细胞凋亡信号传导通路的研究进展

细胞凋亡是机体维持自身稳定的一种基本生理机制,是有许多基因产物及细胞因子参与的一种有序的细胞自我消亡形式。细胞凋亡发生过程的启动和进行受到精确调控,具有独特而复杂的信号系统。各种凋亡信号通过信号传导通路传至细胞内,激活靶分子而产生细胞效应,引发细胞凋亡。一般认为,细胞凋亡存在3条主要通路:线粒体通路、内质网通路和死亡受体通路,各通路间互相联系,共同调节细胞凋亡。     

猪蛋白编码基因3''UTR中IRPRE1元件的鉴定及其基因特征分析

为鉴定猪全基因组范围内蛋白编码基因3'UTR(3'–untranslated region)中反向重复PRE1(inverted repeated PRE1,IRPRE1)元件,对猪全基因组的22342个蛋白编码基因的3'UTR序列进行重复序列元件的生物信息学分析。结果表明:猪蛋白编码基因的3'UTR序列中短散在重复序列与简单重复序列在重复序列的类别中所占比例较高,分别为27.58%与31.08%;在SINE/t RNA的重复元件中,Pre0_SS和PRE1x元件所占的比例较高,分别为41.83%和37.51%;共有1 094个候选蛋白编码基因的3'UTR中含有IRPRE1元件;GO分析发现这些候选基因主要参与m RNA经由剪接体的剪接、细胞分裂、RNA通过酯交换反应发生的剪接、T细胞激活、RNA剪接、T细胞受体信号通路、对糖苷反应、甘油三酯稳态、外源性凋亡信号通路的正调节及胆固醇合成等生物过程;KEGG pathway分析发现这些候选基因参与了缬草碱、亮氨酸和异亮氨酸降解途径、TNF信号通路、T细胞受体信号通路、RIG–I样受体信号通路、吞噬体、剪接体、胆汁分泌、甲状腺激素合成和凋亡;对3个蛋白编码基因的3'UTR中的IRPRE1元件进行鉴定发现,其在多个组织中广泛表达。     

哺乳动物颗粒细胞凋亡研究进展

细胞凋亡是雌性生殖系发育过程中的一个重要组成部分,在哺乳动物中,超过99%的雌性生殖细胞都会在卵子发生的不同阶段发生凋亡.目前,在颗粒细胞凋亡过程中至少发现5个配体受体系统:TNFa和TNF受体系统,Fas配体受体系统,TRAIL和TRAIL受体系统,APO-3配体受体系统,PFG-5配体受体系统,而且发现颗粒细胞凋亡属于依赖于线粒体凋亡信号传导凋亡途径.     

杆状病毒细胞凋亡抑制基因的研究进展

细胞凋亡是多细胞生物为维持自身的正常机能而产生的细胞自杀性行为，杆状病毒为维持自身的生长繁殖而产生了对抗细胞凋亡的基因p35和iap，二者分别作用于细胞凋亡途径的不同部位，以抑制细胞的凋亡。近年来人们对这两种基因的蛋白结构及作用机制等方面进行了大量的研究，对它们的作用机制有了进一步的了解，为其今后在医学及分子生物学等方面的应用打下了基础。     

动物细胞凋亡与疾病的发生

细胞凋亡和细胞坏死是细胞死亡的两种形式，前者属于生理性的平衡机制，后者则是由于致病因子作用下发生的病理过程。免疫系统抑制与细胞凋亡有关，在免疫系统中存在两种细胞程序性死亡，一种是在无生长因子时，Bcl-2基因调控的程序化死亡；另一种是细胞毒介导的靶细胞的程序化死亡。细胞凋亡是动物机体对病毒侵入的一种防御机制之一，当细胞凋亡和细胞增殖平衡破坏时，可引起多种疾病的发生。     

