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Proton-assisted growth of ultra-flat graphene films 期刊论文
NATURE, 2020, 577 (7789) : 204-+
作者:  Yuan, Guowen;  Lin, Dongjing;  Wang, Yong;  Huang, Xianlei;  Chen, Wang;  Xie, Xuedong;  Zong, Junyu;  Yuan, Qian-Qian;  Zheng, Hang;  Wang, Di;  Xu, Jie;  Li, Shao-Chun;  Zhang, Yi;  Sun, Jian;  Xi, Xiaoxiang;  Gao, Libo
收藏  |  浏览/下载:11/0  |  提交时间:2020/07/03

Graphene films grown by chemical vapour deposition have unusual physical and chemical properties that offer promise for applications such as flexible electronics and high-frequency transistors(1-10). However, wrinkles invariably form during growth because of the strong coupling to the substrate, and these limit the large-scale homogeneity of the film(1-4,11,12). Here we develop a proton-assisted method of chemical vapour deposition to grow ultra-flat graphene films that are wrinkle-free. Our method of proton penetration(13-17) and recombination to form hydrogen can also reduce the wrinkles formed during traditional chemical vapour deposition of graphene. Some of the wrinkles disappear entirely, owing to the decoupling of van der Waals interactions and possibly an increase in distance from the growth surface. The electronic band structure of the as-grown graphene films shows a V-shaped Dirac cone and a linear dispersion relation within the atomic plane or across an atomic step, confirming the decoupling from the substrate. The ultra-flat nature of the graphene films ensures that their surfaces are easy to clean after a wet transfer process. A robust quantum Hall effect appears even at room temperature in a device with a linewidth of 100 micrometres. Graphene films grown by proton-assisted chemical vapour deposition should largely retain their intrinsic performance, and our method should be easily generalizable to other nanomaterials for strain and doping engineering.


  
Inverted-V Electron Acceleration Events Concurring With Localized Auroral Observations at Mars by MAVEN 期刊论文
GEOPHYSICAL RESEARCH LETTERS, 2020, 47 (9)
作者:  Xu, Shaosui;  Mitchell, David L.;  McFadden, James P.;  Fillingim, Matthew O.;  Andersson, Laila;  Brain, David A.;  Weber, Tristan;  Schneider, Nicholas M.;  Jain, Sonal;  Fowler, Christopher M.;  Lillis, Robert;  Mazelle, Christian;  Espley, Jared
收藏  |  浏览/下载:13/0  |  提交时间:2020/07/02
inverted-V electron  aurora  Mars  MAVEN  field-aligned potential  magnetic reconnection  
A dominant autoinflammatory disease caused by non-cleavable variants of RIPK1 期刊论文
NATURE, 2020, 577 (7788) : 109-+
作者:  Tao, Panfeng;  Sun, Jinqiao;  Wu, Zheming;  Wang, Shihao;  Wang, Jun;  Li, Wanjin;  Pan, Heling;  Bai, Renkui;  Zhang, Jiahui;  Wang, Ying;  Lee, Pui Y.;  Ying, Wenjing;  Zhou, Qinhua;  Hou, Jia;  Wang, Wenjie;  Sun, Bijun;  Yang, Mi;  Liu, Danru;  Fang, Ran;  Han, Huan;  Yang, Zhaohui;  Huang, Xin;  Li, Haibo;  Deuitch, Natalie;  Zhang, Yuan;  Dissanayake, Dilan;  Haude, Katrina;  McWalter, Kirsty;  Roadhouse, Chelsea;  MacKenzie, Jennifer J.;  Laxer, Ronald M.;  Aksentijevich, Ivona;  Yu, Xiaomin;  Wang, Xiaochuan;  Yuan, Junying;  Zhou, Qing
收藏  |  浏览/下载:29/0  |  提交时间:2020/07/03

