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1. |
Investigated the mechanism of ATR up-regulation by COX-2 and tested our hypothesis that COX-2-induced extracellular signal-regulated kinase (ERK) activation mediates up-regulation of ATR by COX-2. |
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2. |
These findings show a new function for Cdc5L in the regulation of the ATR-mediated cell-cycle checkpoint in response to genotoxic agents. |
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3. |
Here, we demonstrate that ATR (AT mutated and Rad3 related) activity is essential for maintaining high chromatin levels of the Cdc6 protein, thereby delaying entry into mitosis during hydroxyurea (HU)-induced S-phase arrest of HeLa cells. |
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4. |
the restraint of ATR cascade activation may be a novel estrogen action relevant to breast cancer |
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5. |
the ATR-XPA interaction mediated by the helix-turn-helix motif of XPA plays an important role in DNA-damage responses to promote cell survival and genomic stability after UV irradiation. |
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6. |
Data provide a model of how the ATM/ATR pathway acts as a molecular switch for regulating cell fates, flipping between cell death via progress into mitosis, and over-replication via sustained G2 arrest upon DNA damage |
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7. |
we determined the methylation statuso f the promoter in putative modifier genes: BRCA1, BRCA2, ATM, ATR and P53 in Jewish BRCA1/BRCA2 mutation carriers with or without breast cancer. hypermethylation was detected only in the BRCA1 promotor |
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8. |
ATM substrates involved in cell-cycle checkpoint signalling can be minimally phosphorylated independently by ATR, while a small subset of proteins involved in chromatin remodelling are phosphorylated by DNA-PKcs in addition to ATM. |
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9. |
relevant target of caffeine is the ATR-Chk1 pathway and that inhibiting ATR or Chk1 might have promise in preventing or reversing UV damage |
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10. |
ATR mutations in endometrial cancers are associated with biologic aggressiveness as evidenced by reduced disease-free and overall survival |
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11. |
Deficiency in ATR is associatd with marked sensitivity of the cells to cisplatin in osteosarcoma. |
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12. |
Phosphorylation of FANCA on serine 1449 is a DNA damage-specific event that is downstream of ATR and is functionally important in Fanconi anemia |
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13. |
Observational study of gene-disease association and gene-environment interaction. (HuGE Navigator) |
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14. |
The Mre11/Rad50/Nbs1 (MRN) complex is recruited to viral centres only during infection with adenoviruses lacking the early region E4 and ATR signaling is activated. |
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15. |
Ataxia telangiectasia-mutated-Rad3-related DNA damage checkpoint signaling pathway triggered by hepatitis B virus infection. |
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16. |
HCLK2 functions in the same pathway as TopBP1 but that the two proteins regulate different steps in ATR activation. |
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17. |
Single-stranded DNA orchestrates an ATM-to-ATR switch at DNA breaks. |
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18. |
the NBS1/ATR/BRCA1 repair machinery affects centrosome behavior, and this might be a crucial role in the prevention of malignances. |
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19. |
BRCA1, ATR and gammaH2AX in the human may be part of a system which signals unsynapsed chromosomes at pachytene and may lead to their silencing. |
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20. |
ATR-Chk1 signalling pathway plays a major role in the regulation of death in response to DNA replication stress and that the Chk1-suppressed pathway protecting cells from replication stress is clearly distinguishable from that protecting cells from IR |
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21. |
Observational study and meta-analysis of gene-disease association. (HuGE Navigator) |
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22. |
Data show that the basic cleft of the RPA70 N-terminal OB-fold domain binds multiple checkpoint proteins, including RAD9, to promote ATR signaling. |
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23. |
Mcl-1, perhaps acting as an adaptor protein, in controlling the ATR-mediated regulation of Chk1 phosphorylation |
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24. |
These data reveal a highly novel role for ATR in the regulation of global-genomic nucleotide excision repair uniquely during S phase of the cell cycle. |
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25. |
Chk1 is activated by caspase-mediated cleavage during apoptosis and might be implicated in enhancing apoptotic reactions rather than attenuating the ATR-Chk1 pathway |
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26. |
Nbs1 has a function in ATR signalling in a manner distinct to any role at stalled replication forks. Replication-independent ATR signalling also requires the mediator proteins, 53BP1 and MDC1, providing direct evidence for their role in ATR signalling. |
