{"title":"Coordinate regulation of cell cycle and apoptosis during myogenesis.","authors":"K Walsh","doi":"10.1007/978-1-4615-5371-7_5","DOIUrl":"https://doi.org/10.1007/978-1-4615-5371-7_5","url":null,"abstract":"<p><p>During myogenesis, precursor cells irreversibly withdraw from the cell cycle as they differentiate into mature myotubes. The state of myocyte differentiation also influences the propensity of these cells to undergo apoptosis. Proliferative precursor cells are far more susceptible to apoptotic cell death than are terminally differentiated myotubes. The upregulation of the cdk inhibitor p21 and the dephosphorylation of pRb are critical regulatory events that establish both the post-mitotic and apoptosis-resistant states. The coordinate regulation of cell proliferation and death provides the organism with a mechanism to control the deposition of muscle mass during embryonic development.</p>","PeriodicalId":79529,"journal":{"name":"Progress in cell cycle research","volume":"3 ","pages":"53-8"},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20473799","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}
{"title":"Contribution of the dual coding capacity of the p16INK4a/MTS1/CDKN2 locus to human malignancies.","authors":"C J Larsen","doi":"10.1007/978-1-4615-5371-7_9","DOIUrl":"https://doi.org/10.1007/978-1-4615-5371-7_9","url":null,"abstract":"<p><p>During the three last years, the so-called p16 locus on human chromosome band 9p21 has been increasingly implicated in different cancers by a variety of alterations abolishing both copies of the p16INK4a/MTS1/CDKN2 gene and the adjacent p15INK4b gene, two members of a family of specific inhibitors of the cyclin D 1-3-CDK4/6 complexes that control cell cycle progression of the G1 to S phase. While these properties are characteristic of tumor suppressor genes, abundant experimental data have clearly identified a link between the loss of function of p16INK4a and tumorigenic processes. The role of p15INK4b alterations in the onset of natural and experimental tumors is less obvious. New light may be shed on the role of the p16 locus in tumor development by the recent finding that an alternative transcript from the p16INK4a gene encodes p19ARF, a negative regulator of cell cycle progression which is unrelated to p16 and p15 and does not act by binding any CDK. Hence, this protein appears to be an element of a novel negative cell cycle control mechanism, whose impairing might be involved in tumorigenesis.</p>","PeriodicalId":79529,"journal":{"name":"Progress in cell cycle research","volume":"3 ","pages":"109-24"},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20473803","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}
{"title":"Regulation of p34cdc2/cyclinB H1 and NIMA kinases during the G2/M transition and checkpoint responses in Aspergillus nidulans.","authors":"X S Ye, S A Osmani","doi":"10.1007/978-1-4615-5371-7_17","DOIUrl":"https://doi.org/10.1007/978-1-4615-5371-7_17","url":null,"abstract":"<p><p>In A. nidulans, activation of both p34cdc2/cyclinB H1 and NIMA kinases is required to initiate mitosis. These two kinases are regulated at several levels during interphase and are activated independently as protein kinases during G2. They are also targeted for negative regulation, to prevent mitosis by mitotic entry checkpoint controls, when DNA is not replicated or is damaged. Then, to initiate mitosis, they promote each other's mitotic functions to coordinately promote mitosis upon completion of interphase events. In addition, inactivation of both kinases by mitotic specific proteolysis is also required for progression through mitosis into G1.</p>","PeriodicalId":79529,"journal":{"name":"Progress in cell cycle research","volume":"3 ","pages":"221-32"},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20474375","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}
{"title":"Cell cycle regulation of S phase entry in Saccharomyces cerevisiae.","authors":"S Piatti","doi":"10.1007/978-1-4615-5371-7_12","DOIUrl":"https://doi.org/10.1007/978-1-4615-5371-7_12","url":null,"abstract":"<p><p>Eukaryotic DNA replication is restricted to a narrow window of the cell cycle called S phase, and occurs once and only once during each cell cycle. The combination of genetic and biochemical approaches in the budding yeast Saccharomyces cerevisiae has proven extremely helpful for studying the cell cycle regulation of S phase entry. This review will try to summarise the most recent discoveries which led to a new model to explain how entry into S phase is regulated in eukaryotic cells.</p>","PeriodicalId":79529,"journal":{"name":"Progress in cell cycle research","volume":"3 ","pages":"143-56"},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/978-1-4615-5371-7_12","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20473754","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}
{"title":"Organisation and functional regulation of the centrosome in animal cells.","authors":"A Paoletti, M Bornens","doi":"10.1007/978-1-4615-5371-7_23","DOIUrl":"https://doi.org/10.1007/978-1-4615-5371-7_23","url":null,"abstract":"<p><p>Molecular characterisation of centrosomal components is slowly progressing. Recent results indicate that the major aspects of centrosome-mediated microtubule nucleation may soon be understood at the molecular level. In contrast, centrosome reproduction, which is an important aspect of animal cell division, remains terra incognita. The most challenging issue for the future is to understand the molecular mechanisms which control centrosome biogenesis. There is a urgent need to identify with certainty proteins implicated in this process. Comparison between organisms with structurally different centrosomes might be critical for a better understanding of centrosome duplication if a general mechanism has been conserved throughout evolution.</p>","PeriodicalId":79529,"journal":{"name":"Progress in cell cycle research","volume":"3 ","pages":"285-99"},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20474296","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}
