Predicate Object
    1 sg:grant.2779972 schema:about anzsrc-for:2211
    2 schema:amount N0acf799b3e034d29aa8dcf66192c1152
    3 schema:description The World Health Organisation estimates that in the region of 300 million people worldwide now suffer from asthma. Allergic asthma is caused by an abnormal reaction to a variety of environmental agents, called allergens. This leads to long-term lung inflammation and an over-responsiveness of the airways. As the airways become narrowed and irritated, coughing, wheezing and shortness of breath occur. The body is normally protected by its immune system, but during asthma it becomes inappropriately activated by allergens such as pollen and dust. We are trying to understand how the immune system is being controlled and identify points at which we may be able to block it and thereby improve asthma symptoms. Cells of the immune system communicate by sending out protein messengers (called interleukins ) that are received by other cells and cause them to switch on specific functions – for example to start producing mucus in the lung in response to irritation. We have discovered a new immune cell (ILC2) that plays a key role in receiving and sending out messages during asthma-like disease. Recently using mouse asthma models we have shown that blocking the action of Interleukin-25 (IL-25), asthma-like responses. We are now investigating the therapeutic potential of this approach for treating asthma. Technical Summary Allergic asthma is characterised by uncontrollable airways hyperresponsiveness (AHR) induced by a variety of provocative stimuli and is associated with type-2 inflammatory infiltrates into the lungs. The number of sufferers has increased dramatically over recent decades and the World Health Organisation estimates that in the region of 300 million people worldwide suffer from this disorder. Genes residing on human chromosome 5q31-34 have been implicated in the induction and progression of several immune and haematopoietic disorders including asthma and allergy, autoimmunity, parasite susceptibility, and myelodysplasia. We combine information derived from the human and mouse genomes, with techniques to modify the mouse genome to identify and define the functions of disease susceptibility genes. Using transgenic mouse models we have characterised fundamental inter-dependent roles for the type-2 cytokines interleukin-4 (IL-4), IL-5, IL-9 and IL-13 as mediators of asthma and allergy. More recently we have focussed on characterising critical molecules that initiate the type-2 response. These include IL-25 and IL-33. IL-25 is a member of the IL-17 family of cytokines and we have demonstrated an important role for IL-25 in protective immunity to infection and uncovered a critical role for IL-25 in airways hyperresponsiveness and inflammation. We developed a unique monoclonal antibody that blocks the interaction of IL-25 with its receptor, and administration of this antibody prevents airways hyperresponsiveness in a mouse model of allergic asthma. Importantly, since the anti-IL-25 antibody cross-reacts with human IL-25, blocking its interaction with the human IL-25 receptor, we have humanised this antibody in collaboration with MRC Technology, and are continuiing to validate this molecule in asthma models. It is becoming increasingly clear that innate immune cell types, in addition to the classical Th2 cells, can produce type-2 cytokines and that they may play critical roles in the initiation of the type-2 response. Using Il13-eGFP reporter mice, we discovered type-2 innate lymphoid cells (ILC2) and demonstrated that they are the predominant early source of the IL-13 critical for inducing expulsion of the helminth parasite, Nippostrongylus brasiliensis, following infection. ILC2 also expand in experimental models of asthma, where they represent an important source of type-2 cytokines. Our recent studies have indicated that ILC2 interact with dendritic cells and Th2 cells to potentiate type-2 immunity. We have shown that these type-2 ILCs develop from common lymphoid progenitors under signals from IL-7 and IL-33 and Notch. We have gone on to show that the transcription factors ROR, a relative of ROR t, and Bcl11b play important roles in ILC2 development.
