scholarly article | Q13442814 |
P356 | DOI | 10.1016/J.DNAREP.2004.06.017 |
P8608 | Fatcat ID | release_cpjpvdudrzhcvnapgimevkbe2y |
P3181 | OpenCitations bibliographic resource ID | 3751892 |
P698 | PubMed publication ID | 15380105 |
P5875 | ResearchGate publication ID | 8335021 |
P50 | author | Charles Brenner | Q5075760 |
Pawel Bieganowski | Q60716651 | ||
Emma D Deeks | Q102146249 | ||
P2093 | author name string | A Malcolm R Taylor | |
Claire Breslin | |||
Keith W Caldecott | |||
Limei Ju | |||
Maria-Céu Moreira | |||
Paula M Clements | |||
Philip J Byrd | |||
P2860 | cites work | The FHA domain | Q34120305 |
Requirement for Atm in Ionizing Radiation-Induced Cell Death in the Developing Central Nervous System | Q34467644 | ||
Neonatal lethality with abnormal neurogenesis in mice deficient in DNA polymerase beta | Q34668670 | ||
DNA single-strand break repair and spinocerebellar ataxia | Q35044532 | ||
Radiosensitivity in ataxia-telangiectasia: a new explanation | Q36419108 | ||
Chk2 activation and phosphorylation-dependent oligomerization | Q39674829 | ||
Variations in ATM protein expression during normal lymphoid differentiation and among B-cell-derived neoplasias | Q41893936 | ||
A multifunctional vector system for heterologous expression of proteins in Escherichia coli. Expression of native and hexahistidyl fusion proteins, rapid purification of the fusion proteins, and removal of fusion peptide by Kex2 protease. | Q54578918 | ||
Ataxia telangiectasia: a human mutation with abnormal radiation sensitivity | Q59066708 | ||
Aprataxin, the causative protein for EAOH is a nuclear protein with a potential role as a DNA repair protein | Q24306836 | ||
Activation of the ATM kinase by ionizing radiation and phosphorylation of p53 | Q24311891 | ||
Characterization of the XRCC1-DNA ligase III complex in vitro and its absence from mutant hamster cells | Q24313256 | ||
Activity of DNA ligase IV stimulated by complex formation with XRCC4 protein in mammalian cells | Q24320116 | ||
Aprataxin, a novel protein that protects against genotoxic stress | Q24320157 | ||
Mammalian DNA double-strand break repair protein XRCC4 interacts with DNA ligase IV | Q24323238 | ||
A single ataxia telangiectasia gene with a product similar to PI-3 kinase | Q24323579 | ||
Involvement of human polynucleotide kinase in double-strand break repair by non-homologous end joining | Q24536606 | ||
An interaction between the mammalian DNA repair protein XRCC1 and DNA ligase III | Q24615666 | ||
Hint, Fhit, and GalT: function, structure, evolution, and mechanism of three branches of the histidine triad superfamily of nucleotide hydrolases and transferases | Q24649493 | ||
Megabase chromatin domains involved in DNA double-strand breaks in vivo | Q24680284 | ||
XRCC1 stimulates human polynucleotide kinase activity at damaged DNA termini and accelerates DNA single-strand break repair | Q28143501 | ||
Phenotypic variability of aprataxin gene mutations | Q28182302 | ||
Early-onset ataxia with ocular motor apraxia and hypoalbuminemia is caused by mutations in a new HIT superfamily gene | Q28190293 | ||
The gene mutated in ataxia-ocular apraxia 1 encodes the new HIT/Zn-finger protein aprataxin | Q28190324 | ||
Cerebellar ataxia with oculomotor apraxia type 1: clinical and genetic studies | Q28204594 | ||
The protein kinase CK2 facilitates repair of chromosomal DNA single-strand breaks | Q28254858 | ||
The XRCC4 gene encodes a novel protein involved in DNA double-strand break repair and V(D)J recombination | Q28272412 | ||
Defective neurogenesis resulting from DNA ligase IV deficiency requires Atm | Q28510231 | ||
Enhanced Phosphorylation of p53 by ATM in Response to DNA Damage | Q28609838 | ||
P433 | issue | 11 | |
P407 | language of work or name | English | Q1860 |
P921 | main subject | apraxia | Q498916 |
P304 | page(s) | 1493-502 | |
P577 | publication date | 2004-11-02 | |
P1433 | published in | DNA Repair | Q3894086 |
P1476 | title | The ataxia-oculomotor apraxia 1 gene product has a role distinct from ATM and interacts with the DNA strand break repair proteins XRCC1 and XRCC4 | |
P478 | volume | 3 |
Q42408435 | A nonsense mutation of human XRCC4 is associated with adult-onset progressive encephalocardiomyopathy |
Q24301368 | A novel human AP endonuclease with conserved zinc-finger-like motifs involved in DNA strand break responses |
Q36751371 | A unified view of base excision repair: lesion-dependent protein complexes regulated by post-translational modification |
Q24299831 | APLF (C2orf13) is a novel human protein involved in the cellular response to chromosomal DNA strand breaks |
Q35215475 | ATM mediates oxidative stress-induced dephosphorylation of DNA ligase IIIalpha |
Q24295253 | Actions of aprataxin in multiple DNA repair pathways |