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27. |
the ATR-dependent activation of the p38 MAP kinase is a major signaling pathway that induces apoptotic cell death after depletion of Cdc7 in cancer cells |
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28. |
53BP1 bystander foci were induced in an ATR-dependent manner predominantly in S-phase cells, similar to gammaH2AX foci induction |
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29. |
Chk1 is the primary signal transducer linking activation of the ATM/ATR kinases to Cdc25A destruction in response to ionizing radiation. |
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30. |
TopBP1-mediated ATR activation is required for checkpoint signaling and cellular viability |
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31. |
Results describe the control of HIPK2 stability by ubiquitin ligase Siah-1 and checkpoint kinases ATM and ATR. |
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32. |
Data show that Chk1 and the Claspin-Timeless module of replication forks not only participate in ATR signaling, but also protect stressed forks independently of ATR. |
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33. |
an important role for the DNA damage response mediated by ATR-Chk2 in p53 activation and renal cell apoptosis during cisplatin nephrotoxicity. |
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34. |
role of ATR gene alterations in HL lymphomagenesis. |
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35. |
p53 is activated by stimulation of mismatch repair in response to the misincorporation of deoxynucleotides into newly synthesized DNA, long before the lack of pyrimidine nucleoside triphosphates causes the rate of DNA synthesis to slow appreciably. |
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36. |
ectopic activation of ATR leads to a G1/S arrest in ATM-/- cells, providing the first evidence of functional complementation of ATM deficiency by ATR. |
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37. |
Interplay between ATM and ATR in the regulation of common fragile site stability. |
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38. |
Observational study of gene-disease association and gene-gene interaction. (HuGE Navigator) |
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39. |
ATR and DNA-dependent protein kinase cooperate in 2'-C-cyano-2'-deoxy-1-beta-D-arabino-pentofuranosylcytosine-induced activation of the G2 checkpoint pathway |
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40. |
NBS1 mediates ATR-dependent RPA hyperphosphorylation following replication fork stall and collapse. |
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41. |
The increase of cell membranous phosphatidylcholines containing unsaturated fatty acid residues induces phosphorylation of p53 through activation of ATR. |
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42. |
Observational study of gene-disease association. (HuGE Navigator) |
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43. |
Frequent mutations in MSI-H colon cancers were identified within the ATR damage response pathway. |
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44. |
This activation of ATR appeared to result from THIF-induced increases in intracellular oxidative stress, a depletion of cellular GSH and an increase in DNA strand breakage. |
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45. |
The ATR-mediated S phase checkpoint prevents replication in mammalian cells when licensing control is disrupted. |
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46. |
ATR/Chk1 pathway is activated at an early time point after the loss of Geminin and contributes to checkpoint arrest |
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47. |
ATR/ATM-independent checkpoint response to DNA synthesis inhibition exists in HeLa cells. |
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48. |
show that the damage sensor ATR in the presence of topoisomerase II binding protein 1 (TopBP1) mediator/adaptor protein phosphorylates the Chk1 signal-transducing kinase |
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49. |
influence the phosphorylation state of a specific protein substrate of ataxia-telangiectasia mutated (ATM)/ATM- and Rad3-related (ATR) kinases. |
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50. |
Results suggest that protein ubiquitylation is an important regulatory mechanism downstream of ATM (ataxia telangiectasia-mutated) and ATR (ATM-Rad3-related) activation for checkpoint control. |
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51. |
transcription-based stress response involving replication protein A, ATR, and p53 has evolved as a DNA damage-sensing mechanism to safeguard cells against DNA damage-induced mutagenesis |
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52. |
the Mre11-Rad50-Nbs1 complex plays critical roles both upstream and downstream of ATR to regulate the S-phase checkpoint when replication forks are stalled |
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53. |
Data suggest that the UVC-induced S checkpoint response of inhibition of replicon initiation is mediated by ATR signaling through Chk-1 and is independent of ATM, Nbs1, and Mre11. |
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54. |
N-terminal domain of the ATRIP protein contributes to the cell cycle checkpoint by regulating the intranuclear localization of ATR |
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55. |
ATR was indentified as a novel mediator of telomere-dependent senescence in response to interstrand cross-link induced by photoactivated psoralens. |
