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学者姓名：孙玲
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荧光蛋白能够将分子分布与超微结构联系起来,对于光电关联(CLEM)技术的应用至关重要.然而,常规的绿色荧光蛋白及其变体在活体组织的电子显微镜(EM)制样过程中,常因诸多不可控因素导致荧光信号显著减弱,这限制了它们作为光电关联分子探针的应用.本研究在果蝇大脑神经束膜胶质细胞中特异性表达多种GFP变体(mEmerald、hfYFP、mhYFP和CoGFPv0),以评估它们在活体组织光电关联中的应用潜力.通过提高表达量和靶向线粒体等策略,本研究最终筛选出适用于CLEM技术在果蝇神经系统研究中的CoGFPv0.本工作表明,CoGFPv0可作为一种具有良好应用前景的光电关联分子探针,特别适用于复杂的活体组织环境.
Keyword ：
CoGFPv0 CoGFPv0 GFP变体 GFP变体 光电关联技术 光电关联技术 果蝇 果蝇 荧光蛋白 荧光蛋白
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| GB/T 7714 | 陈捷 , 石丹妮 , 齐佳苗 et al. 利用果蝇模型筛选可用于动物组织光电关联的绿色荧光蛋白变体 [J]. | 电子显微学报 , 2025 , 44 (1) : 81-90 . |
| MLA | 陈捷 et al. "利用果蝇模型筛选可用于动物组织光电关联的绿色荧光蛋白变体" . | 电子显微学报 44 . 1 (2025) : 81-90 . |
| APA | 陈捷 , 石丹妮 , 齐佳苗 , 孙玲 , 杨宇丰 , 王道彪 . 利用果蝇模型筛选可用于动物组织光电关联的绿色荧光蛋白变体 . | 电子显微学报 , 2025 , 44 (1) , 81-90 . |
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Background: Alzheimer's disease (AD) is a common cause of dementia among elderly people. Hyperphosphorylation and aggregation of tau correlates with the clinical progression of AD; therefore, therapies targeting the aggregation of tau may have potential applications for anti-AD drug development. Several inhibitors of tau aggregation, including small molecules and antibodies, have been found to decrease the aggregation of tau and the corresponding pathology. Objective: To screen one kind of single-chain variable fragment (scFv) antibody which could inhibit the aggregation of tau and ameliorate its cytotoxicity. Methods/Results: Using phosphorylated tau (pTau) as an antigen, we obtained a scFv antibody via the screening of a high-capacity phage antibody library. Biochemical analysis revealed that this scFv antibody (scFv T1) had a strong ability to inhibit pTau aggregation both in dilute solutions and under conditions of macromolecular crowding. ScFv T1 could also depolymerize preformed pTau aggregates in vitro. Furthermore, scFv T1 was found to be able to inhibit the cytotoxicity of extracellular pTau aggregates and ameliorate tau-mediated toxicity when coexpressed with a hTauR406W mutant in the eye of transgenic Drosophila flies. Conclusion: This scFv T1 antibody may be a potential new therapeutic agent against AD. Our methods can be used to develop novel strategies against protein aggregation for the treatment of neurodegenerative diseases.
Keyword ：
Aggregation Aggregation Alzheimer's disease Alzheimer's disease Drosophila Drosophila single-chain variable fragment antibody single-chain variable fragment antibody tau tau tauopathy tauopathy toxicity toxicity
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| GB/T 7714 | Li, Sen , Yi, Yushan , Cui, Ke et al. A Single-Chain Variable Fragment Antibody Inhibits Aggregation of Phosphorylated Tau and Ameliorates Tau Toxicity in vitro and in vivo [J]. | JOURNAL OF ALZHEIMERS DISEASE , 2021 , 79 (4) : 1613-1629 . |
| MLA | Li, Sen et al. "A Single-Chain Variable Fragment Antibody Inhibits Aggregation of Phosphorylated Tau and Ameliorates Tau Toxicity in vitro and in vivo" . | JOURNAL OF ALZHEIMERS DISEASE 79 . 4 (2021) : 1613-1629 . |
| APA | Li, Sen , Yi, Yushan , Cui, Ke , Zhang, Yanqiu , Chen, Yange , Han, Dou et al. A Single-Chain Variable Fragment Antibody Inhibits Aggregation of Phosphorylated Tau and Ameliorates Tau Toxicity in vitro and in vivo . | JOURNAL OF ALZHEIMERS DISEASE , 2021 , 79 (4) , 1613-1629 . |
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Site-specific DNA double-strand breaks have been used to generate knock-in through the homology-dependent or -independent pathway. However, low efficiency and accompanying negative impacts such as undesirable indels or tumorigenic potential remain problematic. In this study, we present an enhanced reduced-risk genome editing strategy we named as NEO, which used either site-specific trans or cis double-nicking facilitated by four bacterial recombination factors (RecOFAR). In comparison to currently available approaches, NEO achieved higher knock-in (KI) germline transmission frequency (improving from zero to up to 10% efficiency with an average of 5-fold improvement for 8 loci) and 'cleaner' knock-in of long DNA fragments (up to 5.5 kb) into a variety of genome regions in zebrafish, mice and rats. Furthermore, NEO yielded up to 50% knock-in in monkey embryos and 20% relative integration efficiency in non-dividing primary human peripheral blood lymphocytes (hPBLCs). Remarkably, both on-target and off-target indels were effectively suppressed by NEO. NEO may also be used to introduce low-risk unrestricted point mutations effectively and precisely. Therefore, by balancing efficiency with safety and quality, the NEO method reported here shows substantial potential and improves the in vivo gene-editing strategies that have recently been developed.
