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Dissolution hotspots in fractures 期刊论文
Geophysical Research Letters, 2021
作者:  Ran Hu;  Ting Wang;  Zhibing Yang;  Yang Xiao;  Yi-Feng Chen;  Chuang-Bing Zhou
收藏  |  浏览/下载:12/0  |  提交时间:2021/10/07
Divergent evolution of glaciation across High-Mountain Asia during the last four glacial-interglacial cycles 期刊论文
Geophysical Research Letters, 2021
作者:  Qing Yan;  Lewis A. Owen;  Zhongshi Zhang;  Huijun Wang;  Ting Wei;  Nanxuan Jiang;  Ran Zhang
收藏  |  浏览/下载:10/0  |  提交时间:2021/06/07
Stabilizing black-phase formamidinium perovskite formation at room temperature and high humidity 期刊论文
Science, 2021
作者:  Wei Hui;  Lingfeng Chao;  Hui Lu;  Fei Xia;  Qi Wei;  Zhenhuang Su;  Tingting Niu;  Lei Tao;  Bin Du;  Deli Li;  Yue Wang;  He Dong;  Shouwei Zuo;  Bixin Li;  Wei Shi;  Xueqin Ran;  Ping Li;  Hui Zhang;  Zhongbin Wu;  Chenxin Ran;  Lin Song;  Guichuan Xing;  Xingyu Gao;  Jing Zhang;  Yingdong Xia;  Yonghua Chen;  Wei Huang
收藏  |  浏览/下载:22/0  |  提交时间:2021/04/06
Exceptional plasticity in the bulk single-crystalline van der Waals semiconductor InSe 期刊论文
Science, 2020
作者:  Tian-Ran Wei;  Min Jin;  Yuecun Wang;  Hongyi Chen;  Zhiqiang Gao;  Kunpeng Zhao;  Pengfei Qiu;  Zhiwei Shan;  Jun Jiang;  Rongbin Li;  Lidong Chen;  Jian He;  Xun Shi
收藏  |  浏览/下载:10/0  |  提交时间:2020/08/09
Molecular architecture of lineage allocation and tissue organization in early mouse embryo (vol 572, 528, 2019) 期刊论文
NATURE, 2020, 577 (7791) : E6-E6
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:13/0  |  提交时间:2020/07/03
Significant methane ebullition from alpine permafrost rivers on the East Qinghai-Tibet Plateau 期刊论文
NATURE GEOSCIENCE, 2020, 13 (5)
作者:  Zhang, Liwei;  Xia, Xinghui;  Liu, Shaoda;  Zhang, Sibo;  Li, Siling;  Wang, Junfeng;  Wang, Gongqin;  Gao, Hui;  Zhang, Zhenrui;  Wang, Qingrui;  Wen, Wu;  Liu, Ran;  Yang, Zhifeng;  Stanley, Emily H.;  Raymond, Peter A.
收藏  |  浏览/下载:11/0  |  提交时间:2020/05/13
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:23/0  |  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.


  
The wide-binary origin of (2014) MU69-like Kuiper belt contact binaries 期刊论文
NATURE, 2020, 580 (7804) : 463-+
作者:  Jiao, Lin;  Howard, Sean;  Ran, Sheng;  Wang, Zhenyu;  Rodriguez, Jorge Olivares;  Sigrist, Manfred;  Wang, Ziqiang;  Butch, Nicholas P.;  Madhavan, Vidya
收藏  |  浏览/下载:66/0  |  提交时间:2020/07/03

Following its flyby and first imaging of the Pluto-Charon binary, the New Horizons spacecraft visited the Kuiper belt object (KBO) 2014 MU69 (also known as (486958) Arrokoth). The imaging showed MU69 to be a contact binary that rotates at a low spin period (15.92 hours), is made of two individual lobes connected by a narrow neck and has a high obliquity (about 98 degrees)(1), properties that are similar to those of other KBO contact binaries inferred through photometric observations(2). However, all scenarios suggested so far for the origins of such configurations(3-5) have failed to reproduce these properties and their probable frequent occurrence in the Kuiper belt. Here we show that semi-secular perturbations(6,7) operating on only ultrawide KBO binaries close to their stability limit can robustly lead to gentle, slow binary mergers at arbitrarily high obliquities but low rotational velocities, reproducing the characteristics of MU69 and other similar oblique contact binaries. Using N-body simulations, we find that approximately 15 per cent of all ultrawide binaries with a cosine-uniform inclination distribution(5,9) are likely to merge through this process. Moreover, we find that such mergers are sufficiently gentle to deform the shape of the KBO only slightly. The semi-secular contact binary formation channel not only explains the observed properties of MU69, but may also apply to other Kuiper belt or asteroid belt binaries and in the Solar System and extra-solar moon systems.


The high obliquity and low rotation period of the Kuiper belt object (2014) MU69 and other similar contact binaries is successfully reproduced from the collision and post-collision characteristics of initially wide binaries.


  
A self-activating orphan receptor 期刊论文
NATURE, 2020, 579 (7797) : 35-35
作者:  Wang, Lin;  Wu, Juehui;  Li, Jun;  Yang, Hua;  Tang, Tianqi;  Liang, Haijiao;  Zuo, Mianyong;  Wang, Jie;  Liu, Haipeng;  Liu, Feng;  Chen, Jianxia;  Liu, Zhonghua;  Wang, Yang;  Peng, Cheng;  Wu, Xiangyang;  Zheng, Ruijuan;  Huang, Xiaochen;  Ran, Yajun;  Rao, Zihe;  Ge, Baoxue
收藏  |  浏览/下载:11/0  |  提交时间:2020/07/03

The first 3D structure of a full-length G-protein-coupled receptor whose natural activator is unknown has been determined, providing insights into an unusual mode of activation and a basis for discovering therapeutics.


  
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:24/0  |  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.