| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| Richard E Mulnix, Ryan T Pitman, Allison Retzer, Ceyda Bertram, Kavin Arasi, Zachary Crees, Jennifer Girard, Srijayaprakash B Uppada, Amanda L Stone, Neelu Pur. hnRNP C1/C2 and Pur-beta proteins mediate induction of senescence by oligonucleotides homologous to the telomere overhang. OncoTargets and therapy. vol 7. 2013-12-31. PMID:24379680. |
atm (ataxia telangiectasia mutated) was once thought to be the primary driver of t-oligo-induced dna damage responses; however, recent experiments have highlighted other key proteins that may also play a significant role. |
2013-12-31 |
2023-08-12 |
Not clear |
| Peiyee Lee, Nathan T Martin, Kotoka Nakamura, Soheila Azghadi, Mandana Amiri, Uri Ben-David, Susan Perlman, Richard A Gatti, Hailiang Hu, William E Lowr. SMRT compounds abrogate cellular phenotypes of ataxia telangiectasia in neural derivatives of patient-specific hiPSCs. Nature communications. vol 4. 2013-12-30. PMID:23652012. |
ataxia telangiectasia is a devastating neurodegenerative disease caused primarily by loss of function mutations in atm, a hierarchical dna repair gene and tumour suppressor. |
2013-12-30 |
2023-08-12 |
human |
| Peiyee Lee, Nathan T Martin, Kotoka Nakamura, Soheila Azghadi, Mandana Amiri, Uri Ben-David, Susan Perlman, Richard A Gatti, Hailiang Hu, William E Lowr. SMRT compounds abrogate cellular phenotypes of ataxia telangiectasia in neural derivatives of patient-specific hiPSCs. Nature communications. vol 4. 2013-12-30. PMID:23652012. |
here we present a model of human ataxia telangiectasia using induced pluripotent stem cells, and show that small molecule read-through compounds, designed to induce read-through of mrna around premature termination codons, restore atm activity and improve the response to dna damage. |
2013-12-30 |
2023-08-12 |
human |
| Tarek Abdel-Fatah, Arvind Arora, Ipek Gorguc, Rachel Abbotts, Sarah Beebeejaun, Sarah Storr, Vivek Mohan, Claire Hawkes, Irshad Soomro, Dileep N Lobo, Simon L Parsons, Srinivasan Madhusuda. Are DNA repair factors promising biomarkers for personalized therapy in gastric cancer? Antioxidants & redox signaling. vol 18. issue 18. 2013-12-23. PMID:22894650. |
in this study, we profiled key dna repair proteins (single-strand-selective monofunctional uracil-dna glycosylase 1 [smug1], flap endonuclease 1 [fen1], x-ray repair cross-complementing gene 1 [xrcc1], and ataxia telangiectasia mutated [atm]) involved in ros-induced oxidative dna damage repair in gastric cancer and correlated to clinicopathological outcomes. |
2013-12-23 |
2023-08-12 |
Not clear |
| Sylvie Elsen, Véronique Collin-Faure, Xavier Gidrol, Claudie Lemercie. The opportunistic pathogen Pseudomonas aeruginosa activates the DNA double-strand break signaling and repair pathway in infected cells. Cellular and molecular life sciences : CMLS. vol 70. issue 22. 2013-12-16. PMID:23760206. |
chemical inhibition of several kinases known to phosphorylate h2ax demonstrated that ataxia telangiectasia mutated (atm) was the principal kinase in p. aeruginosa-induced h2ax phosphorylation. |
2013-12-16 |
2023-08-12 |
Not clear |
| Te-Chun Hsia, Chia-Wen Tsai, Shinn-Jye Liang, Wen-Shin Chang, Liang-Yi Lin, Wei-Chun Chen, Chih-Yen Tu, Chang-Hai Tsai, Da-Tian Ba. Effects of ataxia telangiectasia mutated (ATM) genotypes and smoking habits on lung cancer risk in Taiwan. Anticancer research. vol 33. issue 9. 2013-11-27. PMID:24023351. |
effects of ataxia telangiectasia mutated (atm) genotypes and smoking habits on lung cancer risk in taiwan. |
