RESUMO
A spin-photon interface should operate with both coherent photons and a coherent spin to enable cluster-state generation and entanglement distribution. In high-quality devices, self-assembled GaAs quantum dots are near-perfect emitters of on-demand coherent photons. However, the spin rapidly decoheres via the magnetic noise arising from the host nuclei. Here, we address this drawback by implementing an all-optical nuclear-spin cooling scheme on a GaAs quantum dot. The electron-spin coherence time increases 156-fold from T_{2}^{*}=3.9 ns to 0.608 µs. The cooling scheme depends on a non-collinear term in the hyperfine interaction. The results show that such a term is present even though the strain is low and no external stress is applied. Our work highlights the potential of optically active GaAs quantum dots as fast, highly coherent spin-photon interfaces.
RESUMO
Restoration of the p53 tumor suppressor for personalised cancer therapy is a promising treatment strategy. However, several high-affinity MDM2 inhibitors have shown substantial side effects in clinical trials. Thus, elucidation of the molecular mechanisms of action of p53 reactivating molecules with alternative functional principle is of the utmost importance. Here, we report a discovery of a novel allosteric mechanism of p53 reactivation through targeting the p53 N-terminus which promotes inhibition of both p53/MDM2 (murine double minute 2) and p53/MDM4 interactions. Using biochemical assays and molecular docking, we identified the binding site of two p53 reactivating molecules, RITA (reactivation of p53 and induction of tumor cell apoptosis) and protoporphyrin IX (PpIX). Ion mobility-mass spectrometry revealed that the binding of RITA to serine 33 and serine 37 is responsible for inducing the allosteric shift in p53, which shields the MDM2 binding residues of p53 and prevents its interactions with MDM2 and MDM4. Our results point to an alternative mechanism of blocking p53 interaction with MDM2 and MDM4 and may pave the way for the development of novel allosteric inhibitors of p53/MDM2 and p53/MDM4 interactions.
RESUMO
Photonic quantum technology provides a viable route to quantum communication1,2, quantum simulation3 and quantum information processing4. Recent progress has seen the realization of boson sampling using 20 single photons3 and quantum key distribution over hundreds of kilometres2. Scaling the complexity requires architectures containing multiple photon sources, photon counters and a large number of indistinguishable single photons. Semiconductor quantum dots are bright and fast sources of coherent single photons5-9. For applications, a roadblock is the poor quantum coherence on interfering single photons created by independent quantum dots10,11. Here we demonstrate two-photon interference with near-unity visibility (93.0 ± 0.8)% using photons from two completely separate GaAs quantum dots. The experiment retains all the emission into the zero phonon line-only the weak phonon sideband is rejected; temporal post-selection is not employed. By exploiting quantum interference, we demonstrate a photonic controlled-not circuit and an entanglement with fidelity of (85.0 ± 1.0)% between photons of different origins. The two-photon interference visibility is high enough that the entanglement fidelity is well above the classical threshold. The high mutual coherence of the photons stems from high-quality materials, diode structure and relatively large quantum dot size. Our results establish a platform-GaAs quantum dots-for creating coherent single photons in a scalable way.
RESUMO
In a radiative Auger process, optical decay leaves other carriers in excited states, resulting in weak red-shifted satellite peaks in the emission spectrum. The appearance of radiative Auger in the emission directly leads to the question if the process can be inverted: simultaneous photon absorption and electronic demotion. However, excitation of the radiative Auger transition has not been shown, neither on atoms nor on solid-state quantum emitters. Here, we demonstrate the optical driving of the radiative Auger transition, linking few-body Coulomb interactions and quantum optics. We perform our experiments on a trion in a semiconductor quantum dot, where the radiative Auger and the fundamental transition form a Λ-system. On driving both transitions simultaneously, we observe a reduction of the fluorescence signal by up to 70%. Our results suggest the possibility of turning resonance fluorescence on and off using radiative Auger as well as THz spectroscopy with optics close to the visible regime.
RESUMO
In this submission, we discuss the growth of charge-controllable GaAs quantum dots embedded in an n-i-p diode structure, from the perspective of a molecular beam epitaxy grower. The QDs show no blinking and narrow linewidths. We show that the parameters used led to a bimodal growth mode of QDs resulting from low arsenic surface coverage. We identify one of the modes as that showing good properties found in previous work. As the morphology of the fabricated QDs does not hint at outstanding properties, we attribute the good performance of this sample to the low impurity levels in the matrix material and the ability of n- and p-doped contact regions to stabilize the charge state. We present the challenges met in characterizing the sample with ensemble photoluminescence spectroscopy caused by the photonic structure used. We show two straightforward methods to overcome this hurdle and gain insight into QD emission properties.
RESUMO
Quantum dots are both excellent single-photon sources and hosts for single spins. This combination enables the deterministic generation of Raman-photons-bandwidth-matched to an atomic quantum-memory-and the generation of photon cluster states, a resource in quantum communication and measurement-based quantum computing. GaAs quantum dots in AlGaAs can be matched in frequency to a rubidium-based photon memory, and have potentially improved electron spin coherence compared to the widely used InGaAs quantum dots. However, their charge stability and optical linewidths are typically much worse than for their InGaAs counterparts. Here, we embed GaAs quantum dots into an n-i-p-diode specially designed for low-temperature operation. We demonstrate ultra-low noise behaviour: charge control via Coulomb blockade, close-to lifetime-limited linewidths, and no blinking. We observe high-fidelity optical electron-spin initialisation and long electron-spin lifetimes for these quantum dots. Our work establishes a materials platform for low-noise quantum photonics close to the red part of the spectrum.