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| GB/T 7714 | He, Xiaozhen , Chen, Wenfeng , Liu, Zhen et al. Efficient and risk-reduced genome editing using double nicks enhanced by bacterial recombination factors in multiple species [J]. | NUCLEIC ACIDS RESEARCH , 2020 , 48 (10) . |
| MLA | He, Xiaozhen et al. "Efficient and risk-reduced genome editing using double nicks enhanced by bacterial recombination factors in multiple species" . | NUCLEIC ACIDS RESEARCH 48 . 10 (2020) . |
| APA | He, Xiaozhen , Chen, Wenfeng , Liu, Zhen , Yu, Guirong , Chen, Youbang , Cai, Yi-Jun et al. Efficient and risk-reduced genome editing using double nicks enhanced by bacterial recombination factors in multiple species . | NUCLEIC ACIDS RESEARCH , 2020 , 48 (10) . |
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Aberrant mitophagy has been implicated in a broad spectrum of disorders. PINK1, Parkin, and ubiquitin have pivotal roles in priming mitophagy. However, the entire regulatory landscape and the precise control mechanisms of mitophagy remain to be elucidated. Here, we uncover fundamental mitophagy regulation involving PINK1 and a non-canonical role of the mitochondrial Tu translation elongation factor (TUFm). The mitochondrion-cytosol dual-localized TUFm interacts with PINK1 biochemically and genetically, which is an evolutionarily conserved Parkin-independent route toward mitophagy. A PINK1-dependent TUFm phosphoswitch at Ser222 determines conversion from activating to suppressing mitophagy. PINK1 modulates differential translocation of TUFm because p-S222-TUFm is restricted predominantly to the cytosol, where it inhibits-mitophagy by impeding Atg5-Atg12 formation. The self-antagonizing feature of PINK1/TUFm is critical for the robustness of mitophagy regulation, achieved by the unique kinetic parameters of p-S222-TUFm, p-S65-ubiquitin, and their common kinase PINK1. Our findings provide new mechanistic insights into mitophagy and mitophagy-associated disorders.
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| GB/T 7714 | Lin, Jingjing , Chen, Kai , Chen, Wenfeng et al. Paradoxical Mitophagy Regulation by PINK1 and TUFm [J]. | MOLECULAR CELL , 2020 , 80 (4) : 607-, . |
| MLA | Lin, Jingjing et al. "Paradoxical Mitophagy Regulation by PINK1 and TUFm" . | MOLECULAR CELL 80 . 4 (2020) : 607-, . |
| APA | Lin, Jingjing , Chen, Kai , Chen, Wenfeng , Yao, Yizhou , Ni, Shiwei , Ye, Meina et al. Paradoxical Mitophagy Regulation by PINK1 and TUFm . | MOLECULAR CELL , 2020 , 80 (4) , 607-, . |
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How complex interactions of genetic, environmental factors and aging jointly contribute to dopaminergic degeneration in Parkinson's disease (PD) is largely unclear. Here, we applied frequent gene co-expression analysis on human patientsubstantia nigra-specific microarray datasets to identify potential novel disease-related genes. In vivoDrosophilastudies validated two of 32 candidate genes, a chromatin-remodeling factor SMARCA4 and a biliverdin reductase BLVRA. Inhibition of SMARCA4 was able to prevent aging-dependent dopaminergic degeneration not only caused by overexpression of BLVRA but also in four most commonDrosophilaPD models. Furthermore, down-regulation of SMARCA4 specifically in the dopaminergic neurons prevented shortening of life span caused by alpha-synuclein and LRRK2. Mechanistically, aberrant SMARCA4 and BLVRA converged on elevated ERK-ETS activity, attenuation of which by either genetic or pharmacological manipulation effectively suppressed dopaminergic degeneration inDrosophilain vivo. Down-regulation of SMARCA4 or drug inhibition of MEK/ERK also mitigated mitochondrial defects inPINK1(a PD-associated gene)-deficient human cells. Our findings underscore the important role of epigenetic regulators and implicate a common signaling axis for therapeutic intervention in normal aging and a broad range of age-related disorders including PD.
