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Journal of Environmental Pathology, Toxicology and Oncology

Publicado 4 números por año

ISSN Imprimir: 0731-8898

ISSN En Línea: 2162-6537

The Impact Factor measures the average number of citations received in a particular year by papers published in the journal during the two preceding years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) IF: 2.4 To calculate the five year Impact Factor, citations are counted in 2017 to the previous five years and divided by the source items published in the previous five years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) 5-Year IF: 2.8 The Immediacy Index is the average number of times an article is cited in the year it is published. The journal Immediacy Index indicates how quickly articles in a journal are cited. Immediacy Index: 0.5 The Eigenfactor score, developed by Jevin West and Carl Bergstrom at the University of Washington, is a rating of the total importance of a scientific journal. Journals are rated according to the number of incoming citations, with citations from highly ranked journals weighted to make a larger contribution to the eigenfactor than those from poorly ranked journals. Eigenfactor: 0.00049 The Journal Citation Indicator (JCI) is a single measurement of the field-normalized citation impact of journals in the Web of Science Core Collection across disciplines. The key words here are that the metric is normalized and cross-disciplinary. JCI: 0.59 SJR: 0.429 SNIP: 0.507 CiteScore™:: 3.9 H-Index: 49

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p53 Binding to Target Sites Is Dynamically Regulated Before and After Ionizing Radiation-Mediated DNA Damage

Volumen 23, Edición 1, 2004, 14 pages
DOI: 10.1615/JEnvPathToxOncol.v23.i1.70
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SINOPSIS

Although radiation therapy has been an important modality for cancer treatment, the molecular mechanisms underlying the overall genomic response of mammalian cells to radiation are not well characterized. The success of radiation therapy using ionizing radiation relies upon the regulation of both the cell cycle and apoptosis, as conferred by the activation of DNA damage-responsive genes. To better understand the key players involved in this response, expression-profiling experiments were performed using custom-made cDNA microarrays. In MOLT-4 lymphoma tumor cells, the induction of target gene products following irradiation supports a major role for p53 as a transcriptional activator, but also invokes questions regarding conditional transcription regulation following irradiation. Using chromatin immunoprecipitation (ChIP), p53 binding to chromatin was examined following irradiation using primers that are specific for p53 binding sites in target genes. PCR analysis indicates dynamic target gene binding.Thus, at 8 hours following radiation treatment, the p21 and puma promoter sites were characterized by relative increases in chromatin precipitation, while the bax promoter site was not. Because the binding of p53 to these sites only changed modestly following radiation, other studies were conducted to characterize the presence of constitutive binding to putative p53 DNA binding sites in several other genes.

CITADO POR
  1. SASANO Nakashi, ENOMOTO Atsushi, HOSOI Yoshio, KATSUMURA Yosuke, MATSUMOTO Yoshihisa, SHIRAISHI Kenshiro, MIYAGAWA Kiyoshi, IGAKI Hiroshi, NAKAGAWA Keiichi, Free Radical Scavenger Edaravone Suppresses X-ray-induced Apoptosis through p53 Inhibition in MOLT-4 Cells, Journal of Radiation Research, 48, 6, 2007. Crossref

  2. Zhang Zheng-Hua, Wang Zhi-Min, Crosby Meredith E., Wang Hai-Feng, Xiang Lei-Hong, Luan Jing, Gu Chao-Ying, Zhou Jun, Niu Zhen-Min, Fang Xu, Huang Wei, Zheng Zhi-Zhong, Gene expression profiling of porokeratosis, Journal of Cutaneous Pathology, 35, 11, 2008. Crossref

  3. Wei Chia-Lin, Wu Qiang, Vega Vinsensius B., Chiu Kuo Ping, Ng Patrick, Zhang Tao, Shahab Atif, Yong How Choong, Fu YuTao, Weng Zhiping, Liu JianJun, Zhao Xiao Dong, Chew Joon-Lin, Lee Yen Ling, Kuznetsov Vladimir A., Sung Wing-Kin, Miller Lance D., Lim Bing, Liu Edison T., Yu Qiang, Ng Huck-Hui, Ruan Yijun, A Global Map of p53 Transcription-Factor Binding Sites in the Human Genome, Cell, 124, 1, 2006. Crossref

  4. Nakano Hisako, Yonekawa Hiromichi, Shinohara Kunio, Threshold Level of p53 Required for the Induction of Apoptosis in X-Irradiated MOLT-4 Cells, International Journal of Radiation Oncology*Biology*Physics, 68, 3, 2007. Crossref

  5. Bansal Nidhi, Kadamb Rama, Mittal Shilpi, Vig Leena, Sharma Raisha, Dwarakanath Bilikere S., Saluja Daman, Gartel Andrei L., Tumor Suppressor Protein p53 Recruits Human Sin3B/HDAC1 Complex for Down-Regulation of Its Target Promoters in Response to Genotoxic Stress, PLoS ONE, 6, 10, 2011. Crossref

  6. Ozyer Tansel, Alhajj Reda, A comprehensive approach for validating p53 binding site predictions, 2017 8th International Conference on Information Technology (ICIT), 2017. Crossref

  7. Bassi CL, Mello SS, Cardoso RS, Godoy PDV, Fachin AL, Junta CM, Sandrin-Garcia P, Carlotti CG, Falcão RP, Donadi EA, Passos GAS, Sakamoto-Hojo ET, Transcriptional changes in U343 MG-a glioblastoma cell line exposed to ionizing radiation, Human & Experimental Toxicology, 27, 12, 2008. Crossref

  8. Kadamb Rama, Mittal Shilpi, Bansal Nidhi, Saluja Daman, Stress-mediated Sin3B activation leads to negative regulation of subset of p53 target genes, Bioscience Reports, 35, 4, 2015. Crossref

  9. Crosby M E, Jacobberger J, Gupta D, Macklis R M, Almasan A, E2F4 regulates a stable G2 arrest response to genotoxic stress in prostate carcinoma, Oncogene, 26, 13, 2007. Crossref

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