2013-11-27 |
2023-08-12 |
Not clear |
| Te-Chun Hsia, Chia-Wen Tsai, Shinn-Jye Liang, Wen-Shin Chang, Liang-Yi Lin, Wei-Chun Chen, Chih-Yen Tu, Chang-Hai Tsai, Da-Tian Ba. Effects of ataxia telangiectasia mutated (ATM) genotypes and smoking habits on lung cancer risk in Taiwan. Anticancer research. vol 33. issue 9. 2013-11-27. PMID:24023351. |
the study aimed to evaluate the association and interaction of ataxia telangiectasia mutated (atm) genetic polymorphisms with lung cancer risk in taiwan, where lung cancer is the primary cause of cancer-related death. |
2013-11-27 |
2023-08-12 |
Not clear |
| Meryem Alagoz, Shih-Chieh Chiang, Abhishek Sharma, Sherif F El-Khamis. ATM deficiency results in accumulation of DNA-topoisomerase I covalent intermediates in neural cells. PloS one. vol 8. issue 4. 2013-11-26. PMID:23626666. |
we subsequently employed this assay to reveal an increased steady state level of top1-ccs in neural cells lacking atm; the protein mutated in ataxia telangiectasia. |
2013-11-26 |
2023-08-12 |
human |
| Meryem Alagoz, Shih-Chieh Chiang, Abhishek Sharma, Sherif F El-Khamis. ATM deficiency results in accumulation of DNA-topoisomerase I covalent intermediates in neural cells. PloS one. vol 8. issue 4. 2013-11-26. PMID:23626666. |
together, these data identify a distinct role for atm during the formation/resolution of neural top1-ccs and suggest that their accumulation contributes to the neuropathology of ataxia telangiectasia. |
2013-11-26 |
2023-08-12 |
human |
| Cenk Kig, Monique Beullens, Lijs Beke, Aleyde Van Eynde, Johannes T Linders, Dirk Brehmer, Mathieu Bolle. Maternal embryonic leucine zipper kinase (MELK) reduces replication stress in glioblastoma cells. The Journal of biological chemistry. vol 288. issue 33. 2013-11-26. PMID:23836907. |
the increased expression of p21 can be explained by the consecutive activation of atm (ataxia telangiectasia mutated), chk2, and p53. |
2013-11-26 |
2023-08-12 |
mouse |
| Shuki Mizutani, Masatoshi Takag. XCIND as a genetic disease of X-irradiation hypersensitivity and cancer susceptibility. International journal of hematology. vol 97. issue 1. 2013-11-19. PMID:23266960. |
ataxia telangiectasia (a-t) is one such disease, and is caused by biallelic germline mutation of the ataxia telangiectasia mutated (atm) gene. |
2013-11-19 |
2023-08-12 |
Not clear |
| Yu Chen, Sichu Liu, Qi Shen, Xianfeng Zha, Haitao Zheng, Lijian Yang, Shaohua Chen, Xiuli Wu, Bo Li, Yangqiu L. Differential gene expression profiles of PPP2R5C-siRNA-treated malignant T cells. DNA and cell biology. vol 32. issue 10. 2013-11-18. PMID:23941244. |
in conclusion, the suppression of ppp2r5c by rna interference could effectively inhibit the proliferation of leukemic t cells, the ppp2r5c-sirna treatment altered gene expression profiles, and the differential expression of the glycogen synthase kinase 3 beta (gsk-3β), ataxia telangiectasia mutated (atm), and mdm2 p53 binding protein homolog (mdm2) genes may play an important role in the effects of ppp2r5c knockdown in jurkat t cells. |
2013-11-18 |
2023-08-12 |
Not clear |
| Dong Wook Choi, Wooju Na, Mohammad Humayun Kabir, Eunbi Yi, Seonjeong Kwon, Jeonghun Yeom, Jang-Won Ahn, Hee-Hyun Choi, Youngha Lee, Kyoung Wan Seo, Min Kyoo Shin, Se-Ho Park, Hae Yong Yoo, Kyo-Ichi Isono, Haruhiko Koseki, Seong-Tae Kim, Cheolju Lee, Yunhee Kim Kwon, Cheol Yong Cho. WIP1, a homeostatic regulator of the DNA damage response, is targeted by HIPK2 for phosphorylation and degradation. Molecular cell. vol 51. issue 3. 2013-11-13. PMID:23871434. |
