Special Issue "Phosphoinositide 3-kinase, a Field in Transition"
A special issue of Biomolecules (ISSN 2218-273X).
Deadline for manuscript submissions: closed (30 June 2019).
The PI3K-TOR signaling axis is a core cellular regulatory component that controls cell proliferation, motility and metabolism. Gain of function in PI3K signaling is an almost universal hallmark of cancer. Several protein members of that signaling pathway, notably class I PI3Ks, have therefore been in the crosshairs of drug developers. However, after more than 20 years of effort, no breakthrough drug has emerged.
With the expansion of basic knowledge of PI3K signaling came the insight that many of the difficulties encountered with PI3K inhibitors derive from the fact that the PI3K-TOR axis is central to the functioning of normal cells and that interference with activity of wildtype proteins in this system is bound to cause side effects. However, it has also become clear that we know far too little about specific aspects of PI3K signaling, especially about isoform-specific activities and their effects in different genetic settings and different states of cellular differentiation.
The PI3K field is in a state of transition. The experiences with small molecule inhibitors define new challenges and opportunities. In this Biomolecules Special Issue “Phosphoinositide 3-kinase, a Field in Transition”, authors will address urgent fundamental questions with the ultimate goal of driving new advances in medical applications.
Prof. Dr. Peter K. Vogt
Manuscript Submission Information
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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2000 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.
- PI3K-AKT-TOR pathway
- PI3K catalytic and regulatory subunits
- isoform-specific functions
- protein-protein interactions
- cancer-specific somatic mutations
- feedback inhibition
- PI3K and immunity
- small molecule inhibitors