PARP-1 and Ku compete for repair of DNA double strand breaks by distinct NHEJ pathways - Wikidata - wikimedia - TriplyDB

PARP-1 and Ku compete for repair of DNA double strand breaks by distinct NHEJ pathways

PARP-1 and Ku compete for repair of DNA double strand breaks by distinct NHEJ pathways

http://www.wikidata.org/entity/Q29616041

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The Role of PARP Inhibitors in the Treatment of Gynecologic Malignancies Knock-in reporter mice demonstrate that DNA repair by non-homologous end joining declines with age DNA ligase III promotes alternative nonhomologous end-joining during chromosomal translocation formation Alternative-NHEJ is a mechanistically distinct pathway of mammalian chromosome break repair Rothmund-Thomson syndrome Ku regulates the non-homologous end joining pathway choice of DNA double-strand break repair in human somatic cells XRCC1 polymorphisms and breast cancer risk from the New York Site of the Breast Cancer Family Registry: A family-based case-control study DNA ligase III and DNA ligase IV carry out genetically distinct forms of end joining in human somatic cells The dynamics of Ku70/80 and DNA-PKcs at DSBs induced by ionizing radiation is dependent on the complexity of damage Dynamics of DNA damage response proteins at DNA breaks: a focus on protein modifications Up-regulation of WRN and DNA ligase IIIalpha in chronic myeloid leukemia: consequences for the repair of DNA double-strand breaks Telomere dysfunction and chromosome instability Two DNA-binding and nick recognition modules in human DNA ligase III Ubc13: the Lys63 ubiquitin chain building machine Targeting DNA Replication Stress for Cancer Therapy Trial watch - inhibiting PARP enzymes for anticancer therapy Role of Biomarkers in the Development of PARP Inhibitors Successes and Challenges of PARP Inhibitors in Cancer Therapy The Role of the COP9 Signalosome and Neddylation in DNA Damage Signaling and Repair Homologous Recombination Deficiency: Exploiting the Fundamental Vulnerability of Ovarian Cancer Beyond Breast and Ovarian Cancers: PARP Inhibitors for BRCA Mutation-Associated and BRCA-Like Solid Tumors Pleiotropic cellular functions of PARP1 in longevity and aging: genome maintenance meets inflammation Replication protein A prevents promiscuous annealing between short sequence homologies: Implications for genome integrity Advances in using PARP inhibitors to treat cancer DNA Damage and Pulmonary Hypertension DNA double-strand-break complexity levels and their possible contributions to the probability for error-prone processing and repair pathway choice Systems modelling of NHEJ reveals the importance of redox regulation of Ku70/80 in the dynamics of dna damage foci Femtosecond near-infrared laser microirradiation reveals a crucial role for PARP signaling on factor assemblies at DNA damage sites.The role of ADP-ribosylation in regulating DNA interstrand crosslink repair The DNA Damage Response: Making It Safe to Play with Knives Understanding specific functions of PARP-2: new lessons for cancer therapy DNA polymerase θ (POLQ), double-strand break repair, and cancer Balancing self-renewal against genome preservation in stem cells: How do they manage to have the cake and eat it too?PARP inhibitors for BRCA1/2-mutated and sporadic ovarian cancer: current practice and future directions Use of poly ADP-ribose polymerase [PARP] inhibitors in cancer cells bearing DDR defects: the rationale for their inclusion in the clinic DNA Polymerase θ: A Unique Multifunctional End-Joining Machine Microhomology-Mediated End Joining: A Back-up Survival Mechanism or Dedicated Pathway?Ubiquitylation, neddylation and the DNA damage response TRF2 interaction with Ku heterotetramerization interface gives insight into c-NHEJ prevention at human telomeres Factors determining DNA double-strand break repair pathway choice in G2 phase

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PARP-1 and Ku compete for repair of DNA double strand breaks by distinct NHEJ pathways

http://www.wikidata.org/entity/Q29616041

description

2006 nî lūn-bûn

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2006 թուականին հրատարակուած գիտական յօդուած

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2006 թվականին հրատարակված գիտական հոդված

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2006年の論文

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2006年論文

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2006年論文

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2006年論文

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2006年論文

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2006年論文

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2006年论文

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name

PARP-1 and Ku compete for repair of DNA double strand breaks by distinct NHEJ pathways

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PARP-1 and Ku compete for repair of DNA double strand breaks by distinct NHEJ pathways

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type

label

PARP-1 and Ku compete for repair of DNA double strand breaks by distinct NHEJ pathways

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PARP-1 and Ku compete for repair of DNA double strand breaks by distinct NHEJ pathways

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prefLabel

PARP-1 and Ku compete for repair of DNA double strand breaks by distinct NHEJ pathways

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PARP-1 and Ku compete for repair of DNA double strand breaks by distinct NHEJ pathways

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Nucleic Acids Research

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PARP-1 and Ku compete for repair of DNA double strand breaks by distinct NHEJ pathways

@en

P2093

Iliakis G

http://www.w3.org/2001/XMLSchema#string

Rosidi B

http://www.w3.org/2001/XMLSchema#string

Wang H

http://www.w3.org/2001/XMLSchema#string

Wang M

http://www.w3.org/2001/XMLSchema#string

Wu W

http://www.w3.org/2001/XMLSchema#string

Zhang L

http://www.w3.org/2001/XMLSchema#string

P2860

Cernunnos, a novel nonhomologous end-joining factor, is mutated in human immunodeficiency with microcephaly

XLF interacts with the XRCC4-DNA ligase IV complex to promote DNA nonhomologous end-joining

Biochemical evidence for Ku-independent backup pathways of NHEJ

The nonhomologous end-joining pathway of DNA repair is required for genomic stability and the suppression of translocations

Poly(ADP-ribose) polymerase (PARP-1) is not involved in DNA double-strand break recovery

XRCC1 is phosphorylated by DNA-dependent protein kinase in response to DNA damage

Targeting the DNA repair defect in BRCA mutant cells as a therapeutic strategy

A pathway of double-strand break rejoining dependent upon ATM, Artemis, and proteins locating to gamma-H2AX foci.

Specific killing of BRCA2-deficient tumours with inhibitors of poly(ADP-ribose) polymerase

DNA repair protein Ku80 suppresses chromosomal aberrations and malignant transformation

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6170-82

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scholarly article

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580552

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10.1093/NAR/GKL840

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21

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34

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2006-01-01T00:00:00Z

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6709409

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17088286

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1693894

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