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N~1-(4-取代氨基-6-甲基-2-嘧啶基)-N~3-(对氯苯基)胍类的合成及其抗丝虫作用
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作者 陈宝珍 俞雄 +1 位作者 金育歧 雷兴翰 《医药工业》 CAS 1987年第5期207-210,共4页
报道了 N~1-[4-[3-(二烷胺基)甲基-和3,5-双[(二烷胺基)甲基]-4-羟基苯基]氨基]-6-甲基-2-嘧啶基]-N~3-(4-氯苯基)胍的合成。所合成的10个化合物进行了药理初筛,其中8个对感染沙鼠的棉鼠丝虫微丝蚴或成虫显示一定的杀灭作用。
关键词 合成 抗丝虫作用 n~1-(4-取代氨基-6-甲基-2-嘧啶基)-n~3-(对氯苯基)胍
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m6A阅读器IGF2BP1在胰腺癌中的表达及意义
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作者 欧阳永灏 易思清 +4 位作者 辛万鹏 孙根 方康 涂书举 肖卫东 《南昌大学学报(医学版)》 2023年第1期27-33,共7页
目的利用生物信息学分析探讨N~6-甲基腺嘌呤(N~6-methyladenosine,m6A)阅读器胰岛素样生长因子2-mRNA结合蛋白1(IGF2BP1)在胰腺癌组织中的表达情况及其临床意义。方法从GEO和TCGA两数据库m6A相关基因的差异分析结果中筛选出本研究的目... 目的利用生物信息学分析探讨N~6-甲基腺嘌呤(N~6-methyladenosine,m6A)阅读器胰岛素样生长因子2-mRNA结合蛋白1(IGF2BP1)在胰腺癌组织中的表达情况及其临床意义。方法从GEO和TCGA两数据库m6A相关基因的差异分析结果中筛选出本研究的目标基因IGF2BP1后,通过HPA、UALCAN网站对IGF2BP1蛋白质水平的表达情况进行分析。利用UALCAN网站分析IGF2BP1的表达与临床病理的关系。通过LinkedOmics网站对IGF2BP1进行共表达分析及GSEA富集分析。STRING网站被用于构建IGF2BP1的蛋白互作(protein-protein interaction,PPI)网络。使用Kaplan-Meier Plotter数据库对IGF2BP1及与其有蛋白互作关系的基因进行Kaplan-Meier生存分析。结果IGF2BP1在胰腺癌组织中高表达且表达水平与胰腺癌患者TP53的突变有关(P<0.05)。共表达分析显示1226个基因与IGF2BP1呈正相关,825个基因与IGF2BP1呈负相关(P<0.01)。GSEA分析显示这些共表达基因主要参与生物调节、代谢、对刺激物的应答等过程,行使与蛋白质、离子和核酸结合等功能。在m6A相关基因的PPI网络中,IGF2BP1与多个m6A相关基因有着蛋白互作关系。Kaplan-Meier分析显示,IGF2BP1及多个与其有着蛋白互作关系的基因表达水平与胰腺癌患者的预后呈负相关(P<0.05)。结论IGF2BP1的表达水平在胰腺癌组织中显著增高,且与胰腺癌不良预后有关,有望成为胰腺癌诊治的潜在新靶点。 展开更多
关键词 n~6-甲基腺嘌呤 胰岛素样生长因子2-mRNA结合蛋白1 胰腺癌 生物信息学 预后
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N~6-甲基腺嘌呤修饰及其调控因子在男性生殖中的作用
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作者 蒋婷 张学广 许文明 《四川大学学报(医学版)》 CAS CSCD 北大核心 2024年第3期527-534,共8页
在哺乳动物中,精子发生是一个高度复杂且协调的生殖细胞分化过程,这一过程受到转录、转录后和翻译水平的精确调控,以确保不同发育阶段的生精细胞正确表达特定基因并维持正常的生精过程。N~6-甲基腺嘌呤(N~6-methyladenosine,m~6A)是真... 在哺乳动物中,精子发生是一个高度复杂且协调的生殖细胞分化过程,这一过程受到转录、转录后和翻译水平的精确调控,以确保不同发育阶段的生精细胞正确表达特定基因并维持正常的生精过程。N~6-甲基腺嘌呤(N~6-methyladenosine,m~6A)是真核生物m RNA上最丰富的修饰,在诸如m RNA剪接、转运和翻译等多个生物过程发挥关键作用。RNA甲基化修饰是一个动态可逆的过程,主要通过编码器(writers)催化、消码器(erasers)去除和读码器(readers)识别来调控修饰水平。本文首先概述了精子发生的主要阶段,然后重点介绍m~6A修饰及相关蛋白在雄性生殖细胞不同发育阶段的关键功能,最后简要总结了目前检测m~6A的主要方法,以期深入了解RNA修饰在调控精子发生以及在男性不育中发挥的作用和机制。 展开更多
关键词 精子发生 n~6-甲基腺嘌呤 RNA修饰 男性不育 表观遗传学 综述
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FTO减少DKK2的m^(6)A修饰和促进DKK2表达而减少心肌纤维化 被引量:1
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作者 李溪 王坤荣 《西安交通大学学报(医学版)》 CAS CSCD 北大核心 2022年第6期807-813,共7页
目的探讨肥胖相关蛋白(FTO)在心肌纤维化过程中与dickkopf2(DKK2)的N~6甲基腺苷(m^(6)A)修饰、表达水平间的关系。方法心肌成纤维细胞分为对照组、AngⅡ处理组、AngⅡ+EV组(空载体和阴性siRNA转染后用AngⅡ处理)、AngⅡ+FTO-O组(FTO过... 目的探讨肥胖相关蛋白(FTO)在心肌纤维化过程中与dickkopf2(DKK2)的N~6甲基腺苷(m^(6)A)修饰、表达水平间的关系。方法心肌成纤维细胞分为对照组、AngⅡ处理组、AngⅡ+EV组(空载体和阴性siRNA转染后用AngⅡ处理)、AngⅡ+FTO-O组(FTO过表达载体转染后用AngⅡ处理)和AngⅡ+FTO-O+DKK2 siRNA组(FTO过表达载体和DKK2 siRNA共转染后用AngⅡ处理);小鼠按对照组(假手术组)、AMI组(构建急性心肌梗死模型)、AMI+EV组(AMI小鼠腹腔注射含空载体的纳米颗粒)和AMI+FTO-O组(AMI小鼠腹腔注射含FTO过表达载体的纳米颗粒)进行处理。用荧光定量PCR和Western blotting检测FTO、DKK2的表达,RNA结合蛋白免疫沉淀检测DKK2的m^(6)A修饰水平,CCK-8检测细胞存活力,评估AMI小鼠的心功能,HE和Masson染色检测小鼠心脏病理变化。结果AngⅡ抑制FTO的表达,进而增强DKK2的m^(6)A修饰水平而下调DKK2的表达(P<0.05);AngⅡ促进细胞存活和增强α-SMA、collagenⅠ和collagenⅢ的表达(P<0.05);FTO过表达能显著阻断AngⅡ的上述调控作用(P<0.05),不过DKK2 siRNA能拮抗FTO过表达对AngⅡ的影响作用。FTO和DKK2在AMI小鼠中的表达下调,且DKK2的m^(6)A修饰水平增加(P<0.05);FTO过表达时,FTO和DKK2在AMI小鼠中的表达显著恢复,DKK2的m^(6)A修饰水平明显减少(P<0.05),且心肌纤维化水平降低,心脏病理变化明显有所改善。结论FTO可通过减少DKK2的m^(6)A修饰水平而促进DKK2的表达,进而抑制心肌纤维化进展,表明FTO/DKK2通路是调控心肌纤维化的关键通路。 展开更多
