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Critical Reviews™ in Eukaryotic Gene Expression

年間 6 号発行

ISSN 印刷: 1045-4403

ISSN オンライン: 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 the p53 Tumor Suppressor Pathway: The Problems and Promises of Studying Mdm2's E3 Ligase Function

巻 20, 発行 1, 2010, pp. 77-86
DOI: 10.1615/CritRevEukarGeneExpr.v20.i1.60
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要約

Mdm2 is a major negative regulator of the tumor suppressor p53 and has long been thought to inhibit p53 in two ways: by ubiquitinating p53 to signal for its degradation, and by binding to p53, masking its transactivation domain. Mdm2 is also believed to control its own levels by autoubiquitination. Despite the widespread acceptance of these hypotheses, the supporting data were drawn primarily from in vitro and ectopic expression studies, which have not always been corroborated when tested in the more physiologically relevant setting of a knock-in or knock-out mouse model. Recently, a mouse model was generated in which a single point mutation (C462A) in Mdm2’s RING domain abrogated Mdm2’s E3 activity while leaving Mdm2-p53 binding intact. This study called into question two major dogmas about Mdm2 by suggesting that when endogenously expressed, (1) Mdm2 cannot inhibit p53 sufficiently by binding without ubiquitination, and (2) Mdm2 may not be regulated by autoubiquitination. Two years later, we are still without definitive answers for why these results conflict with previous findings, but we have gained new insights from subsequent studies. Here, we discuss potential reasons for the discrepancies concerning Mdm2’s functions and how they might be resolved, taking into account new research in the field.

によって引用された
  1. Zak Krzysztof, Pecak Aleksandra, Rys Barbara, Wladyka Benedykt, Dömling Alexander, Weber Lutz, Holak Tad A, Dubin Grzegorz, Mdm2 and MdmX inhibitors for the treatment of cancer: a patent review (2011 – present), Expert Opinion on Therapeutic Patents, 23, 4, 2013. Crossref

  2. Hauck Ludger, Stanley-Hasnain Shanna, Fung Amelia, Grothe Daniela, Rao Vivek, Mak Tak W., Billia Filio, Sadoshima Junichi, Cardiac-specific ablation of the E3 ubiquitin ligase Mdm2 leads to oxidative stress, broad mitochondrial deficiency and early death, PLOS ONE, 12, 12, 2017. Crossref

  3. Dominic Abishai, Banerjee Priyanka, Hamilton Dale J., Le Nhat-Tu, Abe Jun-ichi, Time-dependent replicative senescence vs. disturbed flow-induced pre-mature aging in atherosclerosis, Redox Biology, 37, 2020. Crossref

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