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杂志核酸的publishes original research articles as well as review articles covering all structural, chemical, and functional aspects of DNA and RNA research.
编辑聚光灯
Chief Editor, Professor Basu, is currently based at the University of Connecticut. His research focuses on determination of the consequences of DNA damaged by anti-tumor drugs, chemical carcinogens, oxidation, or radiation.
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Genetic Clearness Novel Strategy of Group IBacillus从发酵食品和饮料隔离种利用纤溶酶基因编码丝氨酸样酶
纤溶酶基因（fibE）中被广泛保守Bacillus属。belonging to group I species. This is encoding a serine-like enzyme (FibE) secreted in extracellular medium. This present work aims to assess the molecular usefulness of this novel conserved housekeeping gene among group IBacillus属。识别和区分传统发酵食品一些相关的菌株和饮料在刚果民主共和国。所有155株首先被筛选使用酪蛋白测定酶活性。使用特异性引物，并用16S相关RNA测序PCR技术和巢式PCR方法中使用。印迹技术已经被用于分子生物学方法比较深的执行。结果是B. amyloliquefaciens (1)，地衣芽孢杆菌（1），B. subtilis (1)，B. pumilus (3)，B. altitudinis(2),B. atrophaeus (1)，andB. safensis (3)已经特别是在发酵食品和饮料中发现了155株中鉴定。遗传分析和谷胱甘肽S-转移酶（GSTs）的过表达融合于成熟的FibE蛋白在Escherichia coliBL21 and TOP10 showed 2-fold higher enzymatic activities by comparison with FibE wild type one. Immunodetection should be associated but this does not clearly discriminateBacillus属于一组
XPF敏感癌细胞对吉西他滨的失活
Gemcitabine (2′, 2′-difluorodeoxycytidine; dFdC) is a deoxycytidine analog and is used primarily against pancreatic cancer. The cytotoxicity of gemcitabine is due to the inhibition of DNA replication. However, a mechanism of removal of the incorporated dFdC is largely unknown. In this report, we discovered that nucleotide excision repair protein XPF-ERCC1 participates in the repair of gemcitabine-induced DNA damage and inactivation of XPF sensitizes cells to gemcitabine. Further analysis identified that XPF-ERCC1 functions together with apurinic/apyrimidinic endonuclease (APE) in the repair of gemcitabine-induced DNA damage. Our results demonstrate the importance of the evaluation of DNA repair activities in gemcitabine treatment.
Netrin Family: Role for Protein Isoforms in Cancer
Netrins形成家庭分泌和膜相关蛋白。Netrins通过调节细胞迁移和存活参与轴突指导，形态发生和血管生成的过程。这些过程在肿瘤生物特别感兴趣的。从导蛋白基因的不同亚型翻译和可变剪接调控。在这里，我们回顾导蛋白家族成员和他们的癌症已知和潜在作用的亚型的多样性。
DNA连接酶IV防止复制叉失速和促进细胞增殖的三阴性乳腺癌
DNA损伤是癌症的标志，并维持基因组的保真度的蛋白质的突变和错误调节与多种癌症的发展有关。DNA双链断裂可以说是被认为是最有害的类型的DNA损伤。的非同源末端连接（NHEJ）途径是一个机制，以修复DNA双链断裂，和参与NHEJ蛋白还可调节DNA的复制。我们先前建立的，即DNA-PKcs的，一个NHEJ蛋白，促进基因组稳定性和细胞活力以下细胞暴露于复制压力;我们希望以辨别是否另一个NHEJ蛋白质，DNA连接酶IV（LIG4），股这种表型。我们的调查集中在三阴性乳腺癌细胞，相比nonbasal乳腺癌，LIG4is frequently amplified, and an increased gene dose is associated with higher Lig4 expression. We depleted Lig4 using siRNA and confirmed our knockdown by qPCR and western blotting. Cell survival diminished with Lig4 depletion alone, and this was associated with increased replication fork stalling. Checkpoint protein Chk1 activation and dephosphorylation were unchanged in Lig4-depleted cells. Lig4 depletion resulted in sustained DNA-PKcs phosphorylation following hydroxyurea exposure. Understanding the effect of Lig4 on genomic replication and the replication stress response will clarify the biological ramifications of inhibiting Lig4 activity. In addition, Lig4 is an attractive clinical target for directing CRISPR/Cas9-mediated repair towards homology-directed repair and away from NHEJ, thus understanding of how diminishing Lig4 impacts cell biology is critical.
SERPINA1基因作为治疗α-1抗胰蛋白酶缺乏
Alpha-1-antitrypsin (AAT)缺乏症是一种遗传性disorder that produces inactive/defective AAT due to mutations in the SERPINA1 gene encoding AAT. This disease is associated with decreased activity of AAT in the lungs and deposition of excessive defective AAT protein in the liver. Currently there is no specific treatment for liver disease associated with AAT deficiency. AAT lung disease is often treated with one of several serum protein replacement products; however, long-term studies of the effectiveness of SerpinA1 replacement therapy are not available, and it does not reduce liver damage in AAT deficiency. mRNA therapy could potentially target both the liver and lungs of AAT deficient patients. AAT patient fibroblasts and AAT patient fibroblast-derived hepatocytes were transfected with SERPINA1-encoding mRNA and cell culture media were tested for SerpinA1 expression. Our data demonstrates increased SerpinA1 protein in culture media from treated AAT patient fibroblasts and AAT patient fibroblast-derived hepatocytes. In vivo studies in wild type mice demonstrate SERPINA1 mRNA biodistribution in liver and lungs, as well as SerpinA1 protein expression in these two target organs which are critically affected in AAT deficiency. Taken together, our data suggests that SerpinA1 mRNA therapy has the potential to benefit patients suffering from AAT deficiency.
5-羟甲基表观遗传修饰对VEGF的稳定性和分子识别的影响的i-Motif和G-四链结构
启动子通常包含不对称G-和C-丰富股线，其中所述的胞嘧啶通过甲基（5-MC）和5-羟甲基化（5-HMC）易于表观遗传学修饰。这些序列还可以形成四股G-四（G4）或I基序（IM）的二级结构。尽管后生调制和IM / G4形成所需的序列是相似的并且可以重叠，它们不可能并存。尽管5-hmC的为5-MC的氧化产物，这两个修饰的碱基在群集不同位点。This study focuses on the intersection of G4/iM formation and 5-hmC modification using the vascular endothelial growth factor (VEGF) gene promoter’s CpG sites and examines whether incorporation of 5-hmC into iM/G4 structures had any physicochemical effect on formation, stability, or recognition by nucleolin or the cationic porphyrin, TMPyP4. No marked changes were found in the formation or stability of iM and G4 structures; however, changes in recognition by nucleolin or TMPyP4 occurred with 5-hmC modification wherein protein and compound binding to 5-hmC modified G4s was notably reduced. G4/iM structures in the VEGF promoter are promising therapeutic targets for antiangiogenic therapy, and this work contributes to a comprehensive understanding of their governing principles related to potential transcriptional control and targeting.