凋亡与自噬性死亡

细胞凋亡是一种由基因控制的自主性死亡过程，而自噬也被认为是非凋亡形式的程序性细胞死亡的方式。本文综述了凋亡、自噬的特征、机制及其联系。     

dSarm/Sarm1 is required for activation of an injury-induced axon death pathway

Axonal and synaptic degeneration is a hallmark of peripheral neuropathy, brain injury, and neurodegenerative disease. Axonal degeneration has been proposed to be mediated by an active autodestruction program, akin to apoptotic cell death; however, loss-of-function mutations capable of potently blocking axon self-destruction have not been described. Here, we show that loss of the Drosophila Toll receptor adaptor dSarm (sterile α/Armadillo/Toll-Interleukin receptor homology domain protein) cell-autonomously suppresses Wallerian degeneration for weeks after axotomy. Severed mouse Sarm1 null axons exhibit remarkable long-term survival both in vivo and in vitro, indicating that Sarm1 prodegenerative signaling is conserved in mammals. Our results provide direct evidence that axons actively promote their own destruction after injury and identify dSarm/Sarm1 as a member of an ancient axon death signaling pathway.     

细胞凋亡与细胞色素C

细胞凋亡是动植物最基本的生命活动,是一个有一系列酶参与的,并且由基因控制的主动的、高度有序的死亡过程。线粒体除了为细胞提供能量外,在细胞凋亡中也起着中心调控作用。研究发现,线粒体释放的细胞色素C是细胞凋亡过程的关键因素,已是近些年研究的热点。本文就细胞色素C从线粒体释放的机制及在凋亡中的作用进行综述。     

皮肤鳞状细胞癌和基底细胞癌中FADD、Caspase-3的表达与细胞凋亡的关系

目的:探讨皮肤鳞状细胞癌(简称鳞癌)、基底细胞癌(简称基癌)组织中FADD、caspase-3(简称casp-3)的表达及其与细胞凋亡的关系。方法:应用原位末端标记(TUNEL)和SABC免疫组化技术检测48例鳞癌、41例基癌中FADD、casp-3表达及细胞凋亡。结果:鳞癌中FADD、casp-3表达及凋亡指数(A I)均明显高于基癌(P<0.01),两种表皮肿瘤的FADD、casp-3表达与A I均呈正相关(r=0.521,P<0.05),FADD与casp-3之间的表达亦呈正相关(r=0.437,P<0.05)。低分化鳞癌中的casp-3表达和A I低于高分化者(P<0.05),鳞癌原发灶中的A I高于转移灶(P<0.01)。结论:Fas凋亡途径可能是鳞癌、基癌的主要凋亡途径,FADD、casp-3是鳞癌、基癌细胞凋亡中重要的促凋亡因子,并有相互协同促凋亡作用。     

Prevention of apoptosis by a baculovirus gene during infection of insect cells

Programmed cell death is an active process of self destruction that is important in both the development and maintenance of multicellular animals. The molecular mechanisms controlling activation or suppression of programmed cell death are largely unknown. Apoptosis, a morphologically and biochemically defined type of programmed cell death commonly seen in vertebrates, was found to be initiated during baculovirus replication in insect cells. A specific viral gene product, p35, was identified as being responsible for blocking the apoptotic response. Identification of the function of this gene will allow further definition of the molecular pathways involved in the regulation of programmed cell death and may identify the role of apoptosis in invertebrate viral defense systems.     

Programmed cell death of T cells signaled by the T cell receptor and the alpha 3 domain of class I MHC

As well as being activated or rendered unresponsive, mature T lymphocytes can be deleted, depending on the signals received by the cell. Deletion by programmed cell death (apoptosis) is triggered if a T cell that has received a signal through its T cell receptor complex also receives a signal through the alpha 3 domain of its class I major histocompatibility complex (MHC) molecule. Such a signal can be delivered by a CD8 molecule, which recognizes the alpha 3 domain, or by an antibody to this domain. Precursors of both cytotoxic T lymphocytes (CTL's) and T helper cells are sensitive to this signal but become resistant at some point before completing differentiation into functioning CTL's or T helper cells. Because CTL's carry CD8, they can induce cell death in T cells that recognize them. This pathway may be important in both removal of autoreactive T cells and immunoregulation.     

