microRNA与免疫调控

微小RNA(microRNA)又简称miRNA,是一类长约21～25个核苷酸的小分子RNA,能与特定的信使RNA靶向结合,在转录后水平调控基因表达.越来越多的证据表明,miRNA可通过靶向免疫系统中关键信号转导分子的表达,从而在多个环节上参与调控机体固有免疫反应和适应性免疫反应.已经发现,miRNA参与调节肿瘤、类风湿...     

微小RNA在肿瘤侵袭转移中的作用

微小RNA(miRNA)是一类长度为19-25个核苷酸对的非编码小分子RNA,通过与靶 mRNA互补配对而在转录水平上对基因的表达进行负调控.实验表明miRNA可通过调控其靶基因参与的信号通路,影响肿瘤的发生、发展和转移,发挥着类似原癌基因或抑癌基因的功能.因此研究miRNA在肿瘤侵袭转移调控中的作用有着重要意义.     

miRNA与lncRNA的相互调控作用在肿瘤中的研究进展

miRNA是一类具有介导基因转录后表达调控功能的非编码小分子RNA,lncRNA是碱基数大于200个核苷酸的非翻译转录本,通过基因印迹、染色质重塑、细胞周期调控等多种机制发挥其生物学功能。miRNA与lncRNA之间存在着相互调控关系,对肿瘤的发生发展以及治疗具有重要作用。     

miRNA,siRNA,saRNA与基因表达调控

近年来的研究发现,生物体内存在着大量的非编码RNA(non-coding RNAs,ncRNA),它们在染色质修饰、基因转录、RNA剪接和mRNA翻译等多种水平上参与了基因表达的调控.ncRNA中的小分子RNA如miRNA能够识别特定的目标mRNA,通过与mRNAs 3'非翻译区结合,影响mRNA转录及蛋白质翻译;siRNA是RNA干扰的引发物,能够导致与dsRNA同源的mRNA降解,进而抑制相应基因表达;saRNA是目前最新发现的一种靶向目的 基因启动子区的在转录水平激活目的基因表达的dsRNA.miRNA、siRNA和saRNA在生成机制、作用途径等方面关系密切,既区别又相互联系,小分子RNA的研究将是今后分子生物学的研究热点之一.     

微小RNAs和细胞周期

微小RNA(microRNAs,miRNAs)对细胞周期的调控已经得到证实,同时细胞周期调控依赖的转录因子(如c-MYC,E2F或P53)对miRNAs也具有调节作用,这些非编码小分子RNAs可通过扰乱关键的细胞周期调节因子而导致肿瘤的发生、发展.miRNAs作为基因表达的调节器,它的存在对于生物体的正常生长发育是非常...     

miR-155调控T细胞分化与功能的研究进展

<正>miRNA是在真核生物中发现的一类内源性具有免疫调控功能的非编码小分子RNA,长约19~24个核苷酸,由具有发夹结构的约70~90个碱基大小的单链RNA前体经Dicer酶加工而成,在转录后水平调控基因表达。miRNA主要通过与特定的靶信使RNA(mRNA)的3'非编码区直接结合,降解靶RNA或抑制其翻译,进而影响目的基因的表达[1-3]。     

MicroRNA与宫颈癌相关性的研究进展

Micro RNA(mi RNA)是一类机体内源性表达的小分子的非编码单链RNA,并参与基因转录后水平的调控。近年的研究表明,mi RNA可参与多个调节途径,由于其既可作为促癌基因引起肿瘤的发生发展,又可作为抑癌基因抑制肿瘤的侵袭转移,因此被认为可能成为一类新的肿瘤标志物及肿瘤治疗的新靶点。     

miRNA与妇科肿瘤的研究进展

miRNA是参与基因转录后水平调控的非编码内源性小分子RNA,参与细胞周期、细胞分化、生长、新陈代谢以及细胞寿命等多个生物过程。在卵巢癌、子宫颈癌和子宫内膜癌中mi RNA表达谱存在明显异常,提示其可能在调控妇科肿瘤的发生和发展中扮演着重要角色。在此阐述mi RNA的生化特征,并分析和总结mi RNA与妇科肿瘤的发生发展、诊断以及预后的关系,本文就mi RNA与妇科恶性肿瘤关系的研究进展作一综述。     

长链非编码RNA与病毒和微小非编码RNA关系的研究进展

非编码RNA,包括以miRNA、siRNA和piRNA等为代表的短小RNA和长链非编码RNA.长链非编码RNA,有别于其他小分子非编码RNA,是目前非编码RNA研究的热点.随着研究的不断推进,人们发现lncRNA与物种进化、胚胎发育、物质代谢以及肿瘤发生等都有着密切的联系.microRNA是一类长度为19～ 23个核苷酸的内源性非编码RNA,可以在转录水平或转录后水平调节基因的表达.     

