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ProMeta SIGNED

Non-histone protein acetylation targets of KAT2A in AML

Total Cost €

0

EC-Contrib. €

0

Partnership

0

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 ProMeta project word cloud

Explore the words cloud of the ProMeta project. It provides you a very rough idea of what is the project "ProMeta" about.

patients    evi1    cell    pkc412    survival    driving    post    aml1    signalling    paves    designation    clonal    deranged    kat2a    mutated    fda    function    modifiers    stages    marrow    diseases    regulates    30    proliferator    ing    free    proteins    supportive    cancer    myeloid    alpha    coactivator    acetyltransferase    flt3    investigation    administration    aml    hijacked    fusion    identity    catalyse    developmental    peroxisome    implicated    gamma    activated    transcriptional    mainstay    modifications    reprogramming    maturation    found    disease    blasts    themes    care    rare    remained    acetylation    complexes    pivotal    histone    decades    mutation    accompanying    fate    receptor    epigenetic    transplantation    essentially    food    considering    first    small    dismal    maintained    received    unchanged    pathogenesis    explore    transferase    interests    break    protein    attributable    therapy    drug    prognosis    translational    acetylates    biology    oncogenic    bone    itd    crucially    heterogeneous    residues    expansion    hat    leukaemia    chains    acetyl       gcn5    acute    dysregulation    extends    yeast    mds1   

Project "ProMeta" data sheet

The following table provides information about the project.

Coordinator
THE CHANCELLOR MASTERS AND SCHOLARSOF THE UNIVERSITY OF CAMBRIDGE 

Organization address
address: TRINITY LANE THE OLD SCHOOLS
city: CAMBRIDGE
postcode: CB2 1TN
website: www.cam.ac.uk

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country United Kingdom [UK]
 Total cost 183˙454 €
 EC max contribution 183˙454 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2017
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2018
 Duration (year-month-day) from 2018-06-01   to  2020-05-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    THE CHANCELLOR MASTERS AND SCHOLARSOF THE UNIVERSITY OF CAMBRIDGE UK (CAMBRIDGE) coordinator 183˙454.00

Map

 Project objective

The importance of an insight into how cell fate is established and maintained, extends far beyond the interests of developmental biology. It is pivotal to our understanding of how these processes can be hijacked and deranged in diseases such as cancer, or of the factors involved in reprogramming cell identity and function. Acute Myeloid Leukaemia (AML) has a dismal prognosis with less than 30% 5-year survival. Mainstay therapy has remained essentially unchanged for the past three decades, with all small advances in disease-free survival attributable to transplantation and improved supportive care. Only recently PKC412 has received Food and Drug Administration (FDA)’s break through therapy designation for the FLT3-ITD AML. This paves the way for investigation considering that FLT3-ITD as a driving oncogenic mutation has been found in ~30% of the AML patients. The pathogenesis of AML is heterogeneous, but there are common themes of epigenetic, transcriptional and signalling dysregulation that contribute to the resulting clonal expansion of blasts at different stages of maturation, and accompanying bone marrow failure. A significant number of the most commonly mutated targets in AML are histone modifiers, i.e. proteins or complexes that catalyse post-translational modifications in specific residues of the histone side chains. A less studied acetyltransferase, but crucially implicated in AML is KAT2A, the first histone acetyl-transferase (HAT) identified in yeast.GCN5 also acetylates the AML1/MDS1/EVI1 fusion protein in rare cases of AML.KAT2A regulates the activity of Peroxisome Proliferator- Activated Receptor Gamma-Coactivator-1α and B through protein acetylation. The goal of this proposal is to explore the role of KAT2A in Acute Myeloid Leukaemia (AML) through investigation of its non-histone protein acetylation activity.

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The information about "PROMETA" are provided by the European Opendata Portal: CORDIS opendata.

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