Keyword ：
aging aging Brahma Brahma Drosophila Drosophila MAPK-ERK-ETS signaling MAPK-ERK-ETS signaling neurodegeneration neurodegeneration Parkinson's disease Parkinson's disease SMARCA4 SMARCA4
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| GB/T 7714 | Sun, Ling , Zhang, Jie , Chen, Wenfeng et al. Attenuation of epigenetic regulator SMARCA4 and ERK-ETS signaling suppresses aging-related dopaminergic degeneration [J]. | AGING CELL , 2020 , 19 (9) . |
| MLA | Sun, Ling et al. "Attenuation of epigenetic regulator SMARCA4 and ERK-ETS signaling suppresses aging-related dopaminergic degeneration" . | AGING CELL 19 . 9 (2020) . |
| APA | Sun, Ling , Zhang, Jie , Chen, Wenfeng , Chen, Yun , Zhang, Xiaohui , Yang, Mingjuan et al. Attenuation of epigenetic regulator SMARCA4 and ERK-ETS signaling suppresses aging-related dopaminergic degeneration . | AGING CELL , 2020 , 19 (9) . |
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MicroRNAs (miRNAs) are post-transcriptional regulators of gene expression that target mRNAs for translational repression or cleavage. The present study was conducted to identify differentially expressed miRNAs in primary tumor tissues of rectal carcinoma (RC) that may be associated with heterochrony hepatic metastasis (HHM). Samples were collected exclusively from patients with RC but not colon cancer (CC); Next-generation high-throughput sequencing technology and bioinformatics tools were used to profile and analyze small RNAs and their corresponding targets in primary tumor tissues with HHM (n=2) or without metastases (non-metastatic, NM; n=2). A total of 24 known miRNAs were identified to be differentially expressed (P< 0.01; absolute value of log(2)-fold change >= 1). Hsa-let-7e-5p exhibited the most significant elevation in tissues with HHM (log(2)-fold change=2.62). By combining online informatics resources and previous mRNA sequencing data, it was identified that 54 validated target genes of let-7e were downregulated in primary tumor tissues with HHM. A number of these target genes have been demonstrated to be directly involved in tumor metastasis (including MYC proto-oncogene, bHLH transcription factor, high-mobility group AT-Hook 2, peptidase inhibitor 3, KIT proto-oncogene receptor tyrosine kinase, Jun proto-oncogene, AP-1 transcription factor subunit and ribonuclease T2), or have physiological associations to immunity (including C-C motif chemokine receptor 4 and cluster of differentiation 40 ligand) and cellular metabolism (including peroxisome proliferator-activated receptor gamma, coactivator 1 alpha). Next, 14 target genes were selected for reverse transcription-quantitative polymerase chain reaction analysis in non-sequenced samples, and the downregulation of 10 target genes in RC samples with HHM was confirmed. In addition, it was demonstrated that hsa-let-7e-5p stimulated colorectal cancer cell migration in vitro. The miRNA hsa-let-7e-5p may serve as a potential biomarker for rectal carcinoma-associated HHM, facilitating the identification of patients with RC who are at risk of developing HHM.
Keyword ：
heterochrony hepatic metastasis heterochrony hepatic metastasis microRNA hsa-let-7e-5p microRNA hsa-let-7e-5p next-generation sequencing next-generation sequencing rectal carcinoma rectal carcinoma
