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

BCR/ABL Stimulates WRN to Promote Survival and Genomic Instability

2 Dec 2010

Abstract excerpt

BCR/ABL-transformed chronic myeloid leukemia (CML) cells accumulate numerous DNA double-strand breaks (DSB) induced by reactive oxygen species (ROS) and genotoxic agents. To repair these lesions BCR/ABL stimulate unfaithful DSB repair pathways, homologous recombination repair (HRR), nonhomologous end-joining (NHEJ), and single-strand annealing (SSA). Here, we show that BCR/ABL enhances the expression and increase...

Read the complete abstract on PubMed

Topics

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

Share to Acute Lymphoblastic Leukemia research
Share to Chronic Myeloid Leukemia Treatments
Share to DNA Repair Mechanisms

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 21123451
DOI: 10.1158/0008-5472.can-10-1066

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

BCR/ABL Stimulates WRN to Promote Survival and Genomic InstabilityPMID 21123451Read ↗

Werner Syndrome Protein Phosphorylation by Abl Tyrosine Kinase Regulates Its Activity and DistributionSemantic proximity Read ↗

Up-regulation of WRN and DNA ligase IIIα in chronic myeloid leukemia: consequences for the repair of DNA double-strand breaksSemantic proximity Read ↗

BCR/ABL modifies the kinetics and fidelity of DNA double-strand breaks repair in hematopoietic cells.Semantic proximity Read ↗

BCR/ABL, DNA damage and DNA repair: Implications for new treatment conceptsSemantic proximity Read ↗

WRN regulates pathway choice between classical and alternative non-homologous end joiningSemantic proximity Read ↗

WRN, the protein deficient in Werner syndrome, plays a critical structural role in optimizing DNA repair.Semantic proximity Read ↗

Werner Syndrome Helicase Is Required for the Survival of Cancer Cells with Microsatellite InstabilitySemantic proximity Read ↗

BCR/ABL oncogenic kinase promotes unfaithful repair of the reactive oxygen species-dependent DNA double-strand breaks.Semantic proximity Read ↗

ATR and ATM differently regulate WRN to prevent DSBs at stalled replication forks and promote replication fork recoverySemantic proximity Read ↗

BCR-ABL promotes the frequency of mutagenic single-strand annealing DNA repair.Semantic proximity Read ↗

WRN as a Novel Target of Synthetic Lethality: Current Advances and Future PerspectivesSemantic proximity Read ↗

The roles of WRN and BLM RecQ helicases in the Alternative Lengthening of Telomeres.Semantic proximity Read ↗

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