雌激素和雄激素对鸡成骨细胞增殖、凋亡、细胞周期及其受体mRNA转录的影响

为探讨雌激素和雄激素对鸡胚额骨成骨细胞(OB)增殖、凋亡、细胞周期及其受体mRNA转录的影响,用雌激素(17β雌二醇)和雄激素(十一酸睾酮)单独以及联合处理鸡胚额骨成骨细胞,MTT法测定细胞增殖率,流式细胞仪检测细胞凋亡和细胞周期的变化,荧光定量PCR检测成骨细胞中雌激素受体(ER)及雄激素受体(AR)mRNA的转录。结果显示:一定浓度的雌激素或雄激素在24h内均能促进成骨细胞的增殖,促进成骨细胞的细胞周期进程,但对细胞凋亡无明显作用。雌激素单独或联合雄激素作用能上调ERmRNA的转录,对ARmRNA的转录无明显作用。     

CCD摄像机内外部参数快速准确的标定方法

导出了一种ＣＣＤ摄像机的成像模型，给出了一种基于这种模型的ＣＣＤ摄像机内部、外部参数标定方法，该方法的特点是无需迭代，且精度高。     

酪氨酸蛋白激酶受体c-Met及靶点药物研究进展

酪氨酸激酶受体c-Met在细胞的代谢、分化以及死亡细胞的信号传导过程中起着重要的作用,其与配体结合,可活化其信号通路,参与胚胎发育、组织损伤修复以及肿瘤的发生和发展。因而,以酪氨酸激酶受体c-Met为靶点的抗肿瘤药物已经成为肿瘤研究中十分活跃的领域,为抗肿瘤治疗提供了新方法。     

利用花粉管通道法将外源DNA导入水稻之研究进展

外源DNA直接导入技术以DNA片断杂交假说为理论基础,直接将目的基因或带有目的性状供体遗传物质(总DNA)通过花粉管通道法导入水稻植株,创造大量的变异材料,通过筛选获得目的性状的后代和新品种。由于简单、易行、不受受体植物种类的限制,已被越多的育种者所接受,在水稻的抗病、米质、丰产性上等各方面广为应用。介绍了外源DNA导入方法、外源基因导入类型、后代遗传变异特点及影响花粉管通道法导入的因素,优点、局限性进行了分析,同时提出了问题和展望。     

The PIDDosome, a protein complex implicated in activation of caspase-2 in response to genotoxic stress

Apoptosis is triggered by activation of initiator caspases upon complex-mediated clustering of the inactive zymogen, as occurs in the caspase-9-activating apoptosome complex. Likewise, caspase-2, which is involved in stress-induced apoptosis, is recruited into a large protein complex, the molecular composition of which remains elusive. We show that activation of caspase-2 occurs in a complex that contains the death domain-containing protein PIDD, whose expression is induced by p53, and the adaptor protein RAIDD. Increased PIDD expression resulted in spontaneous activation of caspase-2 and sensitization to apoptosis by genotoxic stimuli. Because PIDD functions in p53-mediated apoptosis, the complex assembled by PIDD and caspase-2 is likely to regulate apoptosis induced by genotoxins.     

Regulation of an ATG7-beclin 1 program of autophagic cell death by caspase-8

Caspases play a central role in apoptosis, a well-studied pathway of programmed cell death. Other programs of death potentially involving necrosis and autophagy may exist, but their relation to apoptosis and mechanisms of regulation remains unclear. We define a new molecular pathway in which activation of the receptor-interacting protein (a serine-threonine kinase) and Jun amino-terminal kinase induced cell death with the morphology of autophagy. Autophagic death required the genes ATG7 and beclin 1 and was induced by caspase-8 inhibition. Clinical therapies involving caspase inhibitors may arrest apoptosis but also have the unanticipated effect of promoting autophagic cell death.     

p53- and ATM-dependent apoptosis induced by telomeres lacking TRF2

Although broken chromosomes can induce apoptosis, natural chromosome ends (telomeres) do not trigger this response. It is shown that this suppression of apoptosis involves the telomeric-repeat binding factor 2 (TRF2). Inhibition of TRF2 resulted in apoptosis in a subset of mammalian cell types. The response was mediated by p53 and the ATM (ataxia telangiectasia mutated) kinase, consistent with activation of a DNA damage checkpoint. Apoptosis was not due to rupture of dicentric chromosomes formed by end-to-end fusion, indicating that telomeres lacking TRF2 directly signal apoptosis, possibly because they resemble damaged DNA. Thus, in some cells, telomere shortening may signal cell death rather than senescence.