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Critical Reviews™ in Immunology

Publicado 6 números por año

ISSN Imprimir: 1040-8401

ISSN En Línea: 2162-6472

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: 1.3 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: 2.6 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: 0.00079 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: 0.24 SJR: 0.429 SNIP: 0.287 CiteScore™:: 2.7 H-Index: 81

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The Role of Protein Kinase A and A-Kinase Anchoring Proteins in Modulating T-Cell Activation: Progress and Future Directions

Volumen 26, Edición 2, 2006, pp. 113-132
DOI: 10.1615/CritRevImmunol.v26.i2.20
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Robynn V. Schillace
Veterans Affairs Medical Center, Department of Neuroscience, Oregon Health & Science University, Portland, OR 97239
Daniel W. Carr
Department of Medicine, Oregon Health & Science University, Portland, OR 97239

SINOPSIS

Protein kinase A (PKA) is a broad-specificity serine/threonine protein kinase whose spatial and temporal regulation is maintained through interactions with A-kinase anchoring proteins (AKAPs). Subcellular localization of AKAPs through unique targeting domains provides a mechanism by which PKA can respond to localized microdomains of cyclic AMP (cAMP) and phosphorylate nearby substrates.1 For nearly 40 years, cAMP has been known to be a potent modulator of the immune system. cAMP levels are regulated by G-protein−coupled receptors, adenylyl cyclases (AC), and phosphodiesterases (PDEs). This review discusses recent progress made in the discovery of PKA substrates in T lymphocytes and in the identification of AKAPs in T lymphocytes. Because PKA is activated by cAMP, generation and maintenance of cAMP in T cells is also discussed. These findings are framed in the context of understanding the complexity of cAMP and, thus, PKA signaling and are intended to provide the reader with an overview of current literature, as well as an awareness of questions and concerns to consider.

CITADO POR

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