长链非编码RNA分子作用机制研究进展

长链非编码RNA(Long non-coding RNA,lncRNA)是缺乏开放阅读框架,且长度大于200 nt不编码蛋白质的转录本,其绝对数量大、种类多,在表达模式上具有明显的细胞特异性.lncRNA通过碱基配对与DNA或RNA,或通过RNA高级结构与蛋白质结合,发挥多种生物学功能,共同构成了一个复杂而精细的分子调...     

长链非编码RNA及其在斑马鱼中的研究进展

随着测序技术的不断发展和完善,在人类和其他模式生物中,发现了一类具有重要调控功能的RNA,即长链非编码RNA(long non-coding RNA,lncRNA)。长链非编码RNA是一类在生物体内大量存在且无编码功能的RNA,主要参与基础转录、特异基因的转录调控、转录后调控、翻译调控和表观遗传学调控等。本文中综述了长链非编码RNA及其在水生动物斑马鱼中的研究进展,可为水产养殖动物的遗传育种和健康养殖提供参考。     

长链非编码RNA生物学特性和功能研究进展

长链非编码RNA(long non-coding RNA,lncRNA)是近年来备受关注的长度大于200 nt的内源性非蛋白编码RNA。大量资料显示其参与了哺乳动物许多重要生理、病理过程,并在其中起到非常重要的生物学作用。主要针对lncRNA的基本概念、生物学特性及主要生物学功能进行综述,为lncRNA的相关研究提供参考。     

长链非编码RNA及其在斑马鱼中的研究进展

随着测序技术的不断发展和完善,在人类和其他模式生物中,发现了一类具有重要调控功能的RNA,即长链非编码RNA(long non-coding RNA,lncRNA)。长链非编码RNA是一类在生物体内大量存在且无编码功能的RNA,主要参与基础转录、特异基因的转录调控、转录后调控、翻译调控和表观遗传学调控等。本文中综述了长链非编码RNA及其在水生动物斑马鱼中的研究进展,可为水产养殖动物的遗传育种和健康养殖提供参考。     

猪长链非编码RNA lnc-000649在PRRSV感染增殖中的作用

长链非编码RNA(lncRNA)在免疫及病毒与宿主互作中发挥重要作用.本研究在猪PAM细胞中发现一种新的猪长链非编码RNA tnc-000649,其全序列长1 483 bp.利用荧光定量PCR技术检测了猪繁殖与呼吸综合征病毒(PRRSV)感染前后PAM细胞中lnc-000649的表达水平,发现其在PRRSV感染后表达显...     

植物长链非编码 RNA 的研究进展

长链非编码 RNA（long non-coding RNA,lncRNA）是一类长度大于200个核苷酸的非编码RNA,种类很多,能够在表观遗传水平、转录水平和转录后水平调控基因表达,广泛参与生物的生长发育、抗逆、生理和病理过程。相比动物和人类,lncRNA 在植物中的研究相对较少,为深入了解植物长链非编码RNA 的作用机制和拓宽应用范围提供理论依据,对 lncRNA 的研究方法、转录表达与调控方式及其在植物生殖发育和胁迫应答方面的作用进行了综述。     

长链非编码RNA在家畜方面的研究进展

长链非编码RNA（Longnon-codingRNAS,lncRNAs）是一组长度大于200个核苷酸、缺少特异完整的开放阅读框、无蛋白质编码功能的RNA。lncRNA种类繁多,数量庞大,占哺乳动物基因组转录物的绝大部分。相对于研究较多的非编码小RNA,lncRNA的功能目前尚不完全清楚。但越来越多的研究发现,lncRNA在多个水平调控基因的表达,在胚胎发育、物种进化、细胞分化和某些疾病如神经退行性疾病的发生过程中起着重要作用。本文在简要介绍lncRNA基本概念的基础上,结合当前在家畜方面研究成果,就lncRNA在转录水平、转录后水平和表观遗传水平调控基因表达的机制做一综述。     

长链非编码RNA研究现状与趋势的文献计量分析

分析了Web of Science 2003-2012年收录的长链非编码RNA（long non-coding RNA 或long noncoding RNA, lncRNA）文献的发表时间、期刊分布、国家/地区分布、机构分布和学科分布,探讨了lncRNA文献的分布规律,评价了其研究阶段并预测了其未来发展,为我国lncRNA的相关研究提供参考。     

Formaldehyde damage to DNA and inhibition of DNA repair in human bronchial cells

Cultured bronchial epithelial and fibroblastic cells from humans were used to study DNA damage and toxicity caused by formaldehyde. Formaldehyde caused the formation of cross-links between DNA and proteins, caused single-strand breaks in DNA, and inhibited the resealing of single-strand breaks produced by ionizing radiation. Formaldehyde also inhibited the unscheduled DNA synthesis that occurs after exposure of cells to ultraviolet irradiation or to benzo[a]pyrene diolexpoxide but at doses substantially higher than those required to inhibit the resealing of x-ray-induced single-strand breaks. Therefore, formaldehyde could exert its mutagenic and carcinogenic effects by both damaging DNA and inhibiting DNA repair.     