关键词 急性心肌梗死 心肌纤维化 肥胖相关蛋白(FTO) n~6甲基腺苷(m^(6)A) DKK2
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DNA N^6-methyladenine demethylase ALKBH1 enhances osteogenic differentiation of human MSCs 被引量:7
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作者 Chenchen Zhou Yuting Liu +2 位作者 Xiaobing Li Jing Zou Shujuan Zou 《Bone Research》 SCIE CAS CSCD 2016年第3期174-182,共9页
ALKBH1 was recently discovered as a demethylase for DNA N6-methyladenine (N6-mA), a new epigenetic modification, and interacts with the core transcriptional pluripotency network of embryonic stem cells. However, the... ALKBH1 was recently discovered as a demethylase for DNA N6-methyladenine (N6-mA), a new epigenetic modification, and interacts with the core transcriptional pluripotency network of embryonic stem cells. However, the role of ALKBH1 and DNA N6-mA in regulating osteogenic differentiation is largely unknown. In this study, we demonstrated that the expression of ALKBH1 in human mesenchymal stem cells (MSCs) was upregulated during osteogenic induction. Knockdown of ALKBH1 increased the genomic DNA N6-mA levels and significantly reduced the expression of osteogenic-related genes, alkaline phosphatase activity, and mineralization. ALKBHl-depleted MSCs also exhibited a restricted capacity for bone formation in vivo. By contrast, the ectopic overexpression of ALKBH1 enhanced osteoblastic differentiation. Mechanically, we found that the depletion of ALKBH1 resulted in the accumulation of N6-mA on the promoter region of ATF4, which subsequently silenced ATF4 transcription. In addition, restoring the expression of ATP by adenovirus-mediated transduction successfully rescued osteogenic differentiation. Taken together, our results demonstrate that ALKBH1 is indispensable for the osteogenic differentiation of MSCs and indicate that DNA N6-mA modifications area new mechanism for the epigenetic regulation of stem cell differentiation. 展开更多
关键词 ATF Figure MSCS DNA n~6-methyladenine demethylase ALKBH1 enhances osteogenic differentiation of human MSCs
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The N^6-adenine methylation in yeast genome profiled by single-molecule technology 被引量:3
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作者 Zhe Liang Guoliang Yu +5 位作者 Jingrong Liu Yuke Geng Jinghui Mao Depeng Wang Jiapeng Zhou Xiaofeng Gu 《Journal of Genetics and Genomics》 SCIE CAS CSCD 2018年第4期223-225,共3页
The most common and abundant DNA modification is 5-methylcytosine(5mC),which has been well-established as an epigenetic mark regulating gene expression in eukaryotes(Jones,2012).Another DNA modification N^6-methyl... The most common and abundant DNA modification is 5-methylcytosine(5mC),which has been well-established as an epigenetic mark regulating gene expression in eukaryotes(Jones,2012).Another DNA modification N^6-methyldeoxyadenosine(6mA),previously reported as a widespread DNA methylation in prokaryotes. 展开更多
