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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.

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

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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