Activation of RIPK1 controls TNF-mediated apoptosis, necroptosis and inflammatory pathways(1). Cleavage of human and mouse RIPK1 after residues D324 and D325, respectively, by caspase-8 separates the RIPK1 kinase domain from the intermediate and death domains. The D325A mutation in mouse RIPK1 leads to embryonic lethality during mouse development(2,3). However, the functional importance of blocking caspase-8-mediated cleavage of RIPK1 on RIPK1 activation in humans is unknown. Here we identify two families with variants in RIPK1 (D324V and D324H) that lead to distinct symptoms of recurrent fevers and lymphadenopathy in an autosomaldominant manner. Impaired cleavage of RIPK1 D324 variants by caspase-8 sensitized patients'  peripheral blood mononuclear cells to RIPK1 activation, apoptosis and necroptosis induced by TNF. The patients showed strong RIPK1-dependent activation of inflammatory signalling pathways and overproduction of inflammatory cytokines and chemokines compared with unaffected controls. Furthermore, we show that expression of the RIPK1 mutants D325V or D325H in mouse embryonic fibroblasts confers not only increased sensitivity to RIPK1 activation-mediated apoptosis and necroptosis, but also induction of pro-inflammatory cytokines such as IL-6 and TNF. By contrast, patient-derived fibroblasts showed reduced expression of RIPK1 and downregulated production of reactive oxygen species, resulting in resistance to necroptosis and ferroptosis. Together, these data suggest that human non-cleavable RIPK1 variants promote activation of RIPK1, and lead to an autoinflammatory disease characterized by hypersensitivity to apoptosis and necroptosis and increased inflammatory response in peripheral blood mononuclear cells, as well as a compensatory mechanism to protect against several pro-death stimuli in fibroblasts.


  
Engineering covalently bonded 2D layered materials by self-intercalation 期刊论文
NATURE, 2020, 581 (7807) : 171-+
作者:  Shang, Jian;  Ye, Gang;  Shi, Ke;  Wan, Yushun;  Luo, Chuming;  Aihara, Hideki;  Geng, Qibin;  Auerbach, Ashley;  Li, Fang
收藏  |  浏览/下载:11/0  |  提交时间:2020/07/03

Two-dimensional (2D) materials(1-5) offer a unique platform from which to explore the physics of topology and many-body phenomena. New properties can be generated by filling the van der Waals gap of 2D materials with intercalants(6,7)  however, post-growth intercalation has usually been limited to alkali metals(8-10). Here we show that the self-intercalation of native atoms(11,12) into bilayer transition metal dichalcogenides during growth generates a class of ultrathin, covalently bonded materials, which we name ic-2D. The stoichiometry of these materials is defined by periodic occupancy patterns of the octahedral vacancy sites in the van der Waals gap, and their properties can be tuned by varying the coverage and the spatial arrangement of the filled sites(7,13). By performing growth under high metal chemical potential(14,15) we can access a range of tantalum-intercalated TaS(Se)(y), including 25% Ta-intercalated Ta9S16, 33.3% Ta-intercalated Ta7S12, 50% Ta-intercalated Ta10S16, 66.7% Ta-intercalated Ta8Se12 (which forms a Kagome lattice) and 100% Ta-intercalated Ta9Se12. Ferromagnetic order was detected in some of these intercalated phases. We also demonstrate that self-intercalated V11S16, In11Se16 and FexTey can be grown under metal-rich conditions. Our work establishes self-intercalation as an approach through which to grow a new class of 2D materials with stoichiometry- or composition-dependent properties.


  
Electromechanical coupling in the hyperpolarization-activated K+ channel KAT1 期刊论文
NATURE, 2020, 583 (7814) : 145-+
作者:  Jin, Zhenming;  Du, Xiaoyu;  Xu, Yechun;  Deng, Yongqiang;  Liu, Meiqin;  Zhao, Yao;  Zhang, Bing;  Li, Xiaofeng;  Zhang, Leike;  Peng, Chao;  Duan, Yinkai;  Yu, Jing;  Wang, Lin;  Yang, Kailin;  Liu, Fengjiang;  Jiang, Rendi;  Yang, Xinglou;  You, Tian;  Liu, Xiaoce
收藏  |  浏览/下载:28/0  |  提交时间:2020/07/03