关键词 DNA TSS The n~6-adenine methylation in yeast genome profiled by single-molecule technology
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Pan-cancer analysis of DNA epigenetic modifications by hydrophilic interaction liquid chromatography-tandem mass spectrometry
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作者 Yiqiu Hu Xiujuan Hong +6 位作者 Zhijun Yuan Jiayi Mu Xiaoxiao Zhang Zhihao Fang Ying Yuan Shu Zheng Cheng Guo 《Chinese Chemical Letters》 SCIE CAS CSCD 2023年第7期214-218,共5页
Accumulating evidence in recent years indicates that DNA methylation(5-methyl-2-deoxycytidine,5-mdC) and hydroxymethylation(5-hydroxymethyl-2-deoxycytidine, 5-hmd C) have been implicated in various biological processe... Accumulating evidence in recent years indicates that DNA methylation(5-methyl-2-deoxycytidine,5-mdC) and hydroxymethylation(5-hydroxymethyl-2-deoxycytidine, 5-hmd C) have been implicated in various biological processes, and the aberrations of these DNA cytosine modifications is tightly associated with cancer. N6-methyl-2-deoxyadenosine(m~6dA), as a newly discovered epigenetic modification in genome of mammals, has been demonstrated to play vital regulatory roles in tumorigenesis. However, the content information of m~6dA in human tumor tissues is still limited and pan-cancer analysis of these DNA epigenetic modifications is lacked. Herein, we developed a sensitive and robust stable isotopediluted hydrophilic interaction liquid chromatography-tandem mass spectrometry(HILIC-MS/MS) method for accurate quantification of m~6dA, 5-mdC and 5-hmdC in genomic DNA from 82 pairs of human tumor tissues and matched tumor-adjacent normal tissues. The types of tumors included esophagus cancer, lung cancer, breast cancer, liver cancer, pancreatic cancer, gastric cancer, stromal tumor and colorectal cancer.Compared to the normal tissues, we revealed the level of m6dA was increased in tumor tissues of esophagus cancer, lung cancer and liver cancer, whereas the level of m~6dA was diminished in tumor tissues of pancreatic cancer and gastric cancer;while the contents of 5-mdC and 5-hmdC exhibited significant decrease in tumor tissues of most types of cancer. It is worth noting that we revealed, for the first time,the content of genomic m~6dA in pancreatic cancer, stromal tumor and colorectal cancer. The significant changes of these DNA epigenetic modifications indicate they may serve as indicators of cancers. In addition, this study will benefit for better understanding of the regulatory roles of these DNA epigenetic modifications in cancers. 展开更多
关键词 HILIC-MS/MS Pan-cancer analysis n~6-methyl-2-deoxyadenosine 5-Methyl-2-deoxycytidine 5-Hydroxymethyl-2-deoxycytidine
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