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231.
Phytohormones mediate plant development and responses to stresses caused by biotic agents or abiotic factors. The functions of phytohormones in responses to viral infection have been intensively studied, and the emerging picture of complex mechanisms provides insights into the roles that phytohormones play in defense regulation as a whole. These hormone signaling pathways are not simple linear or isolated cascades, but exhibit crosstalk with each other. Here, we summarized the current understanding of recent advances for the classical defense hormones salicylic acid (SA), jasmonic acid (JA), and ethylene (ET) and also the roles of abscisic acid (ABA), auxin, gibberellic acid (GA), cytokinins (CKs), and brassinosteroids (BRs) in modulating plant–virus interactions.  相似文献   
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MicroRNA-24-3p (miR-24-3p) has been implicated as a key promoter of chemotherapy resistance in numerous cancers. Meanwhile, cancer-associated fibroblasts (CAFs) can secret exosomes to transfer miRNAs, which mediate tumour development. However, little is known regarding the molecular mechanism of CAF-derived exosomal miR-24-3p in colon cancer (CC). Hence, this study intended to characterize the functional relevance of CAF-derived exosomal miR-24-3p in CC cell resistance to methotrexate (MTX). We identified differentially expressed HEPH, CDX2 and miR-24-3p in CC through bioinformatics analyses, and validated their expression in CC tissues and cells. The relationship among HEPH, CDX2 and miR-24-3p was verified using ChIP and dual-luciferase reporter gene assays. Exosomes were isolated from miR-24-3p inhibitor–treated CAFs (CAFs-exo/miR-24-3p inhibitor), which were used in combination with gain-of-function and loss-of-function experiments and MTX treatment. CCK-8, flow cytometry and colony formation assays were conducted to determine cell viability, apoptosis and colony formation, respectively. Based on the findings, CC tissues and cells presented with high expression of miR-24-3p and low expression of HEPH and CDX2. CDX2 was a target gene of miR-24-3p and could up-regulate HEPH. Under MTX treatment, overexpressed CDX2 or HEPH and down-regulated miR-24-3p reduced cell viability and colony formation and elevated cell apoptosis. Furthermore, miR-24-3p was transferred into CC cells via CAF-derived exosomes. CAF-derived exosomal miR-24-3p inhibitor diminished cell viability and colony formation and increased cell apoptosis in vitro and inhibited tumour growth in vivo under MTX treatment. Altogether, CAF-derived exosomal miR-24-3p accelerated resistance of CC cells to MTX by down-regulating CDX2/HEPH axis.  相似文献   
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Hepatocellular cancer (HCC) has been reported to belong to one of the highly vascularized solid tumours accompanied with angiogenesis of human umbilical vein endothelial cells (HUVECs). KDM5A, an attractive drug target, plays a critical role in diverse physiological processes. Thus, this study aims to investigate its role in angiogenesis and underlying mechanisms in HCC. ChIP-qPCR was utilized to validate enrichment of H3K4me3 and KDM5A on the promotor region of miR-433, while dual luciferase assay was carried out to confirm the targeting relationship between miR-433 and FXYD3. Scratch assay, transwell assay, Edu assay, pseudo-tube formation assay and mice with xenografted tumours were conducted to investigate the physiological function of KDM5A-miR-433-FXYD3-PI3K-AKT axis in the progression of HCC after loss- and gain-function assays. KDM5A p-p85 and p-AKT were highly expressed but miR-433 was down-regulated in HCC tissues and cell lines. Depletion of KDM5A led to reduced migrative, invasive and proliferative capacities in HCC cells, including growth and a lowered HUVEC angiogenic capacity in vitro. Furthermore, KDM5A suppressed the expression of miR-433 by demethylating H3K4me3 on its promoterregion. miR-433 negatively targeted FXYD3. Depleting miR-433 or re-expressing FXYD3 restores the reduced migrative, invasive and proliferative capacities, and lowers the HUVEC angiogenic capacity caused by silencing KDM5A. Therefore, KDM5A silencing significantly suppresses HCC tumorigenesis in vivo, accompanied with down-regulated miR-433 and up-regulated FXYD3-PI3K-AKT axis in tumour tissues. Lastly, KDM5A activates the FXYD3-PI3K-AKT axis to enhance angiogenesis in HCC by suppressing miR-433.  相似文献   
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Apoptosis - Resistance to epidermal growth factor receptor-tyrosin kinase inhibitors (TKIs, e.g. icotinib) remains a major clinical challenge. Non-small cell lung cancer patients with wild-type...  相似文献   
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Gao  Kai  Liu  Meiyou  Li  Yuan  Wang  Lei  Zhao  Chao  Zhao  Xian  Zhao  Jinyi  Ding  Yi  Tang  Haifeng  Jia  Yanyan  Wang  Jingwen  Wen  Aidong 《Journal of molecular histology》2021,52(3):449-459
Journal of Molecular Histology - Currently, the excessive activation of N-methyl-D-aspartate receptors (NMDARs) is considered to be a crucial mechanism of brain injury. Lycium barbarum A (LyA) is a...  相似文献   
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Yi  Fengshuang  Zhang  Xin  Liang  Ruobing 《The protein journal》2021,40(6):842-848
The Protein Journal - Myo9a is an actin-based molecular motor with a RhoGAP domain in its C-terminal tail. It plays a role in a variety of biological processes, such as in regulating the immune...  相似文献   
240.
位于滇西北的高黎贡山是全球生物多样性研究和保护的热点地区之一, 然而该地区昆虫多样性缺乏系统调查和总结。本研究聚焦蝴蝶类群, 考虑该区域高山峡谷特点, 结合海拔梯度、生境类型和季节变化, 采用样线法调查、分析蝴蝶物种多样性及群落结构变化。结果显示: 共观测记录到蝴蝶2,055只, 隶属于5科85属151种, 在历史记录上新增27种, 使该地区已知蝴蝶种类达488种; 其中蛱蝶科物种多样性最高, 灰蝶科次之, 凤蝶科最低。蝴蝶群落多样性分析结果表明: 中海拔1,000-2,000 m区域种类丰富、多样性指数最高; 低海拔区蝴蝶分布明显聚集, 并且与高海拔地区空间上分离, 少有重叠。该地区不同生境中蝴蝶的种类及数量差异也较大, 物种数及多样性指数在自然保护区最高、边缘交错带居中及农业种植区最低。此外, 蝴蝶的种类和数量也存在季节差异, 春季调查到的个体数少, 夏季观察到的物种数少, 两年秋季调查到的物种丰富度、多样性均高, 但存在季节内变化。总之, 高黎贡山地区不同海拔、生境、季节间和季节内蝴蝶群落组成有自身特点, 共存物种有限, 蝴蝶群落相似性低。综合评估分布于该地区的蝴蝶保护种类, 包括易危种17种、近危种50种, 有国家二级保护蝴蝶3种。本研究弄清了高黎贡山地区蝴蝶的物种本底, 并调查获得其多样性随海拔、生境和季节变化的模式, 为加强区域物种多样性监测、保护生物多样性提供了科学依据。  相似文献   
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