Absence of Ground States for a Class of Translation Invariant Models of Non-relativistic QED

We consider a class of translation invariant models of non-relativistic QED with net charge. Under certain natural assumptions we prove that ground states do not exist in the Fock space

Effective dynamics for particles coupled to a quantized scalar field

We consider a system of N non-relativistic spinless quantum particles (``electrons'') interacting with a quantized scalar Bose field (whose excitations we call ``photons''). We examine the case when the velocity v of the electrons is small with respect to the one of the photons, denoted by c (v/c= epsilon << 1). We show that dressed particle states exist (particles surrounded by ``virtual photons''), which, up to terms of order (v/c)^3, follow Hamiltonian dynamics. The effective N-particle Hamiltonian contains the kinetic energies of the particles and Coulomb-like pair potentials at order (v/c)^0 and the velocity dependent Darwin interaction and a mass renormalization at order (v/c)^{2}. Beyond that order the effective dynamics are expected to be dissipative. The main mathematical tool we use is adiabatic perturbation theory. However, in the present case there is no eigenvalue which is separated by a gap from the rest of the spectrum, but its role is taken by the bottom of the absolutely continuous spectrum, which is not an eigenvalue. Nevertheless we construct approximate dressed electrons subspaces, which are adiabatically invariant for the dynamics up to order (v/c)\sqrt{\ln (v/c)^{-1}}. We also give an explicit expression for the non adiabatic transitions corresponding to emission of free photons. For the radiated energy we obtain the quantum analogue of the Larmor formula of classical electrodynamics.Comment: 67 pages, 2 figures, version accepted for publication in Communications in Mathematical Physic

Infrared problem for the Nelson model on static space-times

We consider the Nelson model with variable coefficients and investigate the problem of existence of a ground state and the removal of the ultraviolet cutoff. Nelson models with variable coefficients arise when one replaces in the usual Nelson model the flat Minkowski metric by a static metric, allowing also the boson mass to depend on position. A physical example is obtained by quantizing the Klein-Gordon equation on a static space-time coupled with a non-relativistic particle. We investigate the existence of a ground state of the Hamiltonian in the presence of the infrared problem, i.e. assuming that the boson mass tends to 0 at infinity

Rapid Internalization of the Oncogenic K+ Channel KV10.1

KV10.1 is a mammalian brain voltage-gated potassium channel whose ectopic expression outside of the brain has been proven relevant for tumor biology. Promotion of cancer cell proliferation by KV10.1 depends largely on ion flow, but some oncogenic properties remain in the absence of ion permeation. Additionally, KV10.1 surface populations are small compared to large intracellular pools. Control of protein turnover within cells is key to both cellular plasticity and homeostasis, and therefore we set out to analyze how endocytic trafficking participates in controlling KV10.1 intracellular distribution and life cycle. To follow plasma membrane KV10.1 selectively, we generated a modified channel of displaying an extracellular affinity tag for surface labeling by α-bungarotoxin. This modification only minimally affected KV10.1 electrophysiological properties. Using a combination of microscopy and biochemistry techniques, we show that KV10.1 is constitutively internalized involving at least two distinct pathways of endocytosis and mainly sorted to lysosomes. This occurs at a relatively fast rate. Simultaneously, recycling seems to contribute to maintain basal KV10.1 surface levels. Brief KV10.1 surface half-life and rapid lysosomal targeting is a relevant factor to be taken into account for potential drug delivery and targeting strategies directed against KV10.1 on tumor cells

Voltage Dependence of Proton Pumping by Bacteriorhodopsin Mutants with Altered Lifetime of the M Intermediate