Q24308872 | Aprataxin forms a discrete branch in the HIT (histidine triad) superfamily of proteins with both DNA/RNA binding and nucleotide hydrolase activities |
Q34937780 | Aprataxin localizes to mitochondria and preserves mitochondrial function |
Q24306648 | Aprataxin, causative gene product for EAOH/AOA1, repairs DNA single-strand breaks with damaged 3'-phosphate and 3'-phosphoglycolate ends |
Q39818706 | Aprataxin, poly-ADP ribose polymerase 1 (PARP-1) and apurinic endonuclease 1 (APE1) function together to protect the genome against oxidative damage. |
Q58451540 | Ataxia with oculomotor apraxia type1 (AOA1): novel and recurrent aprataxin mutations, coenzyme Q10 analyses, and clinical findings in Italian patients |
Q39407990 | CK2 Inhibitor CX-4945 Suppresses DNA Repair Response Triggered by DNA-Targeted Anticancer Drugs and Augments Efficacy: Mechanistic Rationale for Drug Combination Therapy |
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Q37648742 | Cellular radiosensitivity: how much better do we understand it? |
Q47149620 | Characterization of the APLF FHA-XRCC1 phosphopeptide interaction and its structural and functional implications |
Q38963019 | Chronic oxidative damage together with genome repair deficiency in the neurons is a double whammy for neurodegeneration: Is damage response signaling a potential therapeutic target? |
Q41961242 | Complementation of aprataxin deficiency by base excision repair enzymes in mitochondrial extracts. |
Q35131143 | Complementation of aprataxin deficiency by base excision repair enzymes. |
Q39021578 | Coordination of DNA single strand break repair |
Q27674855 | Crystal structures of aprataxin ortholog Hnt3 reveal the mechanism for reversal of 5'-adenylated DNA |
Q42255865 | DNA 3'-phosphatase activity is critical for rapid global rates of single-strand break repair following oxidative stress |
Q36520152 | DNA Repair Gene (XRCC1) Polymorphism (Arg399Gln) Associated with Schizophrenia in South Indian Population: A Genotypic and Molecular Dynamics Study. |
Q38230583 | DNA damage and its links to neurodegeneration |
Q37135926 | DNA double strand break repair via non-homologous end-joining |
Q39866360 | DNA end-processing enzyme polynucleotide kinase as a potential target in the treatment of cancer |
Q37368873 | DNA repair deficiency and neurological disease |
Q34183328 | DNA repair deficiency in neurodegeneration. |
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Q24651990 | Defective DNA ligation during short-patch single-strand break repair in ataxia oculomotor apraxia 1 |
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Q36914594 | Disease-associated mutations inactivate AMP-lysine hydrolase activity of Aprataxin |
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Q35873250 | EEPD1 Rescues Stressed Replication Forks and Maintains Genome Stability by Promoting End Resection and Homologous Recombination Repair |
Q40672836 | Enforced DNA repair enzymes rescue neurons from apoptosis induced by target deprivation and axotomy in mouse models of neurodegeneration |
Q24617266 | Eukaryotic DNA ligases: structural and functional insights |
Q46255285 | Evidence of high-altitude adaptation in the glyptosternoid fish, Creteuchiloglanis macropterus from the Nujiang River obtained through transcriptome analysis. |
Q34441404 | Expression of a pathogenic mutation of SOD1 sensitizes aprataxin-deficient cells and mice to oxidative stress and triggers hallmarks of premature ageing |
Q27933147 | Genetic interactions between HNT3/Aprataxin and RAD27/FEN1 suggest parallel pathways for 5' end processing during base excision repair |
Q35683678 | Genome-wide screens for sensitivity to ionizing radiation identify the fission yeast nonhomologous end joining factor Xrc4. |
Q40132066 | Human Xip1 (C2orf13) is a novel regulator of cellular responses to DNA strand breaks |
Q39233873 | Hypoxia modulates A431 cellular pathways association to tumor radioresistance and enhanced migration revealed by comprehensive proteomic and functional studies |
Q35882559 | Lack of aprataxin impairs mitochondrial functions via downregulation of the APE1/NRF1/NRF2 pathway. |
Q24651265 | Molecular mechanism of DNA deadenylation by the neurological disease protein aprataxin |
Q24672363 | Molecular pathology of ataxia telangiectasia |
Q35562885 | Molecular underpinnings of Aprataxin RNA/DNA deadenylase function and dysfunction in neurological disease |
Q33788936 | Mutational phospho-mimicry reveals a regulatory role for the XRCC4 and XLF C-terminal tails in modulating DNA bridging during classical non-homologous end joining |
Q34535722 | Neurological disorders associated with DNA strand-break processing enzymes |
Q36244602 | New autosomal recessive cerebellar ataxias with oculomotor apraxia |
Q34550224 | Non-homologous end joining: Common interaction sites and exchange of multiple factors in the DNA repair process |
