共查询到16条相似文献，搜索用时 250 毫秒
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p53基因与肿瘤形成 总被引：3，自引：0，他引：3
肿瘤抑制基因的研究已经成为继癌基因之后肿瘤遗传学、分子生物学领域的前沿和热点,尤其是抑癌基因p53越来越被人们重视。研究表明正常的p53,又称野生型p53,在细胞损伤后的修复过程中发挥重要作用。正常p53的功能像"分子警察"一样监视着基因组DNA的完整性。在细胞发生DNA损伤时,p53蛋白能使细胞分裂终止在G1/S期,以使细胞有足够的时间修复损伤,恢复正常状态。若不能修复,野生型p53还能启动细胞的凋亡过程从而引发细胞的程序性死亡,阻止具有癌变倾向的突变细胞产生。而突变型p53基因会导致肿瘤的发生,大多数肿瘤与p53的突变有关。文章着重阐述了p53的表达与突变、p53的稳定调节及p53的转录调控等。 相似文献
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《中国畜牧兽医文摘》2015,(1)
对肿瘤研究最突出的成就是癌基因的发现、染色体畸变与致癌基因表达互相关系的揭示、抑癌基因的发现;癌基因分为两大类型,一是病毒癌基因,一是细胞转化基因。本文仅针对细胞转化基因,即存在于畜禽体中正常细胞中的原癌基因的突变产物,展开论述,表明畜禽肿瘤是畜禽体正常细胞中的原癌基因突变、DNA变化和不正常活动导致的。 相似文献
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野生型p53诱导的磷酸酶1（wild-type p53-induced phosphatase 1,Wip1）是蛋白磷酸酶2C （protein phosphatase type 2C,PP2C）家族中的一员,可以靶向调控机体内多种重要的信号分子,如p53、MAPK和Chk1/Chk2等,在动物细胞周期、增殖、分化、凋亡、衰老、自噬及DNA损伤修复等生理过程中发挥重要作用。Wip1基因缺失会使小鼠生殖激素水平失衡,且该基因通过ATM、Wnt、凋亡和炎症等信号通路影响精子生成过程,导致雄性动物繁殖力下降。此外,Wip1基因还可通过动态平衡调节DNA损伤反应和去磷酸化作用来影响卵母细胞和胚胎发育,从而调控雌性动物的生殖。免疫系统是机体执行免疫应答及免疫功能的重要系统,其与炎症反应和肿瘤发生有着紧密的联系。Wip1基因缺失会使病原体敏感性增强,影响T细胞、B细胞和中性粒细胞迁移及凋亡,进而导致炎症反应。作为原癌基因,Wip1基因通过调控各种信号分子影响DNA损伤修复、细胞周期进程及细胞凋亡等,参与肿瘤发生。因此,Wip1基因在动物繁殖调控和免疫调节中扮演着重要角色。目前,Wip1基因受到越来越多学者的关注,特别是其调控动物疾病发生发展的机制已成为研究热点。本研究主要综述了Wip1基因对动物繁殖及免疫的调节作用,以期为家畜育种、疾病防治及靶向治疗提供新思路。 相似文献
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【目的】 克隆郏县红牛DNA聚合酶β（DNA polymerase beta,POLB）基因,并对其进行生物信息学分析。【方法】 以郏县红牛肌肉组织cDNA为模板,通过PCR方法克隆POLB基因完整CDS区序列;利用在线软件进行遗传距离分析并构建系统进化树,分析POLB蛋白的理化性质、疏水性、磷酸化位点、跨膜结构、信号肽、二级结构、三级结构和互作蛋白。【结果】 郏县红牛POLB基因CDS区序列全长1 008 bp,编码335个氨基酸。系统进化树分析表明,郏县红牛POLB基因氨基酸序列与绵羊等反刍动物的亲缘关系最近,与其他哺乳类动物和禽类次之,与斑马鱼（鱼类）最远。郏县红牛POLB蛋白分子质量为38.26 ku,理论等电点（pI）为9.10,半衰期为30 h,不稳定系数为31.06,总平均亲水系数为－0.659,属于稳定的亲水性蛋白;磷酸化位点预测分析发现,郏县红牛POLB蛋白包含17个丝氨酸磷酸化位点、12个苏氨酸磷酸化位点和4个酪氨酸磷酸化位点;跨膜区和信号肽预测结果显示,郏县红牛POLB蛋白不属于跨膜蛋白和分泌型蛋白;二级结构和三级结构预测发现,其主要包含α-螺旋、β-转角、延伸链和无规则卷曲4种结构;在线软件预测结果表明,POLB蛋白与XRCC1、FEN1、PARP1和LIG3等为互作蛋白。【结论】 本研究成功克隆了郏县红牛POLB基因CDS序列,其与绵羊亲缘关系最近;POLB蛋白为无跨膜结构、无信号肽的亲水性蛋白,与XRCC1蛋白互作程度最高,结果可为进一步探究POLB基因生物学功能提供参考。 相似文献
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《畜牧兽医学报》2015,(5)
Plk1是真核生物中高度保守的丝氨酸/苏氨酸蛋白激酶,作为Polo样激酶家族的重要成员之一,对细胞周期具有重要的调控作用。通过磷酸化不同的特异性底物,Plk1具有促进中心体成熟及纺锤体两极分配,控制有丝分裂启动,促进染色体列队,促进胞质分裂等一系列作用。新近研究表明,Plk1还与DNA损伤应答、肿瘤形成、胚胎早期发育密切相关。本文就Plk1在细胞有丝分裂中发挥的一系列调控作用,DNA损伤发生时如何参与细胞阻滞的启动与逆转,促进DNA损伤修复,Plk1的表达异常与肿瘤发生的因果关系,以及Plk1在促进胚胎早期发育的应用前景等进行综述,以供相关研究参考。 相似文献
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胰岛素样生长因子1（IGF一1）是生长激素发挥促生长作用的重要调节因子,具有调控细胞凋亡、影响蛋白质的合成、调节骨骼肌生长和修复、保护神经系统等生物学功能。本文主要从IGF1基因的结构、生物学功能、作用机制以及发育性变化等方面做一详细综述。 相似文献
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微小RNA（microRNA,miRNA）是长度约16~29 nt的非编码RNA。其功能是通过特异性基因沉默导致靶mRNA降解,抑制蛋白质的合成或在细胞分化、发育和凋亡等关键时期调控转录后的基因表达水平。大量研究结果表明,miRNA既可作为诱癌基因参与恶性肿瘤发生和发育过程,又可作为抑癌基因参与控制恶性肿瘤的形成。迄今,试图以治疗癌症为宗旨进行miRNA的功能与癌症形成的关联性研究已成为国内外的热点课题之一。因此,作者就miRNA产生机制、miRNA的生物学功能、与癌症相关的主要miRNA和癌症治疗的展望等问题进行了概括性的论述,其目的在于为从事miRNA的功能与癌症形成关联性研究的同行提供重要的参考资料,促进该项研究取得新进展。 相似文献
