The Ku-dependent non-homologous end-joining but not other repair pathway is inhibited by high linear energy transfer ionizing radiation.
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Evaluating biomarkers to model cancer risk post cosmic ray exposureVisualization of complex DNA double-strand breaks in a tumor treated with carbon ion radiotherapy.Characteristics of DNA-binding proteins determine the biological sensitivity to high-linear energy transfer radiationCancer risk at low doses of ionizing radiation: artificial neural networks inference from atomic bomb survivors.Radiation-generated short DNA fragments may perturb non-homologous end-joining and induce genomic instabilityA small peptide mimicking the key domain of MEPE/OF45 interacting with CHK1 protects human cells from radiation-induced killing.Carbon Ion Radiotherapy: A Review of Clinical Experiences and Preclinical Research, with an Emphasis on DNA Damage/RepairThe Ku-dependent non-homologous end-joining pathway contributes to low-dose radiation-stimulated cell survival.The radiosensitizing effect of Ku70/80 knockdown in MCF10A cells irradiated with X-rays and p(66)+Be(40) neutrons.DNA double-strand breaks cooperate with loss of Ink4 and Arf tumor suppressors to generate glioblastomas with frequent Met amplification.A stochastic model of DNA fragments rejoiningDistinct roles of Ape1 protein, an enzyme involved in DNA repair, in high or low linear energy transfer ionizing radiation-induced cell killing.Targeting abnormal DNA double strand break repair in cancerHeavier ions with a different linear energy transfer spectrum kill more cells due to similar interference with the Ku-dependent DNA repair pathway.Modeling damage complexity-dependent non-homologous end-joining repair pathway.Bcl2 inhibits recruitment of Mre11 complex to DNA double-strand breaks in response to high-linear energy transfer radiationThe combination of Hsp90 inhibitor 17AAG and heavy-ion irradiation provides effective tumor control in human lung cancer cells.Issues for Simulation of Galactic Cosmic Ray Exposures for Radiobiological Research at Ground-Based Accelerators.Mechanism of cluster DNA damage repair in response to high-atomic number and energy particles radiation.Linear Energy Transfer-Dependent Change in Rice Gene Expression Profile after Heavy-Ion Beam Irradiation.FANCD2 influences replication fork processes and genome stability in response to clustered DSBs.Ku-dependent non-homologous end-joining as the major pathway contributes to sublethal damage repair in mammalian cellsShort DNA Fragments Are a Hallmark of Heavy Charged-Particle Irradiation and May Underlie Their Greater Therapeutic EfficacyBiological characteristics of carbon-ion therapy.Scaffold attachment factor A (SAF-A) and Ku temporally regulate repair of radiation-induced clustered genome lesionsBringing the heavy: carbon ion therapy in the radiobiological and clinical context.Repair of DNA damage induced by accelerated heavy ions--a mini review.Efficient Rejoining of DNA Double-Strand Breaks despite Increased Cell-Killing Effectiveness following Spread-Out Bragg Peak Carbon-Ion Irradiation.Low- and High-LET Ionizing Radiation Induces Delayed Homologous Recombination that Persists for Two Weeks before Resolving.S-phase-specific radiosensitization by gemcitabine for therapeutic carbon ion exposure in vitro.Combining carbon ion irradiation and non-homologous end-joining repair inhibitor NU7026 efficiently kills cancer cells.DNA repair pathway choice at various conditions immediately post irradiation.The major DNA repair pathway after both proton and carbon-ion radiation is NHEJ, but the HR pathway is more relevant in carbon ions.Reduced contribution of thermally labile sugar lesions to DNA double strand break formation after exposure to heavy ions.RBE of α-particles from (211)At for complex DNA damage and cell survival in relation to cell cycle position.Response to multiple radiation doses of human colorectal carcinoma cells infected with recombinant adenovirus containing dominant-negative Ku70 fragment.Chromosome thripsis by DNA double strand break clusters causes enhanced cell lethality, chromosomal translocations and 53BP1-recruitment.The purine scaffold Hsp90 inhibitor PU-H71 sensitizes cancer cells to heavy ion radiation by inhibiting DNA repair by homologous recombination and non-homologous end joining.Complex DSBs: A need for resection.Different mutational function of low- and high-linear energy transfer heavy-ion irradiation demonstrated by whole-genome resequencing of Arabidopsis mutants.
P2860
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P2860
The Ku-dependent non-homologous end-joining but not other repair pathway is inhibited by high linear energy transfer ionizing radiation.
description
2008 nî lūn-bûn
@nan
2008年の論文
@ja
2008年学术文章
@wuu
2008年学术文章
@zh-cn
2008年学术文章
@zh-hans
2008年学术文章
@zh-my
2008年学术文章
@zh-sg
2008年學術文章
@yue
2008年學術文章
@zh
2008年學術文章
@zh-hant
name
The Ku-dependent non-homologou ...... y transfer ionizing radiation.
@en
type
label
The Ku-dependent non-homologou ...... y transfer ionizing radiation.
@en
prefLabel
The Ku-dependent non-homologou ...... y transfer ionizing radiation.
@en
P2093
P1433
P1476
The Ku-dependent non-homologou ...... y transfer ionizing radiation.
@en
P2093
Hongyan Wang
Piyan Zhang
Xiang Wang
P304
P356
10.1016/J.DNAREP.2008.01.010
P577
2008-03-05T00:00:00Z