wip1 (wild-type p53-induced phosphatase 1) functions as a homeostatic regulator of the ataxia telangiectasia mutated (atm)-mediated signaling pathway in response to ionizing radiation (ir). |
2013-11-13 |
2023-08-12 |
mouse |
| Anthony J Cesare, Makoto T Hayashi, Laure Crabbe, Jan Karlsede. The telomere deprotection response is functionally distinct from the genomic DNA damage response. Molecular cell. vol 51. issue 2. 2013-11-11. PMID:23850488. |
we found that, unlike genomic breaks, deprotected telomeres that are recognized as dna damage but remain in the fusion-resistant intermediate state activate differential ataxia telangiectasia mutated (atm) signaling where chk2 is not phosphorylated. |
2013-11-11 |
2023-08-12 |
human |
| F Fallone, S Britton, L Nieto, B Salles, C Mulle. ATR controls cellular adaptation to hypoxia through positive regulation of hypoxia-inducible factor 1 (HIF-1) expression. Oncogene. vol 32. issue 37. 2013-11-08. PMID:23085754. |
recent studies showed that two members of the phosphoinositide 3-kinase-related kinases (pikks) family, atm (ataxia telangiectasia mutated) and dna-pk (dna-dependent protein kinase), regulate the hypoxic-dependent accumulation of hif-1. |
2013-11-08 |
2023-08-12 |
Not clear |
| Abu Baker Qased, Heqing Yi, Nan Liang, Shumei Ma, Shixing Qiao, Xiaodong Li. MicroRNA-18a upregulates autophagy and ataxia telangiectasia mutated gene expression in HCT116 colon cancer cells. Molecular medicine reports. vol 7. issue 2. 2013-11-04. PMID:23229340. |
ataxia telangiectasia mutated (atm) has recently been shown to upregulate the process of autophagy. |
2013-11-04 |
2023-08-12 |
Not clear |
| M P Cataldi, D M McCart. Hairpin-end conformation of adeno-associated virus genome determines interactions with DNA-repair pathways. Gene therapy. vol 20. issue 6. 2013-11-01. PMID:23151519. |
dna molecules with the tr sequences constrained in the t-shaped hp conformation at one or both ends were subject to a loss of gene expression, which was partially relieved in ataxia telangiectasia mutated (atm(-/-)) cells. |
2013-11-01 |
2023-08-12 |
human |
| M A Serrano, Z Li, M Dangeti, P R Musich, S Patrick, M Roginskaya, B Cartwright, Y Zo. DNA-PK, ATM and ATR collaboratively regulate p53-RPA interaction to facilitate homologous recombination DNA repair. Oncogene. vol 32. issue 19. 2013-10-30. PMID:22797063. |
here, we report that dna-dependent protein kinase (dna-pk), the core component of nhej, partnering with dna-damage checkpoint kinases ataxia telangiectasia mutated (atm) and atm- and rad3-related (atr), regulates hr repair of dsbs. |
2013-10-30 |
2023-08-12 |
Not clear |
| R M Jones, O Mortusewicz, I Afzal, M Lorvellec, P García, T Helleday, E Peterman. Increased replication initiation and conflicts with transcription underlie Cyclin E-induced replication stress. Oncogene. vol 32. issue 32. 2013-10-23. PMID:22945645. |
it has become increasingly clear that oncogenes not only provide aberrant growth signals to cells but also cause dna damage at replication forks (replication stress), which activate the ataxia telangiectasia mutated (atm)/p53-dependent tumor barrier. |
2013-10-23 |
2023-08-12 |
Not clear |
| Yuji Okuno, Ayako Nakamura-Ishizu, Kinya Otsu, Toshio Suda, Yoshiaki Kubot. Pathological neoangiogenesis depends on oxidative stress regulation by ATM. Nature medicine. vol 18. issue 8. 2013-10-22. PMID:22797809. |
the ataxia telangiectasia mutated (atm) kinase, a master regulator of the dna damage response (ddr), acts as a barrier to cellular senescence and tumorigenesis. |
2013-10-22 |
2023-08-12 |
mouse |