Journal of cell science. Supplement最新文献_第3页

Coupling of DNA replication and mitosis by fission yeast rad4/cut5. 裂变酵母rad4/cut5对DNA复制与有丝分裂的耦合作用。

Journal of cell science. Supplement Pub Date : 1994-01-01 DOI: 10.1242/jcs.1994.supplement_18.8

Y Saka, P Fantes, M Yanagida

{"title":"Coupling of DNA replication and mitosis by fission yeast rad4/cut5.","authors":"Y Saka, P Fantes, M Yanagida","doi":"10.1242/jcs.1994.supplement_18.8","DOIUrl":"https://doi.org/10.1242/jcs.1994.supplement_18.8","url":null,"abstract":"The fission yeast cut5+ (identical to rad4+) gene is essential for S phase. Its temperature-sensitive (ts) mutation causes mitosis while S phase is inhibited: dependence of mitosis upon the completion of S phase is abolished. If DNA is damaged in mutant cells, however, cell division is arrested. Thus the checkpoint control system for DNA damage is functional, while that for DNA synthesis inhibition is not in the cut5 mutants. Transcription of the cut5+ gene is not under the direct control of cdc10+, which encodes a transcription factor for the START of cell cycle. The transcript level does not change during the cell cycle. The protein product has four distinct domains and is enriched in the nucleus. Its level does not alter during the cell cycle. The N-domain is important for cut5 protein function: it is essential for complementation of ts cut5 mutations and its overexpression blocks cell division. Furthermore, it resembles the N-terminal repeat domain of proto-oncoprotein Ect2, which, in the C-domain, contains a regulator-like sequence for small G proteins. We discuss a hypothesis that the cut5 protein is an essential component of the checkpoint control system for the completion of DNA synthesis. The restraint of mitosis until the completion of S phase is mediated by the cut5 protein, which can sense the state of chromosome duplication and negatively interacts with M phase regulators such as cdc25 and cdc2.","PeriodicalId":77195,"journal":{"name":"Journal of cell science. Supplement","volume":"18 ","pages":"57-61"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1242/jcs.1994.supplement_18.8","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18881464","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: 26

The D-type cyclins and their role in tumorigenesis. d型细胞周期蛋白及其在肿瘤发生中的作用。

Journal of cell science. Supplement Pub Date : 1994-01-01 DOI: 10.1242/jcs.1994.supplement_18.13

G Peters

引用次数: 118

bcl-2 in cancer, development and apoptosis. Bcl-2在癌症、发展和凋亡中的作用。

Journal of cell science. Supplement Pub Date : 1994-01-01 DOI: 10.1242/jcs.1994.supplement_18.7

D M Hockenbery

引用次数: 146

G1 control in mammalian cells. 哺乳动物细胞中的G1控制。

Journal of cell science. Supplement Pub Date : 1994-01-01 DOI: 10.1242/jcs.1994.supplement_18.10

S I Reed, E Bailly, V Dulic, L Hengst, D Resnitzky, J Slingerland

引用次数: 174

The role of cdc25 in checkpoints and feedback controls in the eukaryotic cell cycle. 真核细胞周期中cdc25在检查点和反馈控制中的作用。

Journal of cell science. Supplement Pub Date : 1994-01-01 DOI: 10.1242/jcs.1994.supplement_18.11

I Hoffmann, E Karsenti

引用次数: 69

pRB, p107 and the regulation of the E2F transcription factor. pRB, p107和E2F转录因子的调控。

Journal of cell science. Supplement Pub Date : 1994-01-01 DOI: 10.1242/jcs.1994.supplement_18.12