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56. |
In support of the idea that checkpoint activation and apoptosis induction are functionally linked, we show that Bax activation by Vpr was ablated when ATR or GADD45alpha was knocked down |
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57. |
ATRIP is required for ATR accumulation at intranuclear foci induced by DNA damage. |
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58. |
ATR-checkpoint kinase 1-protein phosphatase 2A regulatory circuit functions to keep Chk1 in a low-activity state during an unperturbed cell division cycle |
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59. |
there are at least two in vitro ATR-ATRIP DNA binding complexes, one which binds DNA with high affinity in an RPA-dependent manner and a second, which binds DNA with lower affinity in an RPA-independent manner |
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60. |
Thus, optimal repair of damaged replication fork lesions likely requires both ATR and ATM. BLM recruits 53BP1 to these lesions independent of its helicase activity, and optimal activation of ATM requires both p53 and BLM helicase activities. |
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61. |
ATR-dependent bystander foci induction in irradiated primary astrocytes and glioma lines is restricted to S-phase cells. |
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62. |
Data show that ultraviolet (UV) radiation-induced ATR signaling is compromised in XPA-deficient human cells during S phase, and this signaling involves UV bypass polymerase eta. |
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63. |
ATR has a role in the DNA damage-signaling pathway by a viral gene product |
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64. |
not required for HIV-1 derived lentivirus vector integration |
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65. |
activity of the ATR kinase is required for successful completion of the viral DNA integration process and/or survival of transduced cells |
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66. |
The G2/M checkpoint-mediated arrest of the cell cycle is critical for the prevention of both apoptosis and the accumulation of cells with rereplicated DNA, because the loss of ATR, BRCA1, or FANCA promotes apoptosis and suppresses the accumulation. |
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67. |
Alterations in the ATR gene result in an abnormal response to DNA double-strand break and single-strand break repair, suggesting a role for ATR gene alterations in NKTCL lymphomagenesis. |
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68. |
lack of role in cellular response to DNA strand-scission enediyne C-1027 |
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69. |
A model in which MSH2 and ATR function upstream to regulate two branches of the response pathway to DNA damage caused by MNNG. |
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70. |
Data suggest that Nijmegen breakage syndrome 1 (Nbs1) functions in both ATR- (ataxia-telangiectasia and Rad3-related protein) and ataxia telangiectasia mutated protein-dependent signalling. |
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71. |
ATR checkpoint kinase and RPA1 are required for efficient FANCD2 monoubiquitination |
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72. |
ATM and Mre11 may stimulate the ATR signaling pathway by converting DNA damage generated by ionizing radiation into structures that recruit and activate ATR |
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73. |
hSMG-1 teams with ATM and ATR to insure the overall quality of the transcriptome in human cells [review] |
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74. |
Polyglutamine-expanded proteins strongly activated ATR. |
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75. |
41 sequence variants, including 16 coding variants, 3 of were unreported, were found. 2 new alternative splice transcripts were found: 1 in intron 41 & 1 resulting from a deletion of 121 nucleotides in exon 33. |
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76. |
ATR kinase has a critical role in the response of hypoxia and reperfusion in solid tumors. |
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77. |
data suggest that RPA-coated ssDNA is the critical structure at sites of DNA damage that recruits the ATR-ATRIP complex and facilitates its recognition of substrates for phosphorylation and the initiation of checkpoint signaling |
|
78. |
the G2 checkpoint in irradiated human cells derives from an overactivation of the ATR/CHK1 pathway. |
|
79. |
ATR is activated in a variety of replication-linked DNA double-strand breaks from ionizing radiation and leads to activation of checkpoints in a checkpoint kinase (Chk)1-dependent manner. |
|
80. |
while ATR mediates the S-phase response, it is not critical for arrest of cells in G(2)/M |
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81. |
ATR has a role in regulating cyclin B1 phosphorylation by inhibiting Plk1 kinase activity |
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82. |
WRN and ATR colocalize after replication fork arrest, suggesting that WRN and the ATR kinase collaborate to prevent genome instability during the S phase. |
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83. |
The transient slow-down of DNA synthesis was abolished in cells lacking ATR, whereas CHK1-siRNA-treated cells, NBS1 or Fanconi anemia cells showed partial S-phase arrest. |
|
84. |