Voltage-gated potassium (K-v) channels coordinate electrical signalling and control cell volume by gating in response to membrane depolarization or hyperpolarization. However, although voltage-sensing domains transduce transmembrane electric field changes by a common mechanism involving the outward or inward translocation of gating charges(1-3), the general determinants of channel gating polarity remain poorly understood(4). Here we suggest a molecular mechanism for electromechanical coupling and gating polarity in non-domain-swapped K-v channels on the basis of the cryo-electron microscopy structure of KAT1, the hyperpolarization-activated K-v channel from Arabidopsis thaliana. KAT1 displays a depolarized voltage sensor, which interacts with a closed pore domain directly via two interfaces and indirectly via an intercalated phospholipid. Functional evaluation of KAT1 structure-guided mutants at the sensor-pore interfaces suggests a mechanism in which direct interaction between the sensor and the C-linker hairpin in the adjacent pore subunit is the primary determinant of gating polarity. We suggest that an inward motion of the S4 sensor helix of approximately 5-7 angstrom can underlie a direct-coupling mechanism, driving a conformational reorientation of the C-linker and ultimately opening the activation gate formed by the S6 intracellular bundle. This direct-coupling mechanism contrasts with allosteric mechanisms proposed for hyperpolarization-activated cyclic nucleotide-gated channels(5), and may represent an unexpected link between depolarization- and hyperpolarization-activated channels.


The cryo-electron microscopy structure of the hyperpolarization-activated K+ channel KAT1 points to a direct-coupling mechanism between S4 movement and the reorientation of the C-linker.


  
A lower X-gate in TASK channels traps inhibitors within the vestibule 期刊论文
NATURE, 2020
作者:  Chen, Tao;  Nomura, Kinya;  Wang, Xiaolin;  Sohrabi, Reza;  Xu, Jin;  Yao, Lingya;  Paasch, Bradley C.;  Ma, Li;  Kremer, James;  Cheng, Yuti;  Zhang, Li;  Wang, Nian;  Wang, Ertao;  Xin, Xiu-Fang;  He, Sheng Yang
收藏  |  浏览/下载:41/0  |  提交时间:2020/07/03

TWIK-related acid-sensitive potassium (TASK) channels-members of the two pore domain potassium (K-2P) channel family-are found in neurons(1), cardiomyocytes(2-4) and vascular smooth muscle cells(5), where they are involved in the regulation of heart rate(6), pulmonary artery tone(5,7), sleep/wake cycles(8) and responses to volatile anaesthetics(8-11). K-2P channels regulate the resting membrane potential, providing background K+ currents controlled by numerous physiological stimuli(12-15). Unlike other K-2P channels, TASK channels are able to bind inhibitors with high affinity, exceptional selectivity and very slow compound washout rates. As such, these channels are attractive drug targets, and TASK-1 inhibitors are currently in clinical trials for obstructive sleep apnoea and atrial fibrillation(16). In general, potassium channels have an intramembrane vestibule with a selectivity filter situated above and a gate with four parallel helices located below  however, the K-2P channels studied so far all lack a lower gate. Here we present the X-ray crystal structure of TASK-1, and show that it contains a lower gate-which we designate as an '  X-gate'  -created by interaction of the two crossed C-terminal M4 transmembrane helices at the vestibule entrance. This structure is formed by six residues ((VLRFMT248)-V-243) that are essential for responses to volatile anaesthetics(10), neurotransmitters(13) and G-protein-coupled receptors(13). Mutations within the X-gate and the surrounding regions markedly affect both the channel-open probability and the activation of the channel by anaesthetics. Structures of TASK-1 bound to two high-affinity inhibitors show that both compounds bind below the selectivity filter and are trapped in the vestibule by the X-gate, which explains their exceptionally low washout rates. The presence of the X-gate in TASK channels explains many aspects of their physiological and pharmacological behaviour, which will be beneficial for the future development and optimization of TASK modulators for the treatment of heart, lung and sleep disorders.


The X-ray crystal structure of the potassium channel TASK-1 reveals the presence of an X-gate, which traps small-molecule inhibitors in the intramembrane vestibule and explains their low washout rates from the channel.


