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Progress in cell cycle research最新文献

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Cap-dependent translation and control of the cell cycle. 帽依赖的翻译和细胞周期的控制。
Progress in cell cycle research Pub Date : 2003-01-01
Patrick Cormier, Stéphane Pyronnet, Patrick Salaün, Odile Mulner-Lorillon, Nahum Sonenberg
{"title":"Cap-dependent translation and control of the cell cycle.","authors":"Patrick Cormier,&nbsp;Stéphane Pyronnet,&nbsp;Patrick Salaün,&nbsp;Odile Mulner-Lorillon,&nbsp;Nahum Sonenberg","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The control of gene expression at the translational level has emerged in the past decade as an important aspect of cell growth, proliferation and malignant transformation. Translation is primarily regulated at the initiation step, and mitogen-dependent signaling pathways converge to modulate the activity of translation initiation factors. In most tumors tested, at least one translation initiation factor is overexpressed and overexpression of translation initiation factors often provokes transformation. Malignant transformation could be caused by the increased translation of a subset of mRNAs encoding important proteins which are required for cell growth and proliferation. These mRNAs usually possess regulatory sequences that render their translation more sensitive to changes in the activity of translation initiation factors. In this chapter, we describe recent advances illustrating the importance of translation in cell cycle progression and cell transformation. Control of translation initiation may represent an excellent target for antitumor drugs.</p>","PeriodicalId":79529,"journal":{"name":"Progress in cell cycle research","volume":"5 ","pages":"469-75"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24054795","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Selective protection of normal proliferating cells against the toxic effects of chemotherapeutic agents. 正常增殖细胞对化疗药物毒性作用的选择性保护。
Progress in cell cycle research Pub Date : 2003-01-01
Khandan Keyomarsi, Arthur B Pardee
{"title":"Selective protection of normal proliferating cells against the toxic effects of chemotherapeutic agents.","authors":"Khandan Keyomarsi,&nbsp;Arthur B Pardee","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>A major problem of cancer therapy is to not kill the normal cells essential for life while killing the great majority of cancer cells. Subtle differences that arise during progression of cancer can provide novel therapies, such as targeting normal cells for protection against chemotoxicity. The increasing understanding gained by applying cellular and molecular biological techniques including expression genetics to detect molecular differences is revealing potential targets, related to cell proliferation, apoptosis, and differentiation. The quantitative differences of gene or enzyme expression between normal and tumor cells have provided the basis for drug discovery that can either reversibly target the normal cells or differentially target the tumor cells. Such differences also emphasize the need for the application of multiple drugs, with different modes of action.</p>","PeriodicalId":79529,"journal":{"name":"Progress in cell cycle research","volume":"5 ","pages":"527-32"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24054800","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Cyclin B1 and CDK1: nuclear localization and upstream regulators. 细胞周期蛋白B1和CDK1:核定位和上游调节因子。
Progress in cell cycle research Pub Date : 2003-01-01
Lisa A Porter, Daniel J Donoghue
{"title":"Cyclin B1 and CDK1: nuclear localization and upstream regulators.","authors":"Lisa A Porter,&nbsp;Daniel J Donoghue","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Formation of an active nuclear cyclin B1-CDK1 complex is a highly intricate procedure requiring many different levels of regulation. Each of these regulatory steps represents a potential target for controlling cell proliferation. Accumulation of threshold levels of cyclin B1 protein at the G2/M transition requires the cooperation of various promoter elements, possibly the activation of several transcription factors, enhanced cyclin B1 mRNA stability and, in some cases, translational activation of dormant mRNA. Binding of cyclin B1 to its inactive partner, CDK1, initiates conformational changes allowing CDK1 to alter its phosphorylation status and to become an active kinase. Lastly, the active cyclin B1-CDK1 complex must translocate to the nucleus to begin phosphorylating nuclear substrates. These phosphorylation events are necessary for mitotic onset. While cyclin B1 is capable of shuttling from the nucleus to the cytoplasm throughout interphase, mitotic onset requires phosphorylation of cyclin B1 within the CRS region, thereby enhancing import and inhibiting export of the cyclin B1-CDK1 complex. Elucidating the role of mediators controlling cyclin B1-CDK1 translocation at the onset of mitosis is essential in developing drug targets for cell cycle control.</p>","PeriodicalId":79529,"journal":{"name":"Progress in cell cycle research","volume":"5 ","pages":"335-47"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24054965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Protein deacetylases: enzymes with functional diversity as novel therapeutic targets. 蛋白质去乙酰化酶:功能多样化的酶作为新的治疗靶点。
