程序性细胞死亡与疾病

程序性细胞死亡（PCD）是有别于病理性细胞死亡——坏死（necrosis）的一种生理性细胞死亡。目前已知,PCD在多细胞生物的发展和成年机体的代谢中均有重要作用。PCD在生物界普遍存在。近年发现PCD异常与某些疾病密切相关。PCD异常主要表现为PCD抑制和PCD过度两方面。PCD的发生由细胞的基因所控制,但是很多细胞外因素均可诱发PCD。弄清PCD在疾病发病中的作用有助于阐明疾病发病机制和探索新型疗法。1PCD与肿瘤PCD受抑制可诱发肿瘤,而通过一定方式诱发癌细胞的PCD又可有助于癌症治疗。肿瘤的发生是细胞内DNAbe变累积的结果…     

环境因子诱导的植物细胞程序性死亡

细胞发生程序性死亡（Programmed cell death,PCD）是多细胞生物用以消除多余的或有害的细胞的一种重要方式。对于植物个体来说,细胞发生程序性死亡（PCD）是抵抗逆境的一种十分有效的途径。因此,揭示环境因子诱导的植物PCD现象的分子本质就具有十分重要的现实意义。近十年来,有关环境因子诱导的植物PCD研究报道逐年增加。本文重点综述了环境因子与植物PCD相关的研究进展,并对植物PCD的主要生物学意义和研究展望进行了讨论。     

液泡信号通路依赖的细胞程序性死亡研究进展

液泡是植物细胞专一性器官之一,具有多种功能,参与细胞内环境调节和细胞解毒等过程。研究表明,液泡在植物细胞程序性死亡（programmed cell death,PCD）中具有重要作用。在液泡介导的PCD过程中,液泡加工酶（vacuolar processing enzyme,VPE）的调控和激活是PCD的关键环节。着眼于液泡信号通路依赖的PCD,对相关细胞事件和分子调控机制进行了讨论,并对未来的研究方向作了展望,以期能推进PCD机制解明。     

蛋白质聚集引起的UPS损伤及其对神经变性疾病的作用

泛蛋白－蛋白酶体系统（UPS）在细胞的质量控制上起关键作用,细胞内的蛋白质聚集能抑制UPS的机能,这或许是许多神经变性疾病神经元死亡的原因。     

胸腺细胞的选择与程序性细胞死亡

胸腺通过阳性和阴性选择作用,保留有功能的并对自身耐受的T细胞,同时通过启动程序性细胞死亡（programmedcelldeath,PCD）机制消除无功能的或对自身有反应性的T细胞。参与胸腺细胞PCD调节的因素中包括胸腺基质细胞和膜分子的作用。胸腺内细胞发生PCD的机理十分复杂。本文从两种选择中PCD出现的特点,PCD与选择作用之间的关系,以及在T细胞耐受形成中PCD的作用等方面,在细胞和分子水平上描述当前这一领域中的研究进展,并提出了若干仍需解决的关键问题。     

植物细胞程序性死亡的研究进展

细胞程序性死亡（PCD）是生物进化过程中受自身基因控制并受多种因子调控的一种细胞主动的死亡过程。PCD在植物的正常生长发育、对环境胁迫的反应和病原体入侵引发的过敏反应中起重要的作用。简要综述了植物PCD的特征、与此相关的蛋白和活性氧在PCD过程中的作用。     

辐射所致程序性细胞死亡的机制

本概述了辐射所致程序性细胞死亡（PCD）的生物形态学与生物化学特征,并重点就辐射诱发PCD机制中的信号转导元件,特征性28S rRNA的丢失,以及细胞膜和重要的癌基因及抑癌基因在PCD生成中的作用等最新进展予以讨论。     

植物细胞编程性死亡的调控

细胞编程性死亡（PCD）在植物生长发育及植物对环境的适应性方面起重要作用。文章主要从PCD相关基因,信号转导途径,蛋白酶及核酸酶等方面介绍植物细胞编程性死亡的调控。     

植物类Caspase及其调控细胞程序性死亡的研究进展

植物细胞程序性死亡（PCD）在植物生长发育和逆境适应中发挥重要作用。半胱氨酸蛋白酶（caspase）调控动物PcD的启动、执行及信号转导。通过人工合成底物、动物caspase抑制剂等方法已证实在植物中存在类caspase,可分为metacas．pases、VPEs（vacuolar processing enzymes）和saspases等。本文综述了植物类caspase的种类、结构、定位、功能及其调控PCD的研究进展,提出植物PCD中类caspase作用的调控途径,为深入研究植物PCD提供参考。     

FRET技术检测植物类caspase-3蛋白酶活性的质粒构建及其瞬时表达

植物细胞程序性死亡（programmed cell death,PCD）是一种由细胞内部程序控制的、主动的细胞死亡过程。在植物发育、逆境胁迫及超敏反应中,PCD都起着重要的作用。为检测植物PCD过程中类似动物细胞凋亡蛋白酶caspase-3的活性,构建了一个能够在活体植物细胞中实时检测类caspase-3蛋白酶激活的质粒PI—ECFP—EYFP。该质粒在植物细胞中可以表达出两端为青色荧光蛋白（ECFP）和黄色荧光蛋白（EYFP）的融合蛋白。这两个荧光蛋白通过含有caspase-3蛋白酶作用靶点DEVD的短肽相连,从而可以根据荧光共振能量转移现象检测类caspase-3凋亡蛋白酶的激活,以为实时检测植物PCD过程中关键蛋白酶的激活及其调控奠定基础。     

