Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Defective nonhomologous end joining blocks B-cell development in FLT3/ITD mice.

Blood - 17 Mar 2011

Li Li, Zhang Li, Fan Jinshui, Greenberg Kathleen, Desiderio Stephen, Rassool Feyruz V, Small Donald

Abstract excerpt

We have generated an FLT3/ITD knock-in mouse model in which mice with an FLT3/ITD mutation develop myeloproliferative disease (MPD) and a block in early B-lymphocyte development. To elucidate the role of FLT3/ITD signaling in B-cell development, we studied VDJ recombination in the pro-B cells of FLT3/ITD mice and discovered an increased frequency of DNA double strand breaks (DSBs) introduced by the VDJ...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Ku Autoantigen
Share to Antigens, Nuclear
Share to Bone Marrow Cells

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cell Lineage

Share to DNA Breaks, Double-Stranded

Share to fms-Like Tyrosine Kinase 3

Share to Poly(ADP-ribose) Polymerases

Share to Precursor Cells, B-Lymphoid

Source

Open in PubMed Open full text

Identifiers

PMID: 21228325
DOI: 10.1182/blood-2010-05-286070
PMCID: PMC3062315

Genes

FLT3
PARP1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Defective nonhomologous end joining blocks B-cell development in FLT3/ITD mice.PMID 21228325Read ↗

Cells expressing FLT3/ITD mutations exhibit elevated repair errors generated through alternative NHEJ pathways: implications for genomic instability and therapySemantic proximity Read ↗

DNA-PKcs suppresses illegitimate chromosome rearrangementsSemantic proximity Read ↗

DNA-PKcs Suppresses Illegitimate Chromosome RearrangementsSemantic proximity Read ↗

Genomic instability is a principle pathologic feature of FLT3 ITD kinase activity in acute myeloid leukemia leading to clonal evolution and disease progression.Semantic proximity Read ↗

MuLV-related endogenous retroviral elements and Flt3 participate in aberrant end-joining events that promote B-cell leukemogenesis.Semantic proximity Read ↗

Leaky severe combined immunodeficiency in mice lacking non-homologous end joining factors XLF and MRI.Semantic proximity Read ↗

Alternative end-joining catalyzes robust IgH locus deletions and translocations in the combined absence of ligase 4 and Ku70Semantic proximity Read ↗

Lymphocyte-specific compensation for XLF/cernunnos end-joining functions in V(D)J recombination.Semantic proximity Read ↗

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.Semantic proximity Read ↗

Leaky severe combined immunodeficiency and aberrant DNA rearrangements due to a hypomorphic RAG1 mutation.Semantic proximity Read ↗

Functional redundancy between repair factor XLF and damage response mediator 53BP1 in V(D)J recombination and DNA repairSemantic proximity Read ↗

DNA double strand breaks (DSB) and non-homologous end joining (NHEJ) pathways in human leukemiaSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.