about
RAG2's acidic hinge restricts repair-pathway choice and promotes genomic stability.RAG2 mutants alter DSB repair pathway choice in vivo and illuminate the nature of 'alternative NHEJ'.Listeria monocytogenes dampens the DNA damage responseB-cell chronic lymphocytic leukaemia: a polymorphic family unified by genomic features.A streamlined method for detecting structural variants in cancer genomes by short read paired-end sequencingNew molecular markers in resistant B-CLL.RAG2 and XLF/Cernunnos interplay reveals a novel role for the RAG complex in DNA repairArtemis and nonhomologous end joining-independent influence of DNA-dependent protein kinase catalytic subunit on chromosome stabilityRoles for NBS1 in alternative nonhomologous end-joining of V(D)J recombination intermediates.Synthetic lethality between PAXX and XLF in mammalian development.Modernizing the nonhomologous end-joining repertoire: alternative and classical NHEJ share the stage.Mutagenicity of non-homologous end joining DNA repair in a resistant subset of human chronic lymphocytic leukaemia B cells.Human chronic lymphocytic leukemia B cells can escape DNA damage-induced apoptosis through the nonhomologous end-joining DNA repair pathway.IgE receptor type I-dependent regulation of a Rab3D-associated kinase: a possible link in the calcium-dependent assembly of SNARE complexes.Specific Roles of XRCC4 Paralogs PAXX and XLF during V(D)J Recombination.Generation and CRISPR/Cas9 editing of transformed progenitor B cells as a pseudo-physiological system to study DNA repair gene function in V(D)J recombination.The RAG recombinase: Beyond breaking.Chronic exposure to sublethal doses of radiation mimetic Zeocin selects for clones deficient in homologous recombination.Shieldin complex promotes DNA end-joining and counters homologous recombination in BRCA1-null cellsChromosomal Translocation Formation Is Sufficient to Produce Fusion Circular RNAs Specific to Patient Tumor Cells[Paralogy and redundancy: maintaining genome integrity during V(D)J recombination]Breakage-Fusion-Bridge Events Trigger Complex Genome Rearrangements and Amplifications in Developmentally Arrested T Cell LymphomasCoordinated signals from the DNA repair enzymes PARP-1 and PARP-2 promotes B-cell development and functionThe immune system profoundly restricts intratumor genetic heterogeneity
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description
researcher, ORCID id # 0000-0002-9673-9525
@en
wetenschapper
@nl
name
Ludovic Deriano
@ast
Ludovic Deriano
@en
Ludovic Deriano
@es
Ludovic Deriano
@fr
Ludovic Deriano
@nl
type
label
Ludovic Deriano
@ast
Ludovic Deriano
@en
Ludovic Deriano
@es
Ludovic Deriano
@fr
Ludovic Deriano
@nl
prefLabel
Ludovic Deriano
@ast
Ludovic Deriano
@en
Ludovic Deriano
@es
Ludovic Deriano
@fr
Ludovic Deriano
@nl
P106
P1153
8786189700
P21
P31
P496
0000-0002-9673-9525