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Neoplasia in both animals and humans results in part from lasting activation of tumor-promoting genes ("oncogenes") or diminished function of genes responsible for preventing neoplastic induction ("tumor suppressor genes"). The concept of "genetic addiction" has emerged to indicate that neoplastic cells cannot maintain a malignant phenotype without sustained genotypic abnormalities related to aberrant activity of oncogene(s) and/or inactivity of tumor suppressor gene(s). Interestingly, some genetic abnormalities reliably produce distinct morphologic patterns that can be used as structural signatures indicating the presence of a specific molecular alteration. Examples of such consistent genetic/microanatomic pairings have been identified for mutated oncogenes, such as rising mucin-producing capacity with RAS overexpression, and mutated tumor suppressor genes-including PTEN eliciting cell hypertrophy, RB1 dictating neuroendocrine differentiation, and TRP53 encouraging sarcomatous transformation. Familiarity with the concept of genetic addiction, as well as the ability to recognize such regular genomic-phenotypic relationships, are of paramount importance for comparative pathologists who are engaged in phenotyping genetically engineered mice to help unravel genomic intricacies in both health and disease. 相似文献
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在哺乳动物中,卵泡抑素（follistatin,FST）不仅参与生殖调控,还与肌肉生长、脂肪沉积等显著相关。为了探究该基因在成纤维细胞中的生物学功能,本研究利用二代测序技术对敲减FST基因的猪成纤维细胞进行转录组测序,筛选差异表达基因,并利用在线生物学软件对差异基因进行GO功能注释及生物学通路富集分析。结果发现,敲减FST基因后共有370个基因显著上调,287个基因显著下调。与细胞增殖、凋亡相关的HOXA6、PARP14、ZBP1、NDUFB9、RAB13、FAM83D、THBS1和BTF3基因以及与疾病相关的ZNF354C、RNF213、IFIT1、CCL5和VPS13C基因均发生了显著变化。这些差异基因共得到51个GO功能注释,生物过程分类下的生物调节、细胞过程、代谢过程、单一生物过程和细胞组分分类下的细胞器、细胞区域、细胞及分子功能分类下的黏合条目下聚集的差异基因数量最多,均>200个。共发现12条显著富集的通路,包括3条与细胞增殖相关的通路（p53信号通路、细胞周期和真核生物中核糖体的生物发生）,4条与疾病相关的通路（阿尔茨海默氏病、沙门氏菌感染、亨廷顿病和非小细胞肺癌）,2条与肌肉收缩相关的通路（血管平滑肌收缩和心肌收缩）以及泛素介导的蛋白水解作用、肌动蛋白细胞骨架的调节和缝隙连接通路。以上研究结果表明,在成纤维细胞中敲减FST基因后,与细胞增殖分化和部分疾病相关的基因和生物学通路被显著富集,暗示FST基因在成纤维细胞的创伤修复过程中发挥重要的作用。 相似文献
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C. Courtay-Cahen S. R. Platt L. De Risio M. P. Starkey 《Veterinary and comparative oncology》2008,6(3):182-192
Cytogenetic detection of unbalanced genomic aberrations in tumours is a strategy for the identification of tumour suppressor genes and oncogenes. When considered in concert with clinical data, the approach also represents a means of identifying markers of prognosis. In a preliminary investigation of the molecular basis of canine meningioma tumorigenesis, we profiled three tumours by comparative genomic hybridization. Distinct patterns of sub-chromosomal deletions were identified suggesting alternative mechanisms of tumour initiation. The deleted chromosomal segments encompass two regions (10q23.1 and 17q22-q23) that are syntenic to the chromosomes (22 and 1p) most often deleted in human meningiomas. A number of genes associated with DNA repair, cell cycle progression and apoptosis are located on both the deleted canine chromosomal segments and the syntenic regions deleted in human meningiomas. This study represents the first report of chromosomal copy number abnormalities in non-cultured canine brain tumour tissue. 相似文献
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Morrison WB 《Journal of veterinary internal medicine / American College of Veterinary Internal Medicine》2012,26(1):18-31