泛素化修饰在DNA损伤修复中的功能研究进展

DNA损伤会导致基因组不稳定,从而导致正常细胞发生癌变。DNA损伤修复过程对于细胞维持基因组稳定性,防止细胞癌变有重要意义。细胞内有许多DNA损伤修复因子参与DNA损伤修复,而许多修复因子在行使修复功能时会发生翻译后修饰,其中泛素化修饰是重要的修饰方式之一。重点介绍泛素化修饰在各种DNA损伤修复途径中的研究进展,从而为相关疾病的治疗和基础研究提供相应的理论依据。     

Interfaces between the detection,signaling, and repair of DNA damage

Left unrepaired, the myriad types of damage that can occur in genomic DNA pose a serious threat to the faithful transmission of the correct complement of genetic material. Defects in DNA damage signaling and repair result in genomic instability, a hallmark of cancer, and often cause lethality, underlining the importance of these processes in the cell and whole organism. The past decade has seen huge advances in our understanding of how the signal transduction pathways triggered by DNA damage radically alter cell behavior. In contrast, it is still unclear how primary DNA damage is detected and how this interfaces with signal transduction and DNA repair proteins.     

Biological damage from intranuclear tritium: DNA strand breaks and their repair

Isotopic decay in tritiated thymidine in the DNA of frozen (-196 degrees C) Chinese hamster cells causes breaks in DNA strands to accumulate at a rate of 2.1 breaks per decay. After DNA is thawed the tritium-induced breaks repair rapidly with a half-time of 15 minutes at 37 degrees C. In comparison to breakage by x-rays, the efficiency of DNA strand breakage by tritium is equivalent to 0.48 rad per decay. This dose per decay is close to that predicted by simple dosimetric considerations (0.38 rad per decay) for irradiation by the beta particles from tritium.     

53BP1, a mediator of the DNA damage checkpoint

53BP1 binds to the tumor suppressor protein p53 and has a potential role in DNA damage responses. We used small interfering RNA (siRNA) directed against 53BP1 in mammalian cells to demonstrate that 53BP1 is a key transducer of the DNA damage checkpoint signal. 53BP1 was required for p53 accumulation, G2-M checkpoint arrest, and the intra-S-phase checkpoint in response to ionizing radiation. 53BP1 played a partially redundant role in phosphorylation of the downstream checkpoint effector proteins Brca1 and Chk2 but was required for the formation of Brca1 foci in a hierarchical branched pathway for the recruitment of repair and signaling proteins to sites of DNA damage.     

SIRT6 promotes DNA repair under stress by activating PARP1

Sirtuin 6 (SIRT6) is a mammalian homolog of the yeast Sir2 deacetylase. Mice deficient for SIRT6 exhibit genome instability. Here, we show that in mammalian cells subjected to oxidative stress SIRT6 is recruited to the sites of DNA double-strand breaks (DSBs) and stimulates DSB repair, through both nonhomologous end joining and homologous recombination. Our results indicate that SIRT6 physically associates with poly[adenosine diphosphate (ADP)-ribose] polymerase 1 (PARP1) and mono-ADP-ribosylates PARP1 on lysine residue 521, thereby stimulating PARP1 poly-ADP-ribosylase activity and enhancing DSB repair under oxidative stress.     

汉族人群聚腺苷二磷酸核糖聚合酶-1遗传多态性的检测

目的:通过检测人聚腺苷二磷酸核糖聚合酶-1(hPARP-1)7个外显子核苷酸多态性,了解在广东的汉族人群中hPARP-1基因多态性分布,为建立民族特色的DNA修复基因多态性数据提供基础资料。方法:选取在广东地区的汉族健康人群320名的基础资料及血液样本,抽提血液DNA,用PCR法扩增hPARP-1基因7个外显子,采用聚合酶链式反应(PCR)-单链构象多态性(SSCP)和银染技术检测hPARP-1基因多态性,并进行DNA序列测定。结果:在广东的汉族正常人320名血标本的7个外显子扩增产物SSCP电泳条带中,4个样本hPARP-1基因外显子17的SSCP电泳条带检出1条多态性条带,3个样本第12内含子检出1条多态性条带,其余6个外显子扩增产物SSCP电泳未见多态性条带。正常带型DNA测序结果与genebank中已知序列完全一致,第17外显子上有1种基因突变类型(T→C)。结论:在广东地区的汉族人群的hPARP-1基因第17外显子和第12内含子上可能存在多态性。     

Ubiquitin-binding protein RAP80 mediates BRCA1-dependent DNA damage response

Mutations in the breast cancer susceptibility gene 1 (BRCA1) are associated with an increased risk of breast and ovarian cancers. BRCA1 participates in the cellular DNA damage response. We report the identification of receptor-associated protein 80 (RAP80) as a BRCA1-interacting protein in humans. RAP80 contains a tandem ubiquitin-interacting motif domain, which is required for its binding with ubiquitin in vitro and its damage-induced foci formation in vivo. Moreover, RAP80 specifically recruits BRCA1 to DNA damage sites and functions with BRCA1 in G2/M checkpoint control. Together, these results suggest the existence of a ubiquitination-dependent signaling pathway involved in the DNA damage response.