data reveal activated ATM and ATR exhibit selective substrate specificity in response to DNA damage |
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85. |
Effects of ATR on cell radiosensitivity are independent of NHEJ but are linked to HRR that may be affected by the deficient S and G(2) checkpoints. |
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86. |
hyperoxia activates the ATR-Chk1 pathway and phosphorylates p53 at multiple sites in an ATM-independent manner, which is different from other forms of oxidative stress such as H2O2 or UV light. |
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87. |
regulated degradation of histone mRNAs requires regulator of nonsense transcripts 1 delta helicase, a key regulator of the nonsense-mediated decay pathway, and ATR, a key regulator of the DNA damage checkpoint pathway activated during replication stress |
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88. |
The activation of ATM/ATR/CHK signaling pathways contributes to this G2 checkpoint and highlight the interrelated roles of p14ARF and the Tip60 protein in the initiation of this DNA damage-signaling cascade. |
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89. |
Herpes simplex virus type I can disrupt the usually tight colocalization of ATR and ATRIP. |
|
90. |
The role of RAS proteins in the activation of ATR and the cell cycle in thyrocytes is reported. |
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91. |
Claspin may be one of the phosphoproteins through which PP2A(Aalpha/Cbeta) affects Chk1 phosphorylation when ATR is activated by human immunodeficiency virus-1 Vpr. |
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92. |
EBNA3C can directly regulate the G2/M component of the host cell cycle machinery through ATM/ATR and Chk2, allowing for the release of the checkpoint block |
|
93. |
ATR activation is facilitated by phosphorylated H2AX stabilizing ATR at the sites of arrested replication forks |
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94. |
low-dose UV radiation activates an S-phase checkpoint requiring ATR-mediated signal transduction pathway |
|
95. |
ATR may function as an initial sensor in the DNA damage checkpoint response to UV. |
|
96. |
ATR is one of the kinases that is likely involved in phosphorylation of Chk2 in response to ionizing radiation when ATM is deficient. |
|
97. |
ATM phosphorylation at Ser1981, a characterised autophosphorylation site, is ATR-dependent and ATM-independent following replication fork stalling or ultraviolet rays treatment. |
|
98. |
a direct physical interaction between BRCA1 and ATRIP is required for the checkpoint function of ATR |
|
99. |
ATR has a role in regulating chromosomal fragile sites and DNA replication |
|
100. |
BRCA1 facilitates the ability of ATM and ATR to phosphorylate downstream substrates that directly influence cell cycle checkpoint arrest and apoptosis |
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101. |
Data show that Artemis interacts with cell cycle checkpoint proteins and is a phosphorylation target of the checkpoint kinases ATM or ATR after exposure of cells to IR or UV irradiation, respectively. |
|
102. |
PP5 plays a critical role in ATR-mediated checkpoint activation |
|
103. |
binds novel protein called ATRIP (ATR-interacting protein); ATRIP and ATR are mutually dependent partners in cell cycle checkpoint signaling pathways |
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104. |
Both 53BP1 and NFBD1 are required for recruitment of ATR to DNA damage sites, as well as for ATR-dependent phosphorylation in response to DNA damage. |
|
105. |
recruitment of ATR to sites of IR-induced DNA damage is concomitant with appearance of large tracts of single-stranded DNA (ssDNA) and that this event is dependent on ATM and components of the Mre11/Rad50/Nbs1 (MRN) protein complex |
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106. |
Data show that recombinant TopBP1 induces a large increase in the kinase activity of both Xenopus and human ATR-ATRIP. |
|
107. |
The response of promyelocytic leukemia nuclear bodies to DNA double-strand breaks is regulated by NBS1, ATM, Chk2, and ATR. |
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108. |
in response to UV-induced DNA damage, ATR rapidly phosphorylates RPA2, disrupting its association with replication centers in the S-phase and contributing to the inhibition of DNA replication |
|
109. |
ATRIP is a CDK2 substrate, and CDK2-dependent phosphorylation of S224 regulates the ability of ATR-ATRIP to promote cell cycle arrest in response to DNA damage |
|
110. |
ATR kinase plays an important role during tumor development in responding to hypoxia-induced replication arrest, and hypoxic conditions could select for the loss of key components of ATR-dependent checkpoint controls |
|
111. |
ATR and Chk1 play critical roles in the cellular response to hypoxia/reoxygenation in cancer cell lines, and inhibitors of ATR and Chk1 represent new hypoxic cell cytotoxins. |
|
112. |
ATR serves as a haploinsufficient tumor suppressor in mismatch repair-deficient cells |
|
113. |
The ATR protein Deltap53 is an essential element of the ATR-intra-S phase checkpoint. |
|
114. |
These results suggest that while TopBP1 is a general regulator of ATR, Claspin operates downstream of TopBP1 to selectively regulate the Chk1-controlled branch of the genotoxic stress response. |
|
115. |
The N-terminus of ATR is sufficient to bind ATRIP and to promote localization to sites of replication stress. |
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116. |
ATR-p53 pathway is suppressed in noncycling lymphocytes via ATR downregulation. |