    4 schema:funder https://www.grid.ac/institutes/grid.14105.31
    5 schema:identifier N1d88d86f954440879b9b679f7eda0ade
    6 N9dc5d8698a0740f9a82d55a820ca315f
    7 schema:inLanguage en
    8 schema:keywords AHR
    9 Bcl11b
    10 IL-13
    11 IL-17 family
    12 IL-25
    13 IL-33
    14 IL-4
    15 IL-5
    16 IL-7
    17 IL-9
    18 ILC
    19 ILC2
    20 ILC2 development
    21 Interleukin-25
    22 MRC Technology
    23 Nippostrongylus brasiliensis
    24 Notch
    25 ROR t
    26 Recent studies
    27 World Health Organization
    28 abnormal reactions
    29 action
    30 addition
    31 administration
    32 airway
    33 airway hyperresponsiveness
    34 allergens
    35 allergic asthma
    36 allergy
    37 anti-IL-25 antibody cross
    38 antibodies
    39 approach
    40 asthma
    41 asthma model
    42 asthma symptoms
    43 asthma-like disease
    44 asthma-like responses
    45 autoimmunity
    46 body
    47 breath
    48 cells
    49 classical Th2 cells
    50 collaboration
    51 common lymphoid progenitors
    52 coughing
    53 critical molecules
    54 critical role
    55 cytokines
    56 dendritic cells
    57 disease susceptibility genes
    58 disorders
    59 dust
    60 environmental agents
    61 example
    62 experimental model
    63 expulsion
    64 function
    65 fundamental inter-dependent roles
    66 genes
    67 haematopoietic disorders
    68 helminth parasites
    69 human IL-25
    70 human IL-25 receptor
    71 human chromosome 5q31
    72 immune system
    73 immunity
    74 important role
    75 important source
    76 induction
    77 infection
    78 inflammation
    79 inflammatory infiltrate
    80 information
    81 initiation
    82 innate immune cell types
    83 innate lymphoid cells
    84 interaction
    85 interleukin
    86 investigation
    87 irritation
    88 key role
    89 long-term lung inflammation
    90 lung
    91 mediators
    92 members
    93 messages
    94 molecules
    95 mouse asthma model
    96 mouse genome
    97 mouse model
    98 mucus
    99 myelodysplasia
    100 new immune cells
    101 number
    102 other cells
    103 parasite susceptibility
    104 people
    105 point
    106 pollen
    107 predominant early source
    108 progression
    109 protective immunity
    110 protein messengers
    111 provocative stimuli
    112 recent decades
    113 receptors
    114 region
    115 relatives
    116 reporter mice
    117 response
    118 responsiveness
    119 shortness
    120 signal
    121 specific functions
    122 sufferers
    123 technical summary
    124 technique
    125 therapeutic potential
    126 transcription factors ROR
    127 transgenic mouse model
    128 type-2 cytokines
    129 type-2 response
    130 unique monoclonal antibody
    131 variety
    132 wheezing
    133 schema:name Investigation of immune and haematopoietic disorders
    134 schema:recipient Ned304c37823f46aeb1cba5bf2536ba61
    135 sg:person.0603056221.77
    136 https://www.grid.ac/institutes/grid.42475.30
    137 schema:sameAs https://app.dimensions.ai/details/grant/grant.2779972
    138 schema:sdDatePublished 2019-03-07T11:34
    139 schema:sdLicense https://scigraph.springernature.com/explorer/license/
    140 schema:sdPublisher N1db2eaad75334c38888607b3d89ef602
    141 schema:startDate 2005-01-01T00:00:00Z
    142 schema:url http://gtr.rcuk.ac.uk/project/D31EBCA2-A303-40E7-A9CD-FD23260BBC69
    143 sgo:license sg:explorer/license/
    144 sgo:sdDataset grants
    145 rdf:type schema:MonetaryGrant
    146 N0acf799b3e034d29aa8dcf66192c1152 schema:currency GBP
    147 schema:value 18006920
    148 rdf:type schema:MonetaryAmount
    149 N1d88d86f954440879b9b679f7eda0ade schema:name dimensions_id
    150 schema:value 2779972
    151 rdf:type schema:PropertyValue
    152 N1db2eaad75334c38888607b3d89ef602 schema:name Springer Nature - SN SciGraph project
    153 rdf:type schema:Organization
    154 N9dc5d8698a0740f9a82d55a820ca315f schema:name gtr_id
    155 schema:value D31EBCA2-A303-40E7-A9CD-FD23260BBC69
    156 rdf:type schema:PropertyValue
    157 Ned304c37823f46aeb1cba5bf2536ba61 schema:member sg:person.0603056221.77
    158 schema:roleName PI
    159 rdf:type schema:Role
    160 anzsrc-for:2211 schema:inDefinedTermSet anzsrc-for:
    161 rdf:type schema:DefinedTerm
    162 sg:person.0603056221.77 schema:affiliation https://www.grid.ac/institutes/grid.42475.30
    163 schema:familyName McKenzie
    164 schema:givenName Andrew
    165 rdf:type schema:Person
    166 https://www.grid.ac/institutes/grid.14105.31 schema:Organization
    167 https://www.grid.ac/institutes/grid.42475.30 schema:name MRC Laboratory of Molecular Biology
    168 rdf:type schema:Organization
     




    Preview window. Press ESC to close (or click here)


    ...