{"title":"Aberrations of the G1- and G1/S-regulating genes in human cancer.","authors":"J Bartkova, J Lukas, J Bartek","doi":"10.1007/978-1-4615-5371-7_16","DOIUrl":"https://doi.org/10.1007/978-1-4615-5371-7_16","url":null,"abstract":"<p><p>Deregulated cell proliferation is the hallmark of cancer, and convergent data from the fields of cell-cycle research and molecular oncology have revealed the key role played by abnormalities of the cell-cycle control genes in multistep tumorigenesis. Along with the p53-mediated DNA damage checkpoint, the G1-governing pathway of D-type cyclins, their partner cyclin-dependent kinases (Cdk), Cdk inhibitors, and the retinoblastoma protein constitute a functional unit and prominent oncogenic target. We have learned a great deal about the molecular basis of G1 phase progression and G1/S transition, their proto-oncogenic defects, and potential clinical significance including diagnostic and prognostic applications and new approaches to gene therapy of cancer.</p>","PeriodicalId":79529,"journal":{"name":"Progress in cell cycle research","volume":"3 ","pages":"211-20"},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20474374","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}
{"title":"Myt1: a Wee1-type kinase that phosphorylates Cdc2 on residue Thr14.","authors":"A Fattaey, R N Booher","doi":"10.1007/978-1-4615-5371-7_18","DOIUrl":"https://doi.org/10.1007/978-1-4615-5371-7_18","url":null,"abstract":"<p><p>Most somatic cell division cycles contain a gap period (G2 phase) between the completion of DNA synthesis and the initiation of mitosis. This delay of mitotic entry is controlled, at least in part, by the repression of Cdc2 kinase activity by the phosphorylation of two conserved residues (Thr14 and Tyr15) within the ATP-binding pocket of the Cdc2 catalytic subunit. The kinases responsible for these two phosphorylation events include the Myt1 and Wee1 kinases, which phosphorylate Cdc2 on Thr14 and Tyr15, respectively. In this discussion, we summarise our current knowledge of the Myt1 kinase and its regulation of Cdc2 kinase activity during the G2-to -M phase transition.</p>","PeriodicalId":79529,"journal":{"name":"Progress in cell cycle research","volume":"3 ","pages":"233-40"},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20474376","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}
{"title":"Regulation of cell division in plants: an Arabidopsis perspective.","authors":"V Mironov, M Van Montagu, D Inzé","doi":"10.1007/978-1-4615-5371-7_3","DOIUrl":"https://doi.org/10.1007/978-1-4615-5371-7_3","url":null,"abstract":"<p><p>Considerable progress has been achieved in the identification and molecular characterisation of genes and/or cDNAs coding for cyclin-dependent kinases (CDK) as well as cyclins in diverse plant species including Arabidopsis thaliana. Their transcriptional control during the cell cycle progression and the response to developmental cues and environmental signals has been studied in much detail, although the transcription factors mediating this regulation have yet to be identified. Experimental evidence has validated the involvement of CDKs and cyclins in cell division control in Arabidopsis and has revealed differential activation of two Arabidopsis CDKs in the course of the cell cycle. Finally, the first active CDK/cyclin pairs are being characterised, providing the basis for elucidation of their specific functions in cell cycle control and for unravelling the mechanisms that control their activity.</p>","PeriodicalId":79529,"journal":{"name":"Progress in cell cycle research","volume":"3 ","pages":"29-41"},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/978-1-4615-5371-7_3","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20476588","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}
{"title":"DNA damage checkpoints: implications for cancer therapy.","authors":"P M O'Connor, S Fan","doi":"10.1007/978-1-4615-5873-6_16","DOIUrl":"https://doi.org/10.1007/978-1-4615-5873-6_16","url":null,"abstract":"<p><p>DNA damage evokes a complex array of cellular responses, including cycle arrest in late G1 and/or G2 phases, and delayed progression through S phase. Arrest at these points in the cell cycle is governed, in large part, by a series of control systems, commonly termed \"checkpoints\". Activation of these checkpoints tends to protect cells from DNA damage by providing cells additional time to complete DNA repair. We discuss the impact of these DNA damage checkpoints on the chemosensitivity of human cancer cells. We focus on some of the complexities of the p53-dependent G1 checkpoint and review some recently discovered vulnerabilities in p53 disrupted cells that might be pharmacologically exploited for cancer treatment.</p>","PeriodicalId":79529,"journal":{"name":"Progress in cell cycle research","volume":"2 ","pages":"165-73"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20474694","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}
P Loyer, G Ilyin, S Cariou, D Glaise, A Corlu, C Guguen-Guillouzo
{"title":"Progression through G1 and S phases of adult rat hepatocytes.","authors":"P Loyer, G Ilyin, S Cariou, D Glaise, A Corlu, C Guguen-Guillouzo","doi":"10.1007/978-1-4615-5873-6_4","DOIUrl":"https://doi.org/10.1007/978-1-4615-5873-6_4","url":null,"abstract":"<p><p>Regenerating liver, hepatocyte primary cultures and differentiated hepatoma cell lines are widely used to study the proliferation/differentiation/apoptosis equilibrium in liver. In hepatocytes, priming factors (TNF alpha, IL6) target G0/G1 transition while growth factors (HGF, EGF, TGF alpha) control a mid-late G1 restriction point. A characteristic pattern of cdk/cyclin expression is observed in hepatocytes, presumably related to their ability to proliferate a limited number of times and to undergo a reversible differentiation. Interestingly, cell-cell interactions between hepatocytes and liver biliary cells in co-cultures, result in a cell cycle arrest in mid G1 of hepatocytes which are insensitive to mitogens. Apoptosis exists in hepatocytes but is still poorly documented. However, hepatoma cell lines stimulated by TGF beta undergo cell death in a p53-independent pathway. In conclusion, the interplay of growth and apoptosis regulators and cell-cell interactions control the proliferation/differentiation/apoptosis balance which is a specific feature of hepatocytes.</p>","PeriodicalId":79529,"journal":{"name":"Progress in cell cycle research","volume":"2 ","pages":"37-47"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/978-1-4615-5873-6_4","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20473990","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}