Rudolph Virchow first speculated on a relationship between inflammation and cancer more than 150 years ago. Subsequently, chronic inflammation and associated reactive free radical overload and some types of bacterial, viral, and parasite infections that cause inflammation were recognized as important risk factors for cancer development and account for one in four of all human cancers worldwide. Even viruses that do not directly cause inflammation can cause cancer when they act in conjunction with proinflammatory cofactors or when they initiate or promote cancer via the same signaling pathways utilized in inflammation. Whatever its origin, inflammation in the tumor microenvironment has many cancer-promoting effects and aids in the proliferation and survival of malignant cells and promotes angiogenesis and metastasis. Mediators of inflammation such as cytokines, free radicals, prostaglandins, and growth factors can induce DNA damage in tumor suppressor genes and post-translational modifications of proteins involved in essential cellular processes including apoptosis, DNA repair, and cell cycle checkpoints that can lead to initiation and progression of cancer. 相似文献
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竞争性内源RNA （competing endogenous RNA,ceRNA）假说提出具有相同短序列非编码微小（microRNA,miRNA）应答元件（microRNA response element,MRE）的转录物通过竞争的方式结合miRNA,从而影响转录物的表达水平。ceRNA假说颠覆了miRNA与靶基因单向调控的传统观念,在RNA调控网络中具有重要的生物学意义。在众多转录物中,长链非编码RNA （long non-coding RNA,lncRNA）是一类序列长度超过200个核苷酸的非编码RNA,对lncRNA的研究涉及到遗传、分子生物、基因调控、疾病（癌症、神经系统疾病等）等领域。miRNA与lncRNA形成了一个相互作用的调控网络,lncRNA可作为ceRNA抑制miRNA的功能,从而影响后续基因的表达。近年来,随着生物信息学技术的发展,科研人员发现ceRNA作用机制不仅涉及到人类癌症疾病,而且在各种复杂动物的肌细胞分化、脂肪细胞分化和颗粒细胞凋亡等生物过程中也发挥重要的调控作用。作者追溯了ceRNA调控机制,分析了ceRNA网络调控的影响因素,综述了ceRNA在不同动物中调控miRNA的研究进展,为进一步研究lncRNA与miRNA的调控网络提供参考,为畜牧业发展及复杂动物疾病治疗提供新的思路。 相似文献
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Maronpot RR 《Journal of toxicologic pathology》2009,22(1):11-33
There is a vast amount of literature related to mouse liver tumorigenesis generated over the past 60 years, not all of which has been captured here. The studies reported in this literature have generally been state of the art at the time they were carried out. A PubMed search on the topic "mouse liver tumors" covering the past 10 years yields over 7000 scientific papers. This review address several important topics related to the unresolved controversy regarding the relevance of mouse liver tumor responses observed in cancer bioassays. The inherent mouse strain differential sensitivities to hepatocarcinogenesis largely parallel the strain susceptibility to chemically induced liver neoplasia. The effects of phenobarbital and halogenated hydrocarbons in mouse hepatocarcinogenesis have been summarized because of recurring interest and numerous publications on these topics. No single simple paradigm fully explains differential mouse strain responses, which can vary more than 50-fold among inbred strains. In addition to inherent genetics, modifying factors including cell cycle balance, enzyme induction, DNA methylation, oncogenes and suppressor genes, diet, and intercellular communication influence susceptibility to spontaneous and induced mouse hepatocarcinogenesis. Comments are offered on the evaluation, interpretation, and relevance of mouse liver tumor responses in the context of cancer bioassays. 相似文献