  
Two-dimensional halide perovskite lateral epitaxial heterostructures 期刊论文
NATURE, 2020, 580 (7805) : 614-+
作者:  Cabrita, Rita;  Lauss, Martin;  Sanna, Adriana;  Donia, Marco;  Larsen, Mathilde;  Mitra, Shamik;  Johansson, Iva;  Phung, Bengt;  Harbst, Katja;  Vallon-Christersson, Johan;  van Schoiack, Alison;  Lovgren, Kristina;  Warren, Sarah;  Jirstrom, Karin;  Olsson, Hakan;  Pietras, Kristian;  Ingvar, Christian;  Isaksson, Karolin
收藏  |  浏览/下载:28/0  |  提交时间:2020/07/03

Epitaxial heterostructures based on oxide perovskites and III-V, II-VI and transition metal dichalcogenide semiconductors form the foundation of modern electronics and optoelectronics(1-7). Halide perovskites-an emerging family of tunable semiconductors with desirable properties-are attractive for applications such as solution-processed solar cells, light-emitting diodes, detectors and lasers(8-15). Their inherently soft crystal lattice allows greater tolerance to lattice mismatch, making them promising for heterostructure formation and semiconductor integration(16,17). Atomically sharp epitaxial interfaces are necessary to improve performance and for device miniaturization. However, epitaxial growth of atomically sharp heterostructures of halide perovskites has not yet been achieved, owing to their high intrinsic ion mobility, which leads to interdiffusion and large junction widths(18-21), and owing to their poor chemical stability, which leads to decomposition of prior layers during the fabrication of subsequent layers. Therefore, understanding the origins of this instability and identifying effective approaches to suppress ion diffusion are of great importance(22-26). Here we report an effective strategy to substantially inhibit in-plane ion diffusion in two-dimensional halide perovskites by incorporating rigid pi-conjugated organic ligands. We demonstrate highly stable and tunable lateral epitaxial heterostructures, multiheterostructures and superlattices. Near-atomically sharp interfaces and epitaxial growth are revealed by low-dose aberration-corrected high-resolution transmission electron microscopy. Molecular dynamics simulations confirm the reduced heterostructure disorder and larger vacancy formation energies of the two-dimensional perovskites in the presence of conjugated ligands. These findings provide insights into the immobilization and stabilization of halide perovskite semiconductors and demonstrate a materials platform for complex and molecularly thin superlattices, devices and integrated circuits.


An epitaxial growth strategy that improves the stability of two-dimensional halide perovskites by inhibiting ion diffusion in their heterostructures using rigid pi-conjugated ligands is demonstrated, and shows near-atomically sharp interfaces.


  
Direct-bandgap emission from hexagonal Ge and SiGe alloys 期刊论文
NATURE, 2020, 580 (7802) : 205-+
作者:  Meiners, Thorsten;  Frolov, Timofey;  Rudd, Robert E.;  Dehm, Gerhard;  Liebscher, Christian H.
收藏  |  浏览/下载:28/0  |  提交时间:2020/07/03

Silicon crystallized in the usual cubic (diamond) lattice structure has dominated the electronics industry for more than half a century. However, cubic silicon (Si), germanium (Ge) and SiGe alloys are all indirect-bandgap semiconductors that cannot emit light efficiently. The goal(1) of achieving efficient light emission from group-IV materials in silicon technology has been elusive for decades(2-6). Here we demonstrate efficient light emission from direct-bandgap hexagonal Ge and SiGe alloys. We measure a sub-nanosecond, temperature-insensitive radiative recombination lifetime and observe an emission yield similar to that of direct-bandgap group-III-V semiconductors. Moreover, we demonstrate that, by controlling the composition of the hexagonal SiGe alloy, the emission wavelength can be continuously tuned over a broad range, while preserving the direct bandgap. Our experimental findings are in excellent quantitative agreement with ab initio theory. Hexagonal SiGe embodies an ideal material system in which to combine electronic and optoelectronic functionalities on a single chip, opening the way towards integrated device concepts and information-processing technologies.