The light-driven proton pump bacteriorhodopsin (BR) from Halobacterium salinarum is tightly regulated by the [H+] gradient and transmembrane potential. BR exhibits optoelectric properties, since spectral changes during the photocycle are kinetically controlled by voltage, which predestines BR for optical storage or processing devices. BR mutants with prolonged lifetime of the blue-shifted M intermediate would be advantageous, but the optoelectric properties of such mutants are still elusive. Using expression in Xenopus oocytes and two-electrode voltage-clamping, we analyzed photocurrents of BR mutants with kinetically destabilized (F171C, F219L) or stabilized (D96N, D96G) M intermediate in response to green light (to probe H+ pumping) and blue laser flashes (to probe accumulation/decay of M). These mutants have divergent M lifetimes. As for BR-WT, this strictly correlates with the voltage dependence of H+ pumping. BR-F171C and BR-F219L showed photocurrents similar to BR-WT. Yet, BR-F171C showed a weaker voltage dependence of proton pumping. For both mutants, blue laser flashes applied during and after green-light illumination showed reduced M accumulation and shorter M lifetime. In contrast, BR-D96G and BR-D96N exhibited small photocurrents, with nonlinear current-voltage curves, which increased strongly in the presence of azide. Blue laser flashes showed heavy M accumulation and prolonged M lifetime, which accounts for the strongly reduced H+ pumping rate. Hyperpolarizing potentials augmented these effects. The combination of M-stabilizing and -destabilizing mutations in BR-D96G/F171C/F219L (BR-tri) shows that disruption of the primary proton donor Asp-96 is fatal for BR as a proton pump. Mechanistically, M destabilizing mutations cannot compensate for the disruption of Asp-96. Accordingly, BR-tri and BR-D96G photocurrents were similar. However, BR-tri showed negative blue laser flash-induced currents even without actinic green light, indicating that Schiff base deprotonation in BR-tri exists in the dark, in line with previous spectroscopic investigations. Thus, M-stabilizing mutations, including the triple mutation, drastically interfere with electrochemical H+ gradient generation

Cortactin controls surface expression of the voltage-gated potassium channel Kv10.1

K(V)10.1 is a voltage-gated potassium channel aberrantly expressed in many cases of cancer, and participates in cancer initiation and tumor progression. Its action as an oncoprotein can be inhibited by a functional monoclonal antibody, indicating a role for channels located at the plasma membrane, accessible to the antibody. Cortactin is an actin-interacting protein implicated in cytoskeletal architecture and often amplified in several types of cancer. In this study, we describe a physical and functional interaction between cortactin and K(V)10.1. Binding of these two proteins occurs between the C terminus of K(V)10.1 and the proline-rich domain of cortactin, regions targeted by many post-translational modifications. This interaction is specific for K(V)10.1 and does not occur with K(V)10.2. Cortactin controls the abundance of K(V)10.1 at the plasma membrane and is required for functional expression of K(V)10.1 channels

Delivery of the Cu-transporting ATPase ATP7B to the plasma membrane in Xenopus oocytes

Cu-transporting ATPase ATP7B (Wilson disease protein) is essential for the maintenance of intracellular copper concentration. In hepatocytes, ATP7B is required for copper excretion, which is thought to occur via a transient delivery of the ATP7B- and copper-containing vesicles to the apical membrane. The currently available experimental systems do not allow analysis of ATP7B at the cell surface. Using epitope insertion, we identified an extracellular loop into which the HA-epitope can be introduced without inhibiting ATP7B activity. The HA-tagged ATP7B was expressed in Xenopus oocytes and the presence of ATP7B at the plasma membrane was demonstrated by electron microscopy, freeze-fracture experiments, and surface luminescence measurements in intact cells. Neither the deletion of the entire N-terminal copper-binding domain nor the inactivating mutation of catalytic Asp1027 affected delivery to the plasma membrane of oocytes. In contrast, surface targeting was decreased for the ATP7B variants with mutations in the ATP-binding site or the intra-membrane copper-binding site, suggesting that ligand-stabilized conformation(s) are important for ATP7B trafficking. The developed system provides significant advantages for studies that require access to both sides of ATP7B in the membrane