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Critical Reviews™ in Eukaryotic Gene Expression

Erscheint 6 Ausgaben pro Jahr

ISSN Druckformat: 1045-4403

ISSN Online: 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

Mechanism of Neurotoxicity of Prion and Alzheimer's Disease−Related Proteins: Molecular Insights from Bioinformatically Identified ω-Conotoxin-Like Pharmacophores

Volumen 23, Ausgabe 4, 2013, pp. 355-373
DOI: 10.1615/CritRevEukaryotGeneExpr.2013007950
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ABSTRAKT

Prion diseases are fatal neurodegenerative disorders caused by altered forms of the prion protein (PrPc). It was reported that dysregulation of cellular Ca2+ homeostasis is recurrent in these diseases and that scrapie-infected cells exhibit Ca2+ perturbation via specific impairment of N-type calcium channels. However, it is not known whether such dysfunction is secondary to the broad neuronal damage accompanying prion diseases or whether it underlies pathological interactions of prions with calcium channels. In this research, we examined this latter possibility by searching for channel binding signatures in PrPc through structural comparison with known N-type channel blockers. To this aim, a computational method devised by us to recognize similar distributions of basic residues in protein structures enabled us to find that the bioactive groups representing the pharmacophores of ω-conotoxins GVIA and MVIIA can be overlaid onto similar residues within the PrPc globular domain. This finding, together with the knowledge that Ca2+ homeostasis disruption is common to other neurodegenerative disorders, led us to search for and identify an ω-conotoxin-like pharmacophore also in the Alzheimer's Aβ(1-42) peptide. These results point to the potential ability of prions and Aβ(1-42) to bind calcium channels as the elusive neurotoxic mechanism common to seemingly unrelated fatal neuropathies.

REFERENZIERT VON
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  2. Zattoni Marco, Garrovo Chiara, Xerxa Elena, Spigolon Giada, Fisone Gilberto, Kristensson Krister, Legname Giuseppe, NMDA Receptor and L-Type Calcium Channel Modulate Prion Formation, Cellular and Molecular Neurobiology, 41, 1, 2021. Crossref

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