Progress in cell cycle research Pub Date : 2003-01-01
Minoru Yoshida, Tadahiro Shimazu, Akihisa Matsuyama
{"title":"Protein deacetylases: enzymes with functional diversity as novel therapeutic targets.","authors":"Minoru Yoshida,&nbsp;Tadahiro Shimazu,&nbsp;Akihisa Matsuyama","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>It is becoming increasingly clear that reversible acetylation of proteins is a signal directly controlling the activity of key cellular regulators. The enzymes controlling protein acetylation were identified as histone acetyltransferases (HATs) and histone deacetylases (HDACs). Following the discovery of HATs and HDACs, a number of non-histone proteins have been identified as substrates for these enzymes. HDACs play important roles in transcriptional regulation and pathogenesis of cancer through removing acetyl groups from histones and other transcriptional regulators. HDAC inhibitors case cell cycle arrest, differentiation and/or apoptosis of many tumors, suggesting their usefulness for chemotherapy and differentiation therapy. Since recent studies have revealed that HDACs are structurally and functionally diverse, it should be possible to develop inhibitors specific to individual HDACs as more promising agents for cancer therapy.</p>","PeriodicalId":79529,"journal":{"name":"Progress in cell cycle research","volume":"5 ","pages":"269-78"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24055040","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The role of ATM and ATR in DNA damage-induced cell cycle control. ATM和ATR在DNA损伤诱导的细胞周期控制中的作用。
Progress in cell cycle research Pub Date : 2003-01-01
Aaron A Goodarzi, Wesley D Block, Susan P Lees-Miller
{"title":"The role of ATM and ATR in DNA damage-induced cell cycle control.","authors":"Aaron A Goodarzi,&nbsp;Wesley D Block,&nbsp;Susan P Lees-Miller","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Ataxia-Telangiectasia mutated (ATM) and ATM- and Rad3-related (ATR) are members of the phosphatidyl inositol 3-kinase-like family of serine/threonine protein kinases (PIKKs), and play important roles in the cellular response to DNA damage. Activation of ATM by ionizing radiation results in the activation of signal transduction pathways that induce cell cycle arrest at G1/S, S and G2/M. ATR is required for cell cycle arrest in response to DNA-damaging agents such as ultraviolet radiation that cause bulky lesions. This review focuses on the role of ATM and ATR in various DNA damage response pathways, and discusses the potential for targeting these pathways for the development of novel therapeutics.</p>","PeriodicalId":79529,"journal":{"name":"Progress in cell cycle research","volume":"5 ","pages":"393-411"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24055420","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The role of cytosolic phospholipase A2 in cell cycle progression. 胞质磷脂酶A2在细胞周期进程中的作用。
Progress in cell cycle research Pub Date : 2003-01-01
Johannes Boonstra, Gerda S van Rossum
{"title":"The role of cytosolic phospholipase A2 in cell cycle progression.","authors":"Johannes Boonstra,&nbsp;Gerda S van Rossum","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Cytosolic phospholipase A2 (cPLA2) cleaves fatty acids from the sn-2 position of phospholipids resulting in the release of arachidonic acid. cPLA2 is activated upon phosphorylation, followed by a Ca(2+)-dependent translocation to cellular membranes. The activity of cPLA2 has been demonstrated to fluctuate during the M, G1 and S-phases of the cell cycle, and it has been shown recently that inhibition of the relatively high activity during the initial phases of the cell cycle results in a drastic reduction in S-phase entry. These findings demonstrate that in addition to a role in the inflammatory response, cPLA2 plays also an important regulatory role in cell cycle progression.</p>","PeriodicalId":79529,"journal":{"name":"Progress in cell cycle research","volume":"5 ","pages":"181-90"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24054412","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The interaction of glycogen synthase kinase-3 (GSK-3) with the cell cycle. 糖原合成酶激酶3 (GSK-3)与细胞周期的相互作用。
Progress in cell cycle research Pub Date : 2003-01-01
W Jonathan Ryves, Adrian J Harwood
