Progress in cell cycle research最新文献

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Airway smooth muscle cell hyperplasia: a therapeutic target in airway remodeling in asthma? 气道平滑肌细胞增生:哮喘气道重塑的治疗靶点?
Progress in cell cycle research Pub Date : 2003-01-01
Alaina J Ammit, Reynold A Panettieri
{"title":"Airway smooth muscle cell hyperplasia: a therapeutic target in airway remodeling in asthma?","authors":"Alaina J Ammit,&nbsp;Reynold A Panettieri","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Severe asthma is characterized by airway remodeling due, in part, to increases in airway smooth muscle (ASM) mass. Regulation of ASM hyperplasia is considered an attractive therapeutic target for the potential treatment of airway remodeling in asthma. In order to develop anti-remodeling drugs, researchers have utilized cell culture techniques to elucidate the cellular and molecular mechanisms underlying ASM cell proliferation and to identify the critical cell cycle events that regulate ASM cell growth. Attractive lead compounds that have emerged from in vitro studies can now be examined in new animal models of airway remodeling, thus providing tools to design novel therapies to prevent or abrogate airway remodeling.</p>","PeriodicalId":79529,"journal":{"name":"Progress in cell cycle research","volume":"5 ","pages":"49-57"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24055156","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
Rheumatoid arthritis: targeting the proliferative fibroblasts. 类风湿关节炎:靶向增殖性成纤维细胞。
Progress in cell cycle research Pub Date : 2003-01-01
Ijsbrand Kramer, Auragun Wibulswas, Daniel Croft, Elisabeth Genot
{"title":"Rheumatoid arthritis: targeting the proliferative fibroblasts.","authors":"Ijsbrand Kramer,&nbsp;Auragun Wibulswas,&nbsp;Daniel Croft,&nbsp;Elisabeth Genot","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Our flexible joints are synovial joints composed of bone, hyaline cartilage, synovial membrane, ligaments and tendons. Rheumatoid arthritis is a disease that affects multiple synovial joints and involves inflammation of the synovial membrane, often resulting in loss of function due to erosion of bone and cartilage. Inflammation is accompanied by an influx of immune-competent cells and by aberrant proliferation of resident fibroblast-like synoviocytes. Accretion of fibroblasts directly contributes to joint destruction, through enhanced production of matrix-degrading enzymes, and indirectly, through excessive release of cytokines that boost the immune system. Targeting the proliferative fibroblast could facilitate regeneration of synovial joints.</p>","PeriodicalId":79529,"journal":{"name":"Progress in cell cycle research","volume":"5 ","pages":"59-70"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24055157","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
Cell cycle control in glomerular disease. 肾小球疾病的细胞周期控制。
Progress in cell cycle research Pub Date : 2003-01-01
Gunter Wolf, Stuart J Shankland
{"title":"Cell cycle control in glomerular disease.","authors":"Gunter Wolf,&nbsp;Stuart J Shankland","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Glomerular diseases are a leading caused of kidney failure. The three resident glomerular cell types respond differently to injury, which includes proliferation, hypertrophy, apoptosis and de-differentiation. Each leads to glomerular scarring, and a decline in renal function. Studies have shown that these events are critically controlled by cell cycle regulatory proteins, providing potential targets for the development of future therapeutics.</p>","PeriodicalId":79529,"journal":{"name":"Progress in cell cycle research","volume":"5 ","pages":"71-9"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24055158","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 mitotic checkpoint: a signaling pathway that allows a single unattached kinetochore to inhibit mitotic exit. 有丝分裂检查点:允许单个未附着着丝点抑制有丝分裂退出的信号通路。
Progress in cell cycle research Pub Date : 2003-01-01
Gordon K Chan, Tim J Yen
{"title":"The mitotic checkpoint: a signaling pathway that allows a single unattached kinetochore to inhibit mitotic exit.","authors":"Gordon K Chan,&nbsp;Tim J Yen","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The mitotic checkpoint is a failsafe mechanism for the cell to ensure accurate chromosome segregation during mitosis. Mutations in genes encoding essential checkpoint proteins lead to chromosome instability and promote carcinogenesis. The BUB and MAD genes are essential components of the mitotic checkpoint pathway. BUB and MAD inhibit the ubiquitin ligase activity of the Anaphase Promoting Complex/Cyclosome (APC/C) during mitosis to ensure cells with unaligned chromosomes do not prematurely enter anaphase. Two models explain how the APC/C is