The ubiquitin-proteasome system in glioma cell cycle control

ABSTRACT: A major determinant of cell fate is regulation of cell cycle. Tight regulation of this process is lost during the course of development and progression of various tumors. The ubiquitin-proteasome system (UPS) constitutes a universal protein degradation pathway, essential for the consistent recycling of a plethora of proteins with distinct structural and functional roles within the cell, including cell cycle regulation. High grade tumors, such as glioblastomas have an inherent potential of escaping cell cycle control mechanisms and are often refractory to conventional treatment. Here, we review the association of UPS with several UPS-targeted proteins and pathways involved in regulation of the cell cycle in malignant gliomas, and discuss the potential role of UPS inhibitors in reinstitution of cell cycle control.     

Real-time observation of autophagic programmed cell death of<Emphasis Type="Italic"> Drosophila</Emphasis> salivary glands in vitro

Autophagy, a form of programmed cell death (PCD) that is morphologically distinguished from apoptosis, is thought to be as prevalent as apoptosis, at least during development. In insect metamorphosis, the steroid hormone 20-hydroxyecdysone (ecdysone) activates autophagic PCD to eliminate larval structures that are no longer needed. However, in comparison with apoptosis, there are not many studies on the regulation mechanisms of autophagy. To provide a useful model for studying autophagic PCD, I established an in vitro culture system that enables real-time observation of the autophagic cell destruction of Drosophila salivary glands. The new system revealed that de novo gene expression was still required for the destruction of salivary glands dissected from phanerocephalic pupae. This indicates the usefulness of the system for exploring genes that participate in the last processes of autophagic PCD.Edited by N. Satoh     

Protein homeostasis and aging: role of ubiquitin protein ligases

Protein homeostasis is fundamental in normal cellular function and cell survival. The ubiquitin-proteasome system (UPS) plays a central role in maintaining the protein homeostasis network through selective elimination of misfolded and damaged proteins. Impaired function of UPS is implicated in normal aging process and also in several age-related neurodegenerative disorders that are characterized by increased accumulation oxidatively modified proteins and protein aggregates. Growing literature also indicate the potential role of various ubiquitin protein ligases in the regulation of aging process by enhancing the degradation of either central lifespan regulators or abnormally folded and damaged proteins. This review mainly focuses on our current understanding of the importance of UPS function in the regulation of normal aging process.     

Functions of E3 Ubiquitin Ligase Hyd in Drosophila Tissues

Molecular Biology - The ubiquitin–proteasome system (UPS) is an important regulator of the main cellular processes. The components of the UPS are involved in the regulation of the cell cycle,...     

Paradoxical roles for programmed cell death signaling during viral infection of the central nervous system

Programmed cell death (PCD) is an essential mechanism of antimicrobial defense. Recent work has revealed an unexpected diversity in the types of PCD elicited during infection, as well as defined unique roles for different PCD modalities in shaping the immune response. Here, we review recent work describing unique ways in which PCD signaling operates within the infected central nervous system (CNS). These studies reveal striking complexity in the regulation of PCD signaling by CNS cells, including both protective and pathological outcomes in the control of infection. Studies defining the specialized molecular mechanisms shaping PCD responses in the CNS promise to yield much needed new insights into the pathogenesis of neuroinvasive viral infection, informing future therapeutic development.     

Early neural cell death: dying to become neurons

The importance of programmed cell death (PCD) during vertebrate development has been well established. During the development of the nervous system in particular, neurotrophic cell death in innervating neurons matches the number of neurons to the size of their target field. However, PCD also occurs during earlier stages of neural development, within populations of proliferating neural precursors and newly postmitotic neuroblasts, all of which are not yet fully differentiated. This review addresses early neural PCD, which is distinct from neurotrophic death in differentiated neurons. Although early neural PCD is observed in a range of organisms, from Caenorhabditis elegans to mouse, the role and the regulation of early neural PCD are not well understood. The regulation of early neural PCD can be inferred from the function of factors such as bone morphogenetic proteins (BMPs), Wnts, fibroblast growth factors (FGFs), and Sonic Hedgehog (Shh), which regulate both early neural development and PCD occurring in other developmental processes. Cell number control, removal of damaged or misspecified cells (spatially or temporally), and selection are the proposed roles early neural PCDs play during neural development. Data from developmental PCD in C. elegans and Drosophila provide insights into the possible signaling pathways integrating PCD with other processes during early neural development and the roles they might play.     

Programmed cell death remodels lace plant leaf shape during development

Programmed cell death (PCD) functions in the developmental remodeling of leaf shape in higher plants, a process analogous to digit formation in the vertebrate limb. In this study, we provide a cytological characterization of the time course of events as PCD remodels young expanding leaves of the lace plant. Tonoplast rupture is the first PCD event in this system, indicated by alterations in cytoplasmic streaming, loss of anthocyanin color, and ultrastructural appearance. Nuclei become terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling positive soon afterward but do not become morphologically altered until late stages of PCD. Genomic DNA is fragmented, but not into internucleosomal units. Other cytoplasmic changes, such as shrinkage and degradation of organelles, occur later. This form of PCD resembles tracheary element differentiation in cytological execution but requires unique developmental regulation so that discrete panels of tissue located equidistantly between veins undergo PCD while surrounding cells do not.