Anomalous electromagnetic coupling via entanglement at the nanoscale

This is the final version of the article. Available from IoP Publishing via the DOI in this record.Understanding unwanted mutual interactions between devices at the nanoscale is crucial for the study of the electromagnetic compatibility in nanoelectronic and nanophotonic systems. Anomalous electromagnetic coupling (crosstalk) between nanodevices may arise from the combination of electromagnetic interaction and quantum entanglement. In this paper we study in detail the crosstalk between two identical nanodevices, each consisting of a quantum emitter (atom, quantum dot, etc), capacitively coupled to a pair of nanoelectrodes. Using the generalized susceptibility concept, the overall system is modeled as a two-port within the framework of the electrical circuit theory and it is characterized by the admittance matrix. We show that the entanglement changes dramatically the physical picture of the electromagnetic crosstalk. In particular, the excitation produced in one of the ports may be redistributed in equal parts between both the ports, in spite of the rather small electromagnetic interactions. Such an anomalous crosstalk is expected to appear at optical frequencies in lateral GaAs double quantum dots. A possible experimental set up is also discussed. The classical concepts of interference in the operation of electronic devices, which have been known since the early days of radio-communications and are associated with electromagnetic compatibility, should then be reconsidered at the nanoscale.This research was supported in part by the EU Horizon 2020 project H2020-MSCA-RISE-2014-644076 CoExAN and EU FP7 projects, FP7-PEOPLE-2012-IRSES-316432 QOCaN and FP7-PEOPLE-2013-IRSES-612285 CANTOR. Discussions of the basic ideas underlying this work with Dr S Starobinets and Dr D Mogilevtsev are acknowledged

Inositol 1,3,4,5,6-pentakisphosphate 2-kinase is a distant IPK member with a singular inositide binding site for axial 2-OH recognition

Inositol phosphates (InsPs) are signaling molecules with multiple roles in cells. In particular Graphic (InsP6) is involved in mRNA export and editing or chromatin remodeling among other events. InsP6 accumulates as mixed salts (phytate) in storage tissues of plants and plays a key role in their physiology. Human diets that are exclusively grain-based provide an excess of InsP6 that, through chelation of metal ions, may have a detrimental effect on human health. Ins(1,3,4,5,6)P5 2-kinase (InsP5 2-kinase or Ipk1) catalyses the synthesis of InsP6 from InsP5 and ATP, and is the only enzyme that transfers a phosphate group to the axial 2-OH of the myo-inositide. We present the first structure for an InsP5 2-kinase in complex with both substrates and products. This enzyme presents a singular structural region for inositide binding that encompasses almost half of the protein. The key residues in substrate binding are identified, with Asp368 being responsible for recognition of the axial 2-OH. This study sheds light on the unique molecular mechanism for the synthesis of the precursor of inositol pyrophosphates

Quantum entanglement in electric circuits: From anomalous crosstalk to electromagnetic compatibility in nano-electronics

This is the author accepted manuscript. The final version is available from the publisher via the DOI in this record..We show that the electromagnetic coupling at the nanoscale may be accompanied by another coupling mechanism, related to quantum entanglement. Consequently, a combined 'electromagnetic-quantum' coupling is created, which stipulates long-distance and long-living interactions in electric circuits. Manifestation of this effect in electromagnetic compatibility (EMC) is discussed. An efficient theoretical framework for EMC analysis in nanoelectronics is developed based on the generalized theory of electric circuits. It is shown that the action of quantum entanglement is equivalent to an addition of the supplementary elements in electric circuit with the effective admittances defined as general susceptibilities that can be calculated using the Kubo-technique.This work was supported in part by EU grants FP7-PEOPLE-2009-IRSES- 247007 CACOMEL and FP7-PEOPLE-2013-IRSES- 612285 CANTOR

Novel roles for class II Phosphoinositide 3-Kinase C2 beta in signalling pathways involved in prostate cancer cell invasion

Phosphoinositide 3-kinases (PI3Ks) regulate several cellular functions such as proliferation, growth, survival and migration. The eight PI3K isoforms are grouped into three classes and the three enzymes belonging to the class II subfamily (PI3K-C2a, ß and ?) are the least investigated amongst all PI3Ks. Interest on these isoforms has been recently fuelled by the identification of specific physiological roles for class II PI3Ks and by accumulating evidence indicating their involvement in human diseases. While it is now established that these isoforms can regulate distinct cellular functions compared to other PI3Ks, there is still a limited understanding of the signalling pathways that can be specifically regulated by class II PI3Ks. Here we show that PI3K-C2ß regulates mitogen-activated protein kinase kinase (MEK1/2) and extracellular signal-regulated kinase (ERK1/2) activation in prostate cancer (PCa) cells. We further demonstrate that MEK/ERK and PI3K-C2ß are required for PCa cell invasion but not proliferation. In addition we show that PI3K-C2ß but not MEK/ERK regulates PCa cell migration as well as expression of the transcription factor Slug. These data identify novel signalling pathways specifically regulated by PI3K-C2ß and they further identify this enzyme as a key regulator of PCa cell migration and invasion