RESUMO
In a multi-electron atom, an excited electron can decay by emitting a photon. Typically, the leftover electrons are in their ground state. In a radiative Auger process, the leftover electrons are in an excited state and a redshifted photon is created1-4. In a semiconductor quantum dot, radiative Auger is predicted for charged excitons5. Here we report the observation of radiative Auger on trions in single quantum dots. For a trion, a photon is created on electron-hole recombination, leaving behind a single electron. The radiative Auger process promotes this additional (Auger) electron to a higher shell of the quantum dot. We show that the radiative Auger effect is a powerful probe of this single electron: the energy separations between the resonance fluorescence and the radiative Auger emission directly measure the single-particle splittings of the electronic states in the quantum dot with high precision. In semiconductors, these single-particle splittings are otherwise hard to access by optical means as particles are excited typically in pairs, as excitons. After the radiative Auger emission, the Auger carrier relaxes back to the lowest shell. Going beyond the original theoretical proposals, we show how applying quantum optics techniques to the radiative Auger photons gives access to the single-electron dynamics, notably relaxation and tunnelling. This is also hard to access by optical means: even for quasi-resonant p-shell excitation, electron relaxation takes place in the presence of a hole, complicating the relaxation dynamics. The radiative Auger effect can be exploited in other semiconductor nanostructures and quantum emitters in the solid state to determine the energy levels and the dynamics of a single carrier.
RESUMO
Escape of tumor cells from cell-intrinsic barrier mediated by tumor suppressors and cell-extrinsic barrier mediated by the immune system is crucial for tumorigenesis. Growing evidence suggests that reactivation of tumor suppressor function or restoration of anticancer immunity is promising strategy for anticancer therapy due to their high potential to combat cancer. p53, a key tumor suppressor, represses tumorigenesis by eliciting growth arrest, apoptosis or senescence in cancer cells. Here, we unravel that, apart from these cell-autonomous effects, p53 activates the innate immune response against cancer cells. Our results show that pharmacological reactivation of p53 can stimulate the expression of ULPB2, a ligand for NK cell activating receptor NKG2D in human tumor cells of different origin, which enhance the susceptibility of tumor cells to NK cell-mediated killing. The molecular mechanism controlling ULPB2 expression by p53 is neither ATM/ATR- nor caspase-dependent. Using several approaches, we identified p53 as a direct transcriptional regulator of ULBP2 and found a p53 response element within ULBP2 gene, which confers the p53 regulation. Furthermore, we demonstrated that demethylation of p53-binding region within ULBP2 gene was required for p53-dependent induction of ULPB2, which can be achieved via repression of DNA methyltransferases (DNMTs) by p53. This molecular evidence for the direct control of immunosurveillance by p53 links tumor suppressor activation to innate immune stimuli and provides a possibility to integrate cell-extrinsic and -intrinsic defenses against tumorigenesis by pharmacological activation of p53, which may increase the probability to achieve a durable therapeutic success.
Assuntos
Imunidade Inata/imunologia , Peptídeos e Proteínas de Sinalização Intercelular/metabolismo , Neoplasias/imunologia , Proteína Supressora de Tumor p53/metabolismo , Linhagem Celular Tumoral , DNA (Citosina-5-)-Metiltransferases/metabolismo , Metilação de DNA , Furanos/farmacologia , Proteínas Ligadas por GPI/metabolismo , Humanos , Células Matadoras Naturais/metabolismo , Células Matadoras Naturais/fisiologia , Subfamília K de Receptores Semelhantes a Lectina de Células NK/antagonistas & inibidores , Subfamília K de Receptores Semelhantes a Lectina de Células NK/metabolismo , Regulação para CimaRESUMO
Disseminating malignant melanoma is a lethal disease highly resistant to radio- and chemotherapy. Therefore, the development of new treatment strategies is strongly needed. Tumor suppressor p53-mediated apoptosis is essential for the response to radio- and chemotherapy. Although p53 is not frequently mutated in melanoma, it is inactivated by integrin αv-mediated signaling, as we previously demonstrated 1, which may account, at least partially, for increased apoptosis resistance of malignant melanoma. In this study we addressed the question whether functional restoration of p53 by APR-246 (PRIMA-1Met), which can reactivate mutant p53 and induce massive apoptosis in cancer cells, is able to restore the function of inactive p53 in melanoma. Using a three-dimensional collagen gel (3D-collagen) to culture melanoma cells carrying wild-type p53, we found that APR-246 treatment resulted in activation of p53, leading to increased expression of p53 pro-apoptotic targets Apaf1 and PUMA and activation of caspase- 9 and -3. Moreover, APR-246 triggered melanoma cell apoptosis that was mediated by p53 and caspase 9. Importantly, APR-246 treatment also suppressed human melanoma xenograft tumors in vivo in a p53-dependent manner. Thus, wild-type p53 reactivation may provide a novel approach for malignant melanoma treatment, with APR-246 as a candidate drug for such a development.