Q33854272 | Non-homologous end joining: emerging themes and unanswered questions |
Q33625010 | Nonhomologous end joining: a good solution for bad ends |
Q28235590 | Nuclear ataxia-telangiectasia mutated (ATM) mediates the cellular response to DNA double strand breaks in human neuron-like cells |
Q24293612 | Nucleolar localization of aprataxin is dependent on interaction with nucleolin and on active ribosomal DNA transcription |
Q27660365 | Oxidation state of the XRCC1 N-terminal domain regulates DNA polymerase binding affinity |
Q24336328 | Phospho-dependent interactions between NBS1 and MDC1 mediate chromatin retention of the MRN complex at sites of DNA damage |
Q36562894 | Phosphorylation of SDT repeats in the MDC1 N terminus triggers retention of NBS1 at the DNA damage-modified chromatin |
Q35160570 | Phosphorylation-regulated binding of Ctp1 to Nbs1 is critical for repair of DNA double-strand breaks |
Q38604020 | Programmed DNA breaks in lymphoid cells: repair mechanisms and consequences in human disease |
Q38492153 | Protein kinase CK2 in breast cancer: the CK2β regulatory subunit takes center stage in epithelial plasticity |
Q39706795 | Radiation-induced XRCC4 association with chromatin DNA analyzed by biochemical fractionation. |
Q35002075 | Recognition and repair of chemically heterogeneous structures at DNA ends |
Q38103528 | Repair of Double-Strand Breaks by End Joining |
Q27026352 | Repair of persistent strand breaks in the mitochondrial genome |
Q36557533 | Repair of topoisomerase I-mediated DNA damage |
Q38070431 | Resolution of complex ends by Nonhomologous end joining - better to be lucky than good? |
Q24309516 | Senataxin, defective in ataxia oculomotor apraxia type 2, is involved in the defense against oxidative DNA damage |
Q29615347 | Single-strand break repair and genetic disease |
Q35932925 | Slow mitochondrial repair of 5'-AMP renders mtDNA susceptible to damage in APTX deficient cells. |
Q44563211 | Specificity of protein interactions mediated by BRCT domains of the XRCC1 DNA repair protein |
Q36589176 | Spinocerebellar ataxia with ocular motor apraxia and DNA repair. |
Q33741181 | Structural and functional characterization of the PNKP-XRCC4-LigIV DNA repair complex |
Q36333360 | Structural basis for phosphorylation-dependent signaling in the DNA-damage response |
Q33914715 | Structural insights into NHEJ: building up an integrated picture of the dynamic DSB repair super complex, one component and interaction at a time |
Q33927202 | Structure and identification of ADP-ribose recognition motifs of APLF and role in the DNA damage response |
Q27674859 | Structure of an aprataxin–DNA complex with insights into AOA1 neurodegenerative disease |
Q60932044 | The Emerging Role of Cohesin in the DNA Damage Response |
Q26768287 | The Response to Oxidative DNA Damage in Neurons: Mechanisms and Disease |
Q41890636 | The Rev1 interacting region (RIR) motif in the scaffold protein XRCC1 mediates a low-affinity interaction with polynucleotide kinase/phosphatase (PNKP) during DNA single-strand break repair. |
Q38563230 | The impact of base excision DNA repair in age-related neurodegenerative diseases |
Q36718848 | The involvement of DNA-damage and -repair defects in neurological dysfunction |
Q24302254 | The neurodegenerative disease protein aprataxin resolves abortive DNA ligation intermediates |
Q27727978 | The role of ADP-ribosylation in regulating DNA interstrand crosslink repair |
Q38498842 | The role of DNA base excision repair in brain homeostasis and disease. |
Q22122018 | The role of double-strand break repair — insights from human genetics |
Q38196597 | The spatial organization of non-homologous end joining: from bridging to end joining |
Q27666268 | The structural basis for partitioning of the XRCC1/DNA ligase III-α BRCT-mediated dimer complexes |
Q35099098 | Tidying up loose ends: the role of polynucleotide kinase/phosphatase in DNA strand break repair |
Q37830005 | To live or to die: a matter of processing damaged DNA termini in neurons |
Q29614976 | Topoisomerase I inhibitors: camptothecins and beyond |
Q38321939 | Understanding the DNA damage response in order to achieve desired gene editing outcomes in mosquitoes |
Q40372217 | Versatility in phospho-dependent molecular recognition of the XRCC1 and XRCC4 DNA-damage scaffolds by aprataxin-family FHA domains |
Q24302150 | XLF interacts with the XRCC4-DNA ligase IV complex to promote DNA nonhomologous end-joining |
Q36629377 | XRCC1 and DNA polymerase beta in cellular protection against cytotoxic DNA single-strand breaks |
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Q34329896 | XRCC4 and XLF form long helical protein filaments suitable for DNA end protection and alignment to facilitate DNA double strand break repair |
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