A hexagonal (rather than cubic) alloy of silicon and germanium that has a direct (rather than indirect) bandgap emits light efficiently across a range of wavelengths, enabling electronic and optoelectronic functionalities to be combined on a single chip.


  
gamma delta T cells and adipocyte IL-17RC control fat innervation and thermogenesis 期刊论文
NATURE, 2020, 578 (7796) : 610-+
作者:  Staus, Dean P.;  Hu, Hongli;  Robertson, Michael J.;  Kleinhenz, Alissa L. W.;  Wingler, Laura M.;  Capel, William D.;  Latorraca, Naomi R.;  Lefkowitz, Robert J.;  Skiniotis, Georgios
收藏  |  浏览/下载:50/0  |  提交时间:2020/07/03

V gamma 6(+) V delta 1(+) gamma delta T cells control tolerance to cold by activating adipocyte IL-17RC and promoting sympathetic innervation of thermogenic adipose tissue in mice.


The sympathetic nervous system innervates peripheral organs to regulate their function and maintain homeostasis, whereas target cells also produce neurotrophic factors to promote sympathetic innervation(1,2). The molecular basis of this bi-directional communication remains to be fully determined. Here we use thermogenic adipose tissue from mice as a model system to show that T cells, specifically gamma delta T cells, have a crucial role in promoting sympathetic innervation, at least in part by driving the expression of TGF beta 1 in parenchymal cells via the IL-17 receptor C (IL-17RC). Ablation of IL-17RC specifically in adipose tissue reduces expression of TGF beta 1 in adipocytes, impairs local sympathetic innervation and causes obesity and other metabolic phenotypes that are consistent with defective thermogenesis  innervation can be fully rescued by restoring TGF beta 1 expression. Ablating gamma delta tau cells and the IL-17RC signalling pathway also impairs sympathetic innervation in other tissues such as salivary glands. These findings demonstrate coordination between T cells and parenchymal cells to regulate sympathetic innervation.


  
Mechanism of adrenergic Ca(V)1.2 stimulation revealed by proximity proteomics 期刊论文
NATURE, 2020, 577 (7792) : 695-+
作者:  Peng, Guangdun;  Suo, Shengbao;  Cui, Guizhong;  Yu, Fang;  Wang, Ran;  Chen, Jun;  Chen, Shirui;  Liu, Zhiwen;  Chen, Guoyu;  Qian, Yun;  Tam, Patrick P. L.;  Han, Jing-Dong J.;  Jing, Naihe
收藏  |  浏览/下载:26/0  |  提交时间:2020/07/03

An in vivo approach to identify proteins whose enrichment near cardiac Ca(V)1.2 channels changes upon beta-adrenergic stimulation finds the G protein Rad, which is phosphorylated by protein kinase A, thereby relieving channel inhibition by Rad and causing an increased Ca2+ current.


Increased cardiac contractility during the fight-or-flight response is caused by beta-adrenergic augmentation of Ca(V)1.2 voltage-gated calcium channels(1-4). However, this augmentation persists in transgenic murine hearts expressing mutant Ca(V)1.2 alpha(1C) and beta subunits that can no longer be phosphorylated by protein kinase A-an essential downstream mediator of beta-adrenergic signalling-suggesting that non-channel factors are also required. Here we identify the mechanism by which beta-adrenergic agonists stimulate voltage-gated calcium channels. We express alpha(1C) or beta(2B) subunits conjugated to ascorbate peroxidase(5) in mouse hearts, and use multiplexed quantitative proteomics(6,7) to track hundreds of proteins in the proximity of Ca(V)1.2. We observe that the calcium-channel inhibitor Rad(8,9), a monomeric G protein, is enriched in the Ca(V)1.2 microenvironment but is depleted during beta-adrenergic stimulation. Phosphorylation by protein kinase A of specific serine residues on Rad decreases its affinity for beta subunits and relieves constitutive inhibition of Ca(V)1.2, observed as an increase in channel open probability. Expression of Rad or its homologue Rem in HEK293T cells also imparts stimulation of Ca(V)1.3 and Ca(V)2.2 by protein kinase A, revealing an evolutionarily conserved mechanism that confers adrenergic modulation upon voltage-gated calcium channels.