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| GB/T 7714 | Chen, Wenfeng , Lin, Guosheng , Yao, Yizhou et al. MicroRNA hsa-let-7e-5p as a potential prognosis marker for rectal carcinoma with liver metastases [J]. | ONCOLOGY LETTERS , 2018 , 15 (5) : 6913-6924 . |
| MLA | Chen, Wenfeng et al. "MicroRNA hsa-let-7e-5p as a potential prognosis marker for rectal carcinoma with liver metastases" . | ONCOLOGY LETTERS 15 . 5 (2018) : 6913-6924 . |
| APA | Chen, Wenfeng , Lin, Guosheng , Yao, Yizhou , Chen, Jishen , Shui, Hanli , Yang, Qinghai et al. MicroRNA hsa-let-7e-5p as a potential prognosis marker for rectal carcinoma with liver metastases . | ONCOLOGY LETTERS , 2018 , 15 (5) , 6913-6924 . |
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本发明属于医药技术领域，其公开了U0126在制备治疗帕金森药物上的应用，是将U0126用于制备延缓多巴胺能神经元退化的药物。所得产品可有效延缓多巴胺能神经元的退行性死亡，从根本上达到治疗帕金森病的作用；且其药物无须进行注射，只通过口服即可达到治疗效果，对多种原因引起的帕金森病有较好疗效，对帕金森病的治疗及治愈具有重要意义。
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| GB/T 7714 | 杨宇丰 , 黄昆 , 张洁 et al. U0126在制备治疗帕金森药物上的应用 : CN201610208601.0[P]. | 2016/4/6 . |
| MLA | 杨宇丰 et al. "U0126在制备治疗帕金森药物上的应用" : CN201610208601.0. | 2016/4/6 . |
| APA | 杨宇丰 , 黄昆 , 张洁 , 张西 , 孙玲 , 陈文锋 et al. U0126在制备治疗帕金森药物上的应用 : CN201610208601.0. | 2016/4/6 . |
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本发明属于医药技术领域，其公开了曲美替尼(Trametinib)在制备治疗帕金森药物上的应用，是将曲美替尼用于制备延缓多巴胺能神经元退化的药物。所得产品可有效延缓多巴胺能神经元的退行性死亡，从根本上达到治疗帕金森病的作用；且其药物无须进行注射，只通过口服即可达到治疗效果，对多种原因引起的帕金森病有较好疗效，对帕金森病的治疗及治愈具有重要意义。
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| GB/T 7714 | 杨宇丰 , 张西 , 孙玲 et al. 曲美替尼在制备治疗帕金森症药物上的应用 : CN201610208591.0[P]. | 2016/4/6 . |
| MLA | 杨宇丰 et al. "曲美替尼在制备治疗帕金森症药物上的应用" : CN201610208591.0. | 2016/4/6 . |
| APA | 杨宇丰 , 张西 , 孙玲 , 陈文锋 , 倪世伟 . 曲美替尼在制备治疗帕金森症药物上的应用 : CN201610208591.0. | 2016/4/6 . |
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本发明属于医药技术领域，其公开了PD0325901在制备治疗帕金森药物上的应用，是将PD0325901用于制备延缓多巴胺能神经元退化的药物。所得产品可有效延缓多巴胺能神经元的退行性死亡，从根本上达到治疗帕金森病的作用；且其药物无须进行注射，只通过口服即可达到治疗效果，对多种原因引起的帕金森病有较好疗效，对帕金森病的治疗及治愈具有重要意义。
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| GB/T 7714 | 杨宇丰 , 张西 , 孙玲 et al. PD0325901在制备治疗帕金森药物上的应用 : CN201610208609.7[P]. | 2016/4/6 . |
| MLA | 杨宇丰 et al. "PD0325901在制备治疗帕金森药物上的应用" : CN201610208609.7. | 2016/4/6 . |
| APA | 杨宇丰 , 张西 , 孙玲 , 陈文锋 , 倪世伟 . PD0325901在制备治疗帕金森药物上的应用 : CN201610208609.7. | 2016/4/6 . |
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实验哺乳动物模型是研究基础生物学及人类疾病的重要工具,对实现转基因操作,尤其是基因敲入(knock-in,KI),具有重大意义.锌指核酸酶(zinc-finger nucleases,ZFN)、类转录激活因子效应物核酸酶(transcription activator-like effector nucleases,TALEN)和RNA介导的、基于成簇的规律间隔的短回文重复序列和Cas9蛋白的DNA核酸内切酶[clustered regulatory interspaced short palindromic repeat (CRISPR)/Cas9-based RNA-guided DNA endonucleases,CRISPR/Cas9]等的出现,为科研工作者提供了革命性的转基因操作工具.这些可编辑核酸酶通过在靶标序列位置产生双链断裂缺口(double strand breaks,DSBs),并在同源修复模板存在的情况下发生同源重组,进而实现精确的基因敲入.该文主要综述了这些技术的原理及其在哺乳动物KI中取得的最新进展、提高KI效率以及降低脱靶效应的举措等,将有助于KI技术在未来转基因实践中的广泛应用.
Keyword ：
CRISPR/Cas9 CRISPR/Cas9 哺乳动物 哺乳动物 基因敲入 基因敲入 类转录因子效应物核酸酶 类转录因子效应物核酸酶 锌指核酸酶 锌指核酸酶
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| GB/T 7714 | 张敏杰 , 孙玲 , 刘真 et al. 可编辑核酸酶介导的哺乳动物基因敲入技术最新进展 [J]. | 中国细胞生物学学报 , 2016 , 38 (1) : 72-80 . |
| MLA | 张敏杰 et al. "可编辑核酸酶介导的哺乳动物基因敲入技术最新进展" . | 中国细胞生物学学报 38 . 1 (2016) : 72-80 . |
| APA | 张敏杰 , 孙玲 , 刘真 , 蔡毅君 , 孙强 , 杨宇丰 et al. 可编辑核酸酶介导的哺乳动物基因敲入技术最新进展 . | 中国细胞生物学学报 , 2016 , 38 (1) , 72-80 . |
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