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Critical Reviews™ in Eukaryotic Gene Expression

Publication de 6  numéros par an

ISSN Imprimer: 1045-4403

ISSN En ligne: 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

Indexed in

AKT as Locus of Cancer Positive Loops Conversion and Chemotherapy

Volume 25, Numéro 3, 2015, pp. 199-202
DOI: 10.1615/CritRevEukaryotGeneExpr.2015013838
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RÉSUMÉ

A cancer positive-feedback loops conversion is the phenomenon and principal mechanism for AKT locus chemotherapy. Such chemotherapy is the approach to target cancer robustness and complexity through the AKT signaling locus. The hypoxic cancer microenvironment generates a powerful signaling interactome with positive-feedback loops that generates cancer robustness through the AKT locus. This complexity and robustness can be successfully halted in leukemia, lymphoma, myeloma, plasmocytoma, sarcoma, and carcinoma by converting cancer positive-feedback loops into negative-feedback loops, achieved through the AKT dephosphorylation by redox balancing change. The hyperphosphorylated AKT locus is down-regulated completely to AKT dephosphorylation by redox balancing change, causing conversion of positive-feedback loops and the disappearance of malignant robustness as a direct effect of AKT locus chemotherapy.

CITÉ PAR
  1. Radisavljevic Ziv, AKT as Locus of Cancer Unknown Primary Site, Journal of Cellular Biochemistry, 117, 5, 2016. Crossref

  2. Radisavljevic Ziv, AKT as Locus of Hydrogen Bond Network in Cancer, Journal of Cellular Biochemistry, 119, 1, 2018. Crossref

  3. Geng Hong-Wei, Yin Feng-Yi, Zhang Zhi-Fa, Gong Xu, Yang Yun, Butyrate Suppresses Glucose Metabolism of Colorectal Cancer Cells via GPR109a-AKT Signaling Pathway and Enhances Chemotherapy, Frontiers in Molecular Biosciences, 8, 2021. Crossref

  4. Radisavljevic Ziv, Lysosome activates AKT inducing cancer and metastasis, Journal of Cellular Biochemistry, 120, 8, 2019. Crossref

  5. Radisavljevic Ziv, Muon disrupts AKT hydrogen bond network in cancer, Journal of Cellular Physiology, 234, 6, 2019. Crossref

  6. Shi Naiming, Shan Ben, Gu Biao, Song Yaqi, Chu Hongjun, Qian Long, Circular RNA circ‐PRKCI functions as a competitive endogenous RNA to regulate AKT3 expression by sponging miR‐3680‐3p in esophageal squamous cell carcinoma, Journal of Cellular Biochemistry, 120, 6, 2019. Crossref

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