Expression, Nuclear Localization and Interactions of Human MCM/P1 Proteins

Tsuruga, Hifumi; Yabuta, Norikazu; Hashizume, Katsuhito; Ikeda, Masako; Endo, Yuichi; Nishimura, Hiroshi

doi:10.1006/bbrc.1997.6865

Cited by 53 publications

(39 citation statements)

References 22 publications

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“…The Mcm proteins are rather abundant proteins even in serum-starved resting ®broblasts (Tsuruga et al, 1997a). Thus, expression of the MCM genes may not be rate limiting for serum-starved ®broblasts to initiate DNA replication after stimulation with serum.…”

Section: Discussionmentioning

confidence: 99%

“…By using RNA probes spanning sequences upstream of HsMCM5 and HsMCM6 cDNAs, fragments with multiple sizes were protected with mRNAs from human T cell lines MT-2 and Kit 225 (Figure 2A), indicating multiple transcriptional start sites around which no typical splicing acceptor consensus sequences were found. These possible transcriptional start sites of the HsMCM5 gene clustered about 15 bp upstream of the 5' end of HsMCM5 cDNA (Tsuruga et al, 1997a). There are two sets of putative E2F binding elements arranged in an overlapping fashion in the 5'¯anking sequence of HsMCM5 cDNA.…”

Section: Hsmcm5 and Hsmcm6 Promotersmentioning

confidence: 99%

“…The Mcm proteins in S. cerevisiae are in the nucleus during G1 phase but disappear from the nucleus upon the initiation of S phase, whereas Mcm proteins in ®ssion yeast and mammalian cells are in the nucleus throughout the mitotic cell cycle. Unlike yeast, in which expression of the Mcm proteins and messages is stable during the cell cycle, mammalian cells show a dramatic induction of MCM mRNAs at G1/S boundary coupled with a signi®cant rise in protein levels upon growth stimulation such as stimulation of resting ®broblasts with serum (Tsuruga et al, 1997a). Thus, in mammalian cells, the transcriptional mechanism of expression of the MCM genes is, at least in part, central to the regulation of Mcm activities.…”

Section: Introductionmentioning

confidence: 99%

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Cell growth-regulated expression of mammalian MCM5 and MCM6 genes mediated by the transcription factor E2F

et al. 1999

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Initiation of DNA replication requires the function of MCM gene products, which participate in ensuring that DNA replication occurs only once in the cell cycle. Expression of all mammalian genes of the MCM family is induced by growth stimulation, unlike yeast, and the mRNA levels peak at G1/S boundary. In this study, we examined the transcriptional activities of isolated human MCM gene promoters. Human MCM5 and MCM6 promoters with mutation in the E2F sites failed in promoter regulation following serum stimulation and exogenous E2F expression. In addition, we identi®ed a novel E2F-like sequence in human MCM6 promoter which cooperates with the authentic E2F sites in E2F-dependent regulation. Forced expression of E2F1 could induce expression of all members of the endogenous MCM genes in rat embryonal ®broblast REF52 cells. Our results demonstrated that the growth-regulated expression of mammalian MCM5 and MCM6 genes, and presumably other MCM members, is primarily regulated by E2F through binding to multiple E2F sites in the promoters.

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Section: Discussionmentioning

confidence: 99%

Section: Hsmcm5 and Hsmcm6 Promotersmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Cell growth-regulated expression of mammalian MCM5 and MCM6 genes mediated by the transcription factor E2F

et al. 1999

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“…Six mammalian homologs of the MCM family members (MCM2 through MCM7) