Mechanisms regulating phosphoinositide 3-kinase signalling in insulin-sensitive tissues
Acta Physiologica Scandinavica, ISSN: 0001-6772, Vol: 183, Issue: 1, Page: 3-12
2005
- 113Citations
- 69Captures
Metric Options: Counts1 Year3 YearSelecting the 1-year or 3-year option will change the metrics count to percentiles, illustrating how an article or review compares to other articles or reviews within the selected time period in the same journal. Selecting the 1-year option compares the metrics against other articles/reviews that were also published in the same calendar year. Selecting the 3-year option compares the metrics against other articles/reviews that were also published in the same calendar year plus the two years prior.
Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations113
- Citation Indexes113
- 113
- CrossRef99
- Captures69
- Readers69
- 69
Review Description
A great deal of evidence has accumulated indicating that the activity of PI 3-kinase is necessary, and in some cases sufficient, for a wide range of insulin's actions in the cell. Most biochemical, genetic and pharmacological studies have focused on identifying potential roles for the class-Ia PI 3-kinases which are rapidly activated following insulin stimulation. However, recent evidence indicates the alpha isoform of class-II PI 3-kinase (PI3K-C2α) may also play a role as insulin causes a very rapid activation of this as well. The basic mechanisms by which insulin activates the various members of the PI 3-kinase family are increasingly well understood and these studies reveal multiple mechanisms for modulating the activity and functionality of PI 3-kinase and for down regulating the signals they generate. These include inhibitory phosphorylation events, lipid phosphatases such as PTEN and SHIP2 and inhibitor proteins of the suppressors of cytokine signalling (SOCS) family. The current review will focus on these mechanisms and how defects in these might contribute to the development of insulin resistance.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=13244252424&origin=inward; http://dx.doi.org/10.1111/j.1365-201x.2004.01382.x; http://www.ncbi.nlm.nih.gov/pubmed/15654916; https://onlinelibrary.wiley.com/doi/10.1111/j.1365-201X.2004.01382.x; http://doi.wiley.com/10.1111/j.1365-201X.2004.01382.x; https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1111%2Fj.1365-201X.2004.01382.x; https://dx.doi.org/10.1111/j.1365-201x.2004.01382.x
Wiley
Provide Feedback
Have ideas for a new metric? Would you like to see something else here?Let us know