Ataxia telangiectasia mutated (ATM) is essential for DNA-PKcs phosphorylations at the Thr-2609 cluster upon DNA double strand break.
about
Hyperactivation of DNA-PK by double-strand break mimicking molecules disorganizes DNA damage responsePhosphorylation: the molecular switch of double-strand break repairRegulation of DNA-dependent protein kinase by protein kinase CK2 in human glioblastoma cellsThe dynamics of Ku70/80 and DNA-PKcs at DSBs induced by ionizing radiation is dependent on the complexity of damageEssential role for DNA-PKcs in DNA double-strand break repair and apoptosis in ATM-deficient lymphocytesAtaxia telangiectasia mutated activation by transcription- and topoisomerase I-induced DNA double-strand breaksDNA damage response and prostate cancer: defects, regulation and therapeutic implicationsDNA-PK: a dynamic enzyme in a versatile DSB repair pathwayTyrosyl-DNA phosphodiesterase and the repair of 3'-phosphoglycolate-terminated DNA double-strand breaks.The DNA-dependent protein kinase: A multifunctional protein kinase with roles in DNA double strand break repair and mitosisTNKS1BP1 functions in DNA double-strand break repair though facilitating DNA-PKcs autophosphorylation dependent on PARP-1MRNIP/C5orf45 Interacts with the MRN Complex and Contributes to the DNA Damage ResponseDNA-PKcs-PIDDosome: a nuclear caspase-2-activating complex with role in G2/M checkpoint maintenanceRole of DNA-dependent protein kinase catalytic subunit in cancer development and treatmentTargeting DNA-PKcs and ATM with miR-101 sensitizes tumors to radiationEstablishment of a γ-H2AX foci-based assay to determine biological dose of radon to red bone marrow in ratsATM limits incorrect end utilization during non-homologous end joining of multiple chromosome breaksIdentification of the DNA repair defects in a case of Dubowitz syndromeFunctional intersection of ATM and DNA-dependent protein kinase catalytic subunit in coding end joining during V(D)J recombinationPP6 regulatory subunit R1 is bidentate anchor for targeting protein phosphatase-6 to DNA-dependent protein kinaseImproved ATM kinase inhibitor KU-60019 radiosensitizes glioma cells, compromises insulin, AKT and ERK prosurvival signaling, and inhibits migration and invasionDNA double-strand breaks induced by cavitational mechanical effects of ultrasound in cancer cell lines.Autophosphorylation of DNA-PKCS regulates its dynamics at DNA double-strand breaks.Increased cancer risk of augmentation cystoplasty: possible role for hyperosmolal microenvironment on DNA damage recognitionRadiation microbeams as spatial and temporal probes of subcellular and tissue response.Nonhomologous end joining: a good solution for bad endsA method for systematic mapping of protein lysine methylation identifies functions for HP1β in DNA damage response.The Ku-dependent non-homologous end-joining pathway contributes to low-dose radiation-stimulated cell survival.Non-homologous end joining: emerging themes and unanswered questions.DNA-PKcs deficiency leads to persistence of oxidatively induced clustered DNA lesions in human tumor cells.Genome-wide reinforcement of cohesin binding at pre-existing cohesin sites in response to ionizing radiation in human cells.miR-18a impairs DNA damage response through downregulation of ataxia telangiectasia mutated (ATM) kinase.More forks on the road to replication stress recoveryProtein kinase CK2 localizes to sites of DNA double-strand break regulating the cellular response to DNA damageAkt: a double-edged sword in cell proliferation and genome stability.Selenium compounds activate ATM-dependent DNA damage response via the mismatch repair protein hMLH1 in colorectal cancer cells.TRIM28 regulates RNA polymerase II promoter-proximal pausing and pause release.BRCA1 modulates the autophosphorylation status of DNA-PKcs in S phase of the cell cycle.Ataxia telangiectasia mutated (Atm) and DNA-PKcs kinases have overlapping activities during chromosomal signal joint formation.Non-homologous end joining: Common interaction sites and exchange of multiple factors in the DNA repair process.
P2860
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P2860
Ataxia telangiectasia mutated (ATM) is essential for DNA-PKcs phosphorylations at the Thr-2609 cluster upon DNA double strand break.
description
2006 nî lūn-bûn
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2006年の論文
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2006年学术文章
@wuu
2006年学术文章
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2006年学术文章
@zh-cn
2006年学术文章
@zh-hans
2006年学术文章
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2006年学术文章
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2006年學術文章
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name
Ataxia telangiectasia mutated ...... upon DNA double strand break.
@en
type
label
Ataxia telangiectasia mutated ...... upon DNA double strand break.
@en
prefLabel
Ataxia telangiectasia mutated ...... upon DNA double strand break.
@en
P2093
P2860
P356
P1476
Ataxia telangiectasia mutated ...... upon DNA double strand break.
@en
P2093
Andrea Krempler
Benjamin P C Chen
David J Chen
Hirohiko Yajima
Junya Kobayashi
Markus Löbrich
Naoya Uematsu
Yaniv Lerenthal
Yosef Shiloh
P2860
P304
P356
10.1074/JBC.M611605200
P407
P577
2006-12-21T00:00:00Z