MicroRNAs在卡波西肉瘤发病机制中的研究进展

MicroRNA是一类内生的、长度约20～24个核苷酸的非编码小分子RNA，广泛存在于真核生物中，其在动物和植物细胞内具有多种重要的基因调控作用，并与其配对的蛋白编码基因来指导转录后表达。     

Our changing ideas about steroid effects on an ever-changing brain

Steroid hormone actions on gene expression in the brain provide a vast array of examples of environmentally-controlled gene expression. Recent studies of steroid hormone receptors and the effects they mediate have led to new findings which change our notions about the type and speed of plastic changes which the brain is capable of undergoing. We have found that estradiol and progesterone induce dendritic spines and new synapses as well as regulate oxytocin receptors in hypothalamus, whereas adrenal steroids affect neuronal survival and dendrite structure in the hippocampus as well as regulate several neurochemical processes throughout the brain related to the diurnal rhythm and adaptation to stress. Studies of estrogen and progesterone action in the hypothalamus have also shed some light on the nature of developmentally programmed sex differences in the brain. Moreover, recent work indicates that progesterone is a versatile steroid which not only affects gene expression but also produces effects via membrane receptors which alter release of neuroactive substances, chloride flux and the distribution of oxytocin receptors of the hypothalamus.     

The vascular endothelial growth factor family; proteins which guide the development of the vasculature

The development of the vascular tree during embryogenesis involves vasculogenesis, angiogenesis and tissue-specific differentiation of endothelium which gives rise to many different vessel types. These processes are physiologically complex and are therefore difficult to study in vitro. However, the discovery of endothelial cell-specific receptors and cognate ligands has led to the generation of transgenic and knockout mouse models which have shed light on the molecular mechanisms that regulate the development of blood and lymphatic vessels during embryogenesis. Such mouse models have demonstrated that members of the vascular endothelial growth factor (VEGF) family of proteins and the VEGF receptors are critical regulators of vasculogenesis, angiogenesis and endothelial cell differentiation. The availability of purified VEGF family members and of inhibitors of these growth factors may provide a means to modulate blood vessel growth for the treatment of cancer, retinopathies and diseases of ischemia.     

Inside the microcluster: antigen receptor signalling viewed with molecular imaging tools

Over the last decade, live cell imaging has revealed the surprisingly complex orchestration of antigen receptor signalling at the immunological synapse. The imaging studies showed that one of the earliest steps in antigen receptor activation is the formation of submicroscopic clusters, which regulate the early signalling events. However, the molecular mechanisms operating inside these microclusters have remained beyond the resolution of optical microscopy. Recent development of imaging techniques that approach molecular resolution in intact cells offers a first view of the molecular processes inside these structures. Here I review the contributions of molecular imaging of the immunological synapse to our understanding of antigen receptor clustering, binding to antigens, and recruitment of signalling molecules. Finally, I provide an outlook on the future prospects of this rapidly advancing technology.     

Flies and their golden apples: the effect of dietary restriction on Drosophila aging and age-dependent gene expression

Reduced nutrient availability (dietary restriction) extends lifespan in species as diverse as yeast, nematode worms, Daphnia, Drosophila, and mammals. Recent demographic experiments have shown that moderate nutrient manipulation in adult Drosophila affects current mortality rate in a completely reversible manner, which suggests that dietary restriction in Drosophila increases lifespan through a reduction of the current risk of death rather than a slowing of aging-related damage. When examined in the light of the new demographic data, age-dependent changes in gene expression in normal and diet-restricted flies can provide unique insight into the biological processes affected by aging and may help identify molecular pathways that regulate it.     

