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Critical Reviews™ in Eukaryotic Gene Expression

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ISSN Печать: 1045-4403

ISSN Онлайн: 2162-6502

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: 1.6 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: 2.2 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: 0.3 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: 0.00058 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: 0.33 SJR: 0.345 SNIP: 0.46 CiteScore™:: 2.5 H-Index: 67

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Regulation of Apoptosis by E1A and Myc Oncoproteins

Том 10, Выпуск 3&4, 2000, 8 pages
DOI: 10.1615/CritRevEukarGeneExpr.v10.i3-4.50
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Краткое описание

E1A and c-myc are oncogenes that can deregulate the cell cycle and promote transformation under conditions where normal cell-cycle checkpoints are inactivated. In situations where cell-cycle checkpoints are intact, the E1A and c-Myc proteins potently induce apoptosis, a property that is believed to be the end result of a cellular response to uncontrolled growth-promoting signals. p53 is a key regulator of E1A and c-myc-induced apoptosis and, together with the oncoproteins, may transcriptionally activate numerous genes whose products influence, or are themselves, members of the core apoptotic machinery. The upstream signaling events and the ultimate apoptotic pathways activated by E1A and c-Myc are discussed in this review.

ЦИТИРОВАНО В
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  2. Oving Irma M., Clevers Hans C., Molecular causes of colon cancer, European Journal of Clinical Investigation, 32, 6, 2002. Crossref

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  4. LEVINE A. J., HU W., FENG Z., GIL G., Reconstructing Signal Transduction Pathways: Challenges and Opportunities, Annals of the New York Academy of Sciences, 1115, 1, 2007. Crossref

  5. Liao Yong, Yu Dihua, Hung Mien-Chie, Novel Approaches for Chemosensitization of Breast Cancer Cells: The E1A Story, in Breast Cancer Chemosensitivity, 608, 2007. Crossref

  6. Nag Alo, Datta Abhishek, Yoo Kyung, Bhattacharyya Dibyendu, Chakrabortty Amit, Wang Xinhi, Slagle Betty L., Costa Robert H., Raychaudhuri Pradip, DDB2 Induces Nuclear Accumulation of the Hepatitis B Virus X Protein Independently of Binding to DDB1, Journal of Virology, 75, 21, 2001. Crossref

  7. Fu Loning, Lee Cheng Chi, The circadian clock: pacemaker and tumour suppressor, Nature Reviews Cancer, 3, 5, 2003. Crossref

  8. Mathai Jaigi P, Germain Marc, Marcellus Richard C, Shore Gordon C, Induction and endoplasmic reticulum location of BIK/NBK in response to apoptotic signaling by E1A and p53, Oncogene, 21, 16, 2002. Crossref

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