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APOBEC SIGNED

Enzymatic DNA deamination and the immunity/cancer balance

Total Cost €

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EC-Contrib. €

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Partnership

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 APOBEC project word cloud

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

double    directed    uracil    abasic    polynucleotide    excision    edits    substrate    rosa26    gene    understand    intestine    antibody    residue    preceded    produces    ubiquitously    shown    small    time    deaminate    base    loci    aid    site    reagents    sequence    intermediates    permits    breaks    dsb    enzymes    viral    clinical    science    oncogenic    mice    mammalian    introduction    translocations    tumours    transcripts    introduces    misexpression    nuclear    mrna    expressed    act    generate    dna    tagged    activated    cells    causing    locus    genome    progression    incisions    ligation    off    ends    vivo    trigger    mutations    nucleotide    hallmark    oncology    tumourigenesis    conventional    apobec3b    members    flag    acts    apobec3a    sequencing    damage    contexts    pairs    inserted    genomic    apobec3    basic    stop    trans    residues    deamination    restriction    conditional    context    apobec    endogenous    forms    host    proximal    apobec1    replication    cdna    transgenic    regulate    containing    floxed    cancer    rearrangements    family    broken    chromosomal    tissue    expression    instability    incision    nucleus    physiologically    harbour    intermediate    initiate    chromosome    repair    tumour    diversification    lymphocyte    substitutions    liver    cytosine    translocation    strand    strands    immunoglobulin   

Project "APOBEC" data sheet

The following table provides information about the project.

Coordinator
MAX DELBRUECK CENTRUM FUER MOLEKULARE MEDIZIN IN DER HELMHOLTZ-GEMEINSCHAFT (MDC) 

Organization address
address: ROBERT ROSSLE STRASSE 10
city: BERLIN
postcode: 13125
website: www.mdc-berlin.de

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 Germany [DE]
 Project website https://www.mdc-berlin.de/research-report-2016
 Total cost 159˙460 €
 EC max contribution 159˙460 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2014
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2015
 Duration (year-month-day) from 2015-04-01   to  2017-03-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    MAX DELBRUECK CENTRUM FUER MOLEKULARE MEDIZIN IN DER HELMHOLTZ-GEMEINSCHAFT (MDC) DE (BERLIN) coordinator 159˙460.00

Map

 Project objective

Genomic instability is a key hallmark of cancer. Chromosome translocations require the formation of pairs of double-strand breaks (DSB) and trans-chromosomal ligation of the broken ends. Members of the AID/APOBEC family of enzymes deaminate cytosine (C) to uracil (U) in the context of a polynucleotide substrate. Excision of the U residue from DNA produces an abasic site, leading to incision of the DNA strand containing the abasic site by the conventional base-excision repair pathway. The introduction of proximal incisions on both DNA strands can generate a DSB intermediate for chromosomal translocation. AID acts on C residues at immunoglobulin loci in activated B cells to trigger antibody gene diversification and is the only member of the AID/APOBEC family that is currently known to act physiologically on endogenous nuclear DNA. Off-target deamination by AID results in nucleotide substitutions and genomic rearrangements in B lymphocyte tumours. APOBEC1 edits mRNA transcripts in the small intestine. Liver-directed misexpression of APOBEC1 is oncogenic in transgenic mice. APOBEC3 enzymes are ubiquitously expressed and act on C residues in the cDNA viral replication intermediates as part of a host restriction pathway. APOBEC3A and APOBEC3B have been shown to be capable of causing genomic damage in mammalian cells. Access to the nucleus by APOBEC family members likely permits DNA deamination activity that introduces mutations and genomic instability during tumourigenesis. I have generated mice that harbour FLAG-tagged forms of AID, APOBEC1, APOBEC3A or APOBEC3B inserted at the ROSA26 locus, preceded by a floxed stop sequence for conditional expression. This system will be used to understand the role of cytosine deamination in tumour progression in tissue- and time-specific contexts in vivo through whole genome sequencing of tumours. The long-term goal is to initiate the development of reagents to regulate APOBEC activity in basic science and clinical oncology.

 Publications

year authors and title journal last update
List of publications.
2015 Sandrine Sander, Van Trung Chu, Tomoharu Yasuda, Andrew Franklin, Robin Graf, Dinis Pedro Calado, Shuang Li, Koshi Imami, Matthias Selbach, Michela Di Virgilio, Lars Bullinger, Klaus Rajewsky
PI3 Kinase and FOXO1 Transcription Factor Activity Differentially Control B Cells in the Germinal Center Light and Dark Zones
published pages: 1075-1086, ISSN: 1074-7613, DOI: 10.1016/j.immuni.2015.10.021
Immunity 43/6 2019-06-18
2015 Kevin L. Otipoby, Ari Waisman, Emmanuel Derudder, Lakshmi Srinivasan, Andrew Franklin, Klaus Rajewsky
The B-cell antigen receptor integrates adaptive and innate immune signals
published pages: 12145-12150, ISSN: 0027-8424, DOI: 10.1073/pnas.1516428112
Proceedings of the National Academy of Sciences 112/39 2019-06-18

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