The fine structure and innervation of the cushion veins of the human nasal respiratory mucosa

Cushion veins of the human nasal lining were studied in eight patients of both sexes ranging in age from 11 to 59 years. It was found that the subendothelial cushions were part of the tunica media and consisted of smooth muscle cells, collagen and elastic fibers and occasional fibrocytes. The muscle fibers of the cushion nearest to the endothelium were circular. They extended processes towards the endothelium through gaps in the endothelial basement membrane and formed appositional junctions with the endothelial cells. The rest of the cushion consisted of longitudinal muscle fibers. The sarcoplasm of the muscle cells was characterized by large areas filled with vesicles of various sizes. In addition, these cells possessed cytoplasmic processes which were devoid of a basement membrane and which did not show the regular structure of sarcoplasm. The subendothelial cushion possessed a rich, intrinsic nerve supply of adrenergic and cholinergic axons. It is suggested that the cushion veins regulate the drainage of the cavernous tissue and are under nervous and humoral control. The increase in girth of the subendothelial cushion is effected by contraction of the longitudinal muscle cells and probably by uptake of extracellular fluid by means of the specialized cytoplasmic processes. The single layer of circular muscle cells situated between the endothelial lining and the longitudinal musculature, may provide protection to the endothelium against distension when the cushion expands.     

骨生长因子在骨修复中的研究进展

骨代谢和损伤后的修复过程高度复杂,涉及到多种生长因子间的相互作用。骨生长因子是指可以增加骨细胞生长活性,调节骨生长、分化以及重塑等多种生物学过程的因子,在骨修复过程中具有重要作用。目前,研究较多的参与骨形成的生长因子包括骨形态发生蛋白(bone morphogenetic protein,BMPs)、转化生长因子β(transforming growth factorβ,TGF-β)、成纤维细胞生长因子(fibroblast growth factors,FGF)、血小板衍生因子(platelet-derived growth factor,PDGF)等。本研究总结国内外相关研究,综述了骨生长因子在骨修复中的作用机制及临床应用,以期为骨生长因子的临床应用提供一定的理论基础。     

Mechanisms regulating the development of the corpus callosum and its agenesis in mouse and human

The development of the corpus callosum depends on a large number of different cellular and molecular mechanisms. These include the formation of midline glial populations, and the expression of specific molecules required to guide callosal axons as they cross the midline. An additional mechanism used by callosal axons from neurons in the neocortex is to grow within the pathway formed by pioneering axons derived from neurons in the cingulate cortex. Data in humans and in mice suggest the possibility that different mechanisms may regulate the development of the corpus callosum across its rostrocaudal and dorsoventral axes. The complex developmental processes required for formation of the corpus callosum may provide some insight into why such a large number of human congenital syndromes are associated with agenesis of this structure.     

胃癌相关MicroRNA研究进展

MicroRNA简称MiRNA,是近年来的研究热点。它们是一类内源性短链非编码小分子核糖核苷酸,长度一般为19～24个核糖核苷酸。MiRNA从DNA转录后经Drosha和Dicer酶修饰后能够与靶点mRNA互补结合从而调控其靶基因的表达。越来越多的的研究证实它们在器官发育和癌症形成过程中都起到了一定的调节作用。近年来MiRNA在癌症形成以及进展中的调节作用得到了广泛的研究。其中,MiRNA在胃癌发生、发展、侵袭、转移中的作用的研究也日益增多。特别是2009年以来,这方面的文献数量有了前所未有的提高。本文目的在于对目前MiRNA分子在胃癌形成、进展、预后以及耐药等方面的作用进行综述,以便研究者能够更好地把握胃癌相关MiR-NA分子的研究进展,为将来的研究以及临床应用打下基础。     

Viruses exploit the function of epidermal growth factor receptor

Epidermal growth factor receptor (EGFR) is a receptor tyrosine kinase that regulates cellular homeostatic processes. Following ligand binding, EGFR activates different downstream signalling cascades that promote cell survival, proliferation, motility, and angiogenesis and induces F‐actin‐dependent EGFR endocytosis, which relocalises the activated receptors for degradation or recycling. The responses that are induced by ligand binding to EGFR, including cell signalling activation, protein kinase phosphorylation and cytoskeletal network rearrangement, resemble those induced by virus infection. Increasing evidence demonstrates that many viruses usurp EGFR endocytosis or EGFR‐mediated signalling for entry, replication, inflammation, and viral antagonism to the host antiviral system. In addition, viruses have acquired sophisticated mechanisms to regulate EGFR functions by interrupting the EGFR‐recycling process and modulating EGFR expression. In this review, we provide an overview of the mechanisms by which viruses alter EGFR signalling in favour of their continued survival. Copyright © 2014 John Wiley & Sons, Ltd.