N Dyson

{"title":"pRB, p107 and the regulation of the E2F transcription factor.","authors":"N Dyson","doi":"10.1242/jcs.1994.supplement_18.12","DOIUrl":"https://doi.org/10.1242/jcs.1994.supplement_18.12","url":null,"abstract":"Small DNA tumor viruses, such as adenovirus, encode proteins that deregulate the cell cycle. These proteins are potent transforming agents when tested in standard oncogenic assays. For adenovirus the best characterized viral oncoproteins are the early region 1A (E1A) products. Mutational studies have shown that E1A's oncogenic ability is determined primarily by its ability to bind to certain cellular proteins and interfere with their function. One of these cellular targets for E1A is the product of the retinoblastoma tumor suppressor gene, pRB. pRB is a negative regulator of cell proliferation, and its inactivation has been shown to be an important oncogenic step in the development of many human cancers. In adenovirusmediated transformation, E1A binds to pRB and inactivates it, thus functionally mimicking the loss of pRB often seen in human tumors. There is now compelling evidence to suggest that pRB regulates transcription at specific phases of the cell cycle by physically associating with key transcription factors. The best characterized target of pRB is the transcription factor E2F. The interaction of pRB and E2F leads to the inhibition of E2F-mediated transactivation. Most of the genes that are known to be controlled by E2F have key roles in the regulation of cell proliferation. During cell cycle progression, phosphorylation of pRB appears to change its conformation and E2F is released. In pathogenic settings E2F transactivation is not regulated by pRB binding. In human tumors with mutations in the retinoblastoma gene, functional pRB is absent and hence can no longer inhibit E2F activity.(ABSTRACT TRUNCATED AT 250 WORDS)","PeriodicalId":77195,"journal":{"name":"Journal of cell science. Supplement","volume":"18 ","pages":"81-7"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1242/jcs.1994.supplement_18.12","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18880759","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: 68

Pax genes in development. 发育中的Pax基因。

Journal of cell science. Supplement Pub Date : 1994-01-01 DOI: 10.1242/jcs.1994.supplement_18.5

A Mansouri, A Stoykova, P Gruss

引用次数: 81

Focal adhesion kinase: structure and signalling. 局灶黏附激酶:结构和信号传导。

Journal of cell science. Supplement Pub Date : 1994-01-01 DOI: 10.1242/jcs.1994.supplement_18.16

J T Parsons, M D Schaller, J Hildebrand, T H Leu, A Richardson, C Otey

引用次数: 86

Signal transduction by the macrophage-colony-stimulating factor receptor (CSF-1R). 巨噬细胞集落刺激因子受体(CSF-1R)信号转导。

Journal of cell science. Supplement Pub Date : 1994-01-01 DOI: 10.1242/jcs.1994.supplement_18.15

M F Roussel

{"title":"Signal transduction by the macrophage-colony-stimulating factor receptor (CSF-1R).","authors":"M F Roussel","doi":"10.1242/jcs.1994.supplement_18.15","DOIUrl":"https://doi.org/10.1242/jcs.1994.supplement_18.15","url":null,"abstract":"The macrophage-specific colony-stimulating factor 1 (CSF-1 or M-CSF) is required throughout the G1 phase of the cell cycle to regulate both immediate and delayed early responses necessary for cell proliferation. These are triggered by the binding of the growth factor to the colony-stimulating factor 1 receptor and the activation of its intrinsic tyrosine-specific protein kinase. Phosphorylation of the colony-stimulating factor 1 receptor on specific tyrosine residues enables it to bind directly to cytoplasmic effector proteins, which in turn relay receptor-induced signals through multiple-signal transduction pathways. The activity of p21ras as well as transcription factors of the ets gene family appears to be required for colony-stimulating factor 1 to induce the c-myc gene, and the latter response is essential to ensure cell proliferation. Genes within the fos/jun or activator protein 1 family are targeted via a parallel and independently regulated signal transduction pathway. The continuous requirement for colony-stimulating factor 1 after the immediate early response is initiated indicates that expression of additional delayed early response genes, although contingent on previously induced gene products, might also depend on colony-stimulating factor 1-induced signals. Among the growth factor-regulated delayed early response genes are D-type G1 cyclins, which play an important role in cell-cycle progression.","PeriodicalId":77195,"journal":{"name":"Journal of cell science. Supplement","volume":"18 ","pages":"105-8"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1242/jcs.1994.supplement_18.15","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18881548","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: 41

Structure and function of SH2 domains. SH2结构域的结构和功能。

Journal of cell science. Supplement Pub Date : 1994-01-01 DOI: 10.1242/jcs.1994.supplement_18.14

L E Marengere, T Pawson

引用次数: 57