inhibited by the checkpoint. The Sequestration Model postulates that Mad2 and BubR1 bind and sequester Cdc20, an APC/C activator, away from APC/C so substrates whose destruction drives mitotic exit are no longer ubiquitinated. In this model, the unattached kinetochore is postulated to catalytically convert Mad2 to a form that binds Cdc20. In the Direct Inhibition Model, the Mitotic Checkpoint Complex (MCC) consisting of BubR1, Bub3, Mad2 and Cdc20 binds and inhibits the APC/C independently of the kinetochore. However, the \"wait anaphase\" signal generated by unattached kinetochores sensitizes the APC/C to prolonged inhibition by the MCC. A single unattached kinetochore is proposed to amplify the \"wait anaphase\" signal through a kinase cascade involving checkpoint kinases such as hBubR1, hBub1 and Mps1.</p>","PeriodicalId":79529,"journal":{"name":"Progress in cell cycle research","volume":"5 ","pages":"431-9"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24055423","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 contemporary drug development process: advances and challenges in preclinical and clinical development. 当代药物开发过程:临床前和临床开发的进展和挑战。
Progress in cell cycle research Pub Date : 2003-01-01
Michelle D Garrett, Mike I Walton, Edward McDonald, Ian Judson, Paul Workman
{"title":"The contemporary drug development process: advances and challenges in preclinical and clinical development.","authors":"Michelle D Garrett,&nbsp;Mike I Walton,&nbsp;Edward McDonald,&nbsp;Ian Judson,&nbsp;Paul Workman","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>We are in a new era of drug discovery, in which it is feasible to develop therapeutic agents targeted at a particular protein or biological activity in a living cell. This has been made possible by major advances in our understanding of cell and molecular biology, epitomized by the 2001 Nobel prize award for Physiology or Medicine to Lee Hartwell, Tim Hunt and Paul Nurse, who were recognised for their work on key regulators of the cell cycle. Technological advances have also played a decisive role, leading to the sequencing of the human genome and increased throughput at many stages of the drug discovery and development process. For example, developments in high throughput screening, structural biology and microarray technology are increasing the speed of drug discovery. In this chapter we focus on the long, and often difficult, pathway which leads from identification of a hit in a screen to regulatory approval of a drug for disease treatment. The emphasis in this chapter is on the development of anticancer drugs, as this is our own area of expertise and also because cancer is a disease in which the cell cycle is already a major target for therapeutic intervention. However, many of the concepts, approaches and issues are generally common to other therapeutic areas.</p>","PeriodicalId":79529,"journal":{"name":"Progress in cell cycle research","volume":"5 ","pages":"145-58"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24054408","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
Proteomic approaches for the identification of cell cycle-related drug targets. 鉴定细胞周期相关药物靶点的蛋白质组学方法。
Progress in cell cycle research Pub Date : 2003-01-01
Mark R Flory, Ruedi Aebersold
{"title":"Proteomic approaches for the identification of cell cycle-related drug targets.","authors":"Mark R Flory,&nbsp;Ruedi Aebersold","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Drugs affecting the cell cycle provide insights into mechanisms underlying cancer and suggest strategies for ablating uncontrolled growth. Essential to an understanding of the activity of such compounds is the identification of the set of proteins affected, either directly or indirectly, by the drug. The combination of novel technologies for stable isotope protein tagging, chromatographic separation, tandem mass spectrometry, and data processing is an extremely powerful means for providing such identifications and, in addition, for establishing a proteome-wide profile of all proteins whose abundance levels or phosphorylation state are affected by the drug.</p>","PeriodicalId":79529,"journal":{"name":"Progress in cell cycle research","volume":"5 ","pages":"167-71"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24054410","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 the replication licensing system in cell proliferation and cancer. 复制许可制度在细胞增殖和癌症中的作用。
Progress in cell cycle research Pub Date : 2003-01-01
S Shreeram, J Julian Blow
