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ProteomicsPARG is Essential for Pol-theta-Mediated DNA End-Joining by Removing Repressive Poly-ADP Ribose Marks
DNA polymerase theta (Pol-theta)-mediated end-joining (TMEJ) repairs DNA double-strand breaks and confers resistance to genotoxic agents. How Pol-theta is regulated at the molecular level to exert TMEJ remains unknown. We find that Pol-theta interacts with and is PARylated by PARP1 in vitro and in c...
ORGANISM(S): Homo Sapiens (ncbitaxon:9606) 
MSV000092839 | MassIVE
UnknownAKT-induced reactive oxygen species generate imatinib-resistant clones emerging from chronic myeloid leukemia progenitor cells.
Not available
S-EPMC4262587 | biostudies-literature
TranscriptomicsComparing gene expression in stem/progenitor cells from patients with CML in chronic, accelerated and blastic phase with normal volunteers
A comparison of global gene expression between rigorously defined stem and progenitor cells from patients with chronic myeloid leukaemia (CML) in chronic (CP), accelerated (AP) and blastic (BC) phase and similar populations isolated from normal volunteers. Cryopreserved CD34+ enriched cell populatio...
ORGANISM(S): Homo sapiens 
2013-09-06 | E-GEOD-47927 | biostudies-arrayexpress
UnknownInhibition of the mutated c-KIT kinase in AML1-ETO-positive leukemia cells restores sensitivity to PARP inhibitor.
Not available
S-EPMC6963253 | biostudies-literature
UnknownTargeting RAD51 phosphotyrosine-315 to prevent unfaithful recombination repair in BCR-ABL1 leukemia.
Chronic myeloid leukemia chronic phase (CML-CP) CD34(+) cells contain numerous DNA double-strand breaks whose unfaithful repair may contribute to chromosomal instability and disease progression to blast phase (CML-BP). These phenomena are often associated with the appearance of imatinib-resistant BC...
S-EPMC3148158 | biostudies-literature
UnknownBCR/ABL and other kinases from chronic myeloproliferative disorders stimulate single-strand annealing, an unfaithful DNA double-strand break repair.
Myeloproliferative disorders (MPD) are stem cell-derived clonal diseases arising as a consequence of acquired aberrations in c-ABL, Janus-activated kinase 2 (JAK2), and platelet-derived growth factor receptor (PDGFR) that generate oncogenic fusion tyrosine kinases (FTK), including BCR/ABL, TEL/ABL, ...
S-EPMC2531069 | biostudies-literature
UnknownBCR/ABL kinase induces self-mutagenesis via reactive oxygen species to encode imatinib resistance.
Mutations in the BCR/ABL kinase domain play a major role in resistance to imatinib mesylate (IM). We report here that BCR/ABL kinase stimulates reactive oxygen species (ROS), which causes oxidative DNA damage, resulting in mutations in the kinase domain. The majority of mutations involved A/T-->G/C ...
S-EPMC1895841 | biostudies-literature
UnknownEnhanced phosphorylation of Nbs1, a member of DNA repair/checkpoint complex Mre11-RAD50-Nbs1, can be targeted to increase the efficacy of imatinib mesylate against BCR/ABL-positive leukemia cells.
Nbs1, a member of the Mre11-RAD50-Nbs1 complex, is phosphorylated by ATM, the product of the ataxia-telangiectasia mutated gene and a member of the phosphatidylinositol 3-kinase-related family of serine-threonine kinases, in response to DNA double-strand breaks (DSBs) to regulate DNA damage checkpoi...
S-EPMC1924483 | biostudies-literature
UnknownClonal medicine targeting DNA damage response eradicates leukemia.
Not available
S-EPMC10912018 | biostudies-literature
UnknownSimultaneous Targeting of DNA Polymerase Theta and PARP1 or RAD52 Triggers Dual Synthetic Lethality in Homologous Recombination-Deficient Leukemia Cells.
DNA polymerase theta (Polθ, encoded by POLQ gene) plays an essential role in Polθ-mediated end-joining (TMEJ) of DNA double-strand breaks (DSB). Inhibition of Polθ is synthetic lethal in homologous recombination (HR)-deficient tumor cells. However, DSBs can be also repaired by PARP1 and RAD52-mediat...
S-EPMC10654933 | biostudies-literature
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