{"title":"The interaction of glycogen synthase kinase-3 (GSK-3) with the cell cycle.","authors":"W Jonathan Ryves,&nbsp;Adrian J Harwood","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>GSK-3 is a multifunctional protein kinase known to play a pivotal role in the regulation of metabolism, the cytoskeleton and gene expression. It also interacts with the cell cycle in a number of ways. GSK-3 forms part of both Wnt and Hh signalling pathways and hence controls expression of a number of cell cycle regulatory genes. Prominent among these is cyclin D1. GSK-3 also phosphorylates cyclin D1 to promote its nuclear export and subsequent degradation. In this chapter we examine how GSK-3 mediates these effects and consider how therapeutic strategies may be developed to specifically target these pathways.</p>","PeriodicalId":79529,"journal":{"name":"Progress in cell cycle research","volume":"5 ","pages":"489-95"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24054797","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Survivin in apoptosis control and cell cycle regulation in cancer. Survivin在肿瘤细胞凋亡调控和细胞周期调控中的作用。
Progress in cell cycle research Pub Date : 2003-01-01
Dario C Altieri
{"title":"Survivin in apoptosis control and cell cycle regulation in cancer.","authors":"Dario C Altieri","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Evasion of apoptosis, and the ability to proliferate uncontrollably are two of the molecular traits found perhaps in all human cancers (1). Positioned at the interface between the regulation of apoptosis and the control of cell proliferation, survivin is a recently described molecule that is expressed in most human cancers but not in normal tissues. Encouraging new studies demonstrate that it may be possible to exploit the survivin pathway for cancer diagnosis and therapy.</p>","PeriodicalId":79529,"journal":{"name":"Progress in cell cycle research","volume":"5 ","pages":"447-52"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24055425","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Polo-like kinases and the microtubule organization center: targets for cancer therapies. Polo样激酶和微管组织中心：癌症疗法的靶点。
Progress in cell cycle research Pub Date : 2003-01-01
Wei Dai, John P Cogswell
{"title":"Polo-like kinases and the microtubule organization center: targets for cancer therapies.","authors":"Wei Dai, John P Cogswell","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Studies from eukaryotic model systems, ranging from yeast to human, indicate that Polo and Polo-like kinases (Plks) are essential for the activity of the microtubule organization center. Polo/Plks localize to centrosomes or spindle pole bodies and undergo dramatic subcellular relocation during the cell cycle. Deregulated activities of Plks often result in abnormalities in centrosome duplication, maturation, and/or microtubule dynamics. Genetic and biochemical approaches have identified several candidate genes that either lie in the same pathway as POLO/PLKs or whose products are direct targets of Polo/Plks during the centrosome cycle. Recent studies have demonstrated that mammalian Plks also regulate the function of the Golgi complex, a cellular organelle closely associated with the centrosome and also having microtubule organization activity. Furthermore, deregulated expression of human PLK1 and PLK3 is strongly correlated with the development of many types of malignancies, and ectopic expression of kinase-active Plk3 or Plk1 dominant negative protein leads to rapid cell death. Given that several effective anti-tumor drugs directly interfere with microtubule dynamics, mammalian Plks are excellent targets for the development of anticancer drugs.</p>","PeriodicalId":79529,"journal":{"name":"Progress in cell cycle research","volume":"5 ","pages":"327-34"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24054964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Dynamics of the mitotic spindle--potential therapeutic targets. 有丝分裂纺锤体动力学——潜在的治疗靶点。
Progress in cell cycle research Pub Date : 2003-01-01
David T Miyamoto, Zachary E Perlman, Timothy J Mitchison, Mimi Shirasu-Hiza
{"title":"Dynamics of the mitotic spindle--potential therapeutic targets.","authors":"David T Miyamoto,&nbsp;Zachary E Perlman,&nbsp;Timothy J Mitchison,&nbsp;Mimi Shirasu-Hiza","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Inhibition of mitosis is a useful strategy for treating diseases involving excessive cell proliferation. Antimitotic drugs currently in clinical use perturb microtubule dynamics and thereby disrupt the function of the mitotic spindle. Protein regulators of microtubule dynamics and microtubule motors are also essential for mitotic spindle function. In this chapter, we evaluate the potential of these proteins as candidate targets for antimitotic drugs. We review in depth a number of proteins of particular interest, highlighting their known functions in mitosis and the effects of their inhibition on cell cycle progression.</p>","PeriodicalId":79529,"journal":{"name":"Progress in cell cycle research","volume":"5 ","pages":"349-60"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24054966","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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