{"title":"The role of the replication licensing system in cell proliferation and cancer.","authors":"S Shreeram,&nbsp;J Julian Blow","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The precise duplication of chromosomal DNA during each cell cycle is essential for the maintenance of genetic stability. Failure to correctly regulate chromosomal DNA replication could lead to losses or duplication of chromosome segments. The precise duplication of chromosomes is normally achieved by correct regulation of the replication licensing system. Here we review our current knowledge of the licensing system and how this might be defective in cancer cells. We also review how detection of licensing components can be used for the diagnosis and prognosis of cancer. Finally we discuss the potential of the replication licensing system as a novel anti-cancer target.</p>","PeriodicalId":79529,"journal":{"name":"Progress in cell cycle research","volume":"5 ","pages":"287-93"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3604915/pdf/emss-50617.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24055042","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Small-molecule inhibitors of the cell cycle: an overview. 细胞周期的小分子抑制剂:综述。
Progress in cell cycle research Pub Date : 2003-01-01
Craig M Crews, J Brad Shotwell
{"title":"Small-molecule inhibitors of the cell cycle: an overview.","authors":"Craig M Crews,&nbsp;J Brad Shotwell","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Potent and selective small-molecule mediated inhibition of the cell's replication machinery remains a principal aim in the development of novel therapeutics and biological probes. Recent efforts have identified small molecules capable of arresting the cell cycle via specific interaction with a variety of intracellular protein targets. Advances in combinatorial and diversity oriented synthetic methods, coupled with a continued effort to identify sources of bioactive natural products, promise to contribute to the growing library of small-molecule inhibitors of the cell cycle.</p>","PeriodicalId":79529,"journal":{"name":"Progress in cell cycle research","volume":"5 ","pages":"125-33"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24055162","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
Inhibitors of the G2 DNA damage checkpoint and their potential for cancer therapy. G2 DNA损伤检查点抑制剂及其在癌症治疗中的潜力。
Progress in cell cycle research Pub Date : 2003-01-01
Hilary J Anderson, Raymond J Andersen, Michel Roberge
{"title":"Inhibitors of the G2 DNA damage checkpoint and their potential for cancer therapy.","authors":"Hilary J Anderson,&nbsp;Raymond J Andersen,&nbsp;Michel Roberge","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Cells normally respond to DNA damage by activating checkpoints that delay the transition from G1 to S and from G2 to M while DNA is repaired. The checkpoints thus protect cells by blocking replication of damaged DNA and segregation of damaged chromosomes. Most cancer cells have an inoperative G1 checkpoint due to p53 inactivation, and a functioning but impaired G2 checkpoint. Inhibitors of the G2 checkpoint can selectively sensitize cells with inactive p53 to killing by DNA-damaging drugs or ionizing radiation and might be useful in cancer therapy. Cell-based and target-directed screens for checkpoint inhibitors have been developed and several checkpoint inhibitors have been identified. This review describes their chemical structures, biochemical targets and cellular effects and discusses their therapeutic potential.</p>","PeriodicalId":79529,"journal":{"name":"Progress in cell cycle research","volume":"5 ","pages":"423-30"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24055422","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 peptidyl-prolyl isomerase Pin1. 肽基脯氨酸异构酶Pin1。
Progress in cell cycle research Pub Date : 2003-01-01
James D Joseph, Elisabeth S Yeh, Katherine I Swenson, Anthony R Means, Winkler
{"title":"The peptidyl-prolyl isomerase Pin1.","authors":"James D Joseph,&nbsp;Elisabeth S Yeh,&nbsp;Katherine I Swenson,&nbsp;Anthony R Means,&nbsp;Winkler","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The phospho-Ser/Thr-Pro specific prolyl-isomerase Pin1 has been implicated in multiple aspects of cell cycle regulation. It has been suggested that Pin1 function is required for both normal mitotic progression and reentry into the cell cycle from quiescence. In support of this hypothesis, numerous key regulators of G1 and mitosis have been identified as Pin1 interacting proteins. However, the cellular consequence of Pin1 binding to these proteins has rarely been rigorously characterized. In this review we focus on the role of Pin1 and its binding proteins in cell cycle regulation and the potential value of Pin1 as a therapeutic target.</p>","PeriodicalId":79529,"journal":{"name":"Progress in cell cycle research","volume":"5 ","pages":"477-87"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24054796","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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