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| 1 | Grhl3 induces human epithelial tumor cell migration and invasion via downregulation of E-cadherin显示文摘Grainyhead 基因涉及愈合弯屈和发展神经试管闭合。转移在细胞从主要肿瘤的地点传播哪个癌症并且在远器官建立第二等的肿瘤期间是一个 multistep 过程。粘附蛋白质 E-cadherin 在转移起一个必要作用。考虑到在在皮或乳癌发生在侵略的获得期间的愈合创伤的过程和 EMT 发生的 epithelialmesenchymal 转变(EMT ) 的类似的高度,我们在癌症侵略调查了 Grainyhead 基因的角色。这里,我们证明在象 Grainyhead 一样之间有一种反的关系 3 (Grhl3 ) 并且在某上皮的肿瘤房间的 E-cadherin 表示排队。在 E-cadherin-positive 上皮的肿瘤房间线的 Grhl3 的 Overexpression,由更少的侵略描绘了,产生了 E-cadherin 基因的 transcriptional 阻塞并且支持了房间移植和房间侵略。相反地, Grhl3 弄空禁止了房间移植和房间侵略并且与 E-cadherin 表示的获得被联系。为了推进,探索 Grhl3 由调整了 E-cadherin 表示的机制, E-cadherin 倡导者报告分析被表现,结果出现了那 Grhl3 镇压 E-cadherin 基因表示由对在近似 E-cadherin 倡导者在场的电子盒子直接或间接地有约束力。一起拿,我们的调查结果在癌症房间由 E-cadherin 的 downregulation 在移植和侵略的正式就职为 Grhl3 定义一个主要角色。 | Pan Zhao Sijia Guo Zhenzhen Tu Lijun Di Xiaoiun Zha Haisheng Zhou Xuejun Zhang | 2016 | Acta Biochimica et Biophysica Sinica2016，0，3： | 9 |
| 2 | Interlayer-expanded MoS2 assemblies for enhanced electrochemical storage of potassium ions显示文摘Potassium-ion batteries are regarded as the low-cost alternative to lithium-ion batteries.However,their development is hampered by the lack of suitable electrode materials.In this work,we demonstrate that MoS2 with expanded interlayers represents a promising candidate for the electrochemical storage of potassium ions.Hierarchical interlayer-expanded MoS2 assemblies supported on carbon nanotubes are prepared via a straightforward solution method.The increased interlayer spacing not only enables the better accommodation of foreign ions,but also lowers the diffusion energy barrier and improves diffusion kinetics of ions.When investigated as the anode material of potassium ion batteries,our interlayer-expanded MoS2 assemblies exhibit an excellent electrochemical performance with large capacity(up to∼520 mAhg^−1),good rate capability(∼310 mAhg^−1 at 1,000 mAg^−1)and impressive cycling stability,superior to most competitors. | Sijia Di Pan Ding Yeyun Wang Yunling Wu Jun Deng Lin Jia Yanguang Li | 2020 | Nano Research2020，13，1： | 6 |
| 3 | CPAL, as a New Mediator of Cardiomyocyte Metabolic Alterations and Pyroptosis, Regulates Myocardial Infarction Injury in Mice显示文摘Myocardial infarction (MI), the most serious of the ischemic heart diseases, is accompanied by myocardial metabolic disorders and the loss of cardiomyocytes. Increasing evidence has shown that long noncoding RNAs (lncRNAs) are involved in various pathological conditions such as cancer and cardiovascular diseases (CVDs), and are emerging as a novel biomarker for these disorders. This study aims to investigate the regulatory role and mechanisms of lncRNAs in myocardial remodeling in the setting of MI. We find that post-infarcted hearts exhibit a reduction of adenosine triphosphate (ATP) and an alteration of the glucose and lipid metabolism genes cluster of differentiation 36 (CD36), hexokinase 1 (HK1), and clucose transporter 4 (GLUT4), accompanied by cardiomyocyte pyroptosis. We then identify a previously unknown conserved lncRNA, AK009126 (cardiomyocyte pyroptosis-associated lncRNA, CPAL), which is remarkably upregulated in the myocardial border zone of MI mice. Importantly, the adeno-associated virus 9 (AAV9)-mediated silencing of endogenous CPAL by its short hairpin RNA (shRNA) partially abrogates myocardial metabolic alterations and cardiomyocyte pyroptosis during MI in mice. Mechanistically, CPAL is shown to bind directly to nuclear factor kappa B (NFκB) and to act as an activator of NFκB to induce NFκB phosphorylation in cardiomyocytes. We also find that CPAL upregulates caspase-1 expression at the transcriptional level and consequently promotes the release of interleukin (IL)-18 and IL-1β from cardiomyocytes. Collectively, our findings reveal the conserved lncRNA CPAL as a new regulator of cardiac metabolic abnormalities and cardiomyocyte pyroptosis in the setting of MI and suggest CPAL as a new therapeutic target to protect cardiomyocytes against ischemic injury in infarcted hearts. | Jiamin Li Hongru Xue Ning Xu Liling Gong Ming Li Sijia Li Di Huang Qingwei Zhang Pengyu Li Qingsui Li Hang Yu Yining Liu Yadong Xue Haixin Chen Jiali Liu Wanyu Zhang Mingbin Liu Siyu Chang Xianzhi Lang Xingmiao Zhao Weijie Du Benzhi Cai Ning Wang Baofeng Yang | 2023 | Engineering2023，，1： | 0 |
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