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Critical Reviews™ in Eukaryotic Gene Expression

Publicou 6 edições por ano

ISSN Imprimir: 1045-4403

ISSN On-line: 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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Transcriptional Targets of p53 That Regulate Cellular Proliferation

Volume 17, Edição 1, 2007, pp. 73-86
DOI: 10.1615/CritRevEukarGeneExpr.v17.i1.50
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RESUMO

In response to various forms of cellular stress, including DNA damage, ribonucleotide depletion, and abnormal proliferative signals, p53 becomes activated as a transcription factor, targeting genes that induce cell-cycle arrest and apoptosis. Eliminating damaged, stressed, or abnormally proliferating cells from the replicating cell population prevents the propagation of potentially cancer-prone cells. Here we focus on the transcriptional targets of p53 that regulate the cell cycle. p53 induction of G1/S cell-cycle arrest is largely attributed to the transcriptional upregulation of p21WAF1, and more recently, to the transcriptional repression of c-MYC. The role of p53 in G2/M cell-cycle arrest in response to DNA damage is more complex, involving multiple targets that can generally be considered to impinge upon either the cell cycle (e.g., Cyclin-B, cdc2, cdc25C) or the mitotic machinery (i.e., Topoisomerase II, B99/Gtse-1, and MAP4). The ability of p53 to regulate these two types of gene targets may reflectp53-mediated early versus late events in the G2/M cell-cycle arrest response. Together the information presented illustrates the need for further studies to precisely delineate the nature of G2/M cell-cycle arrest in response to cell stress, and defines the role of p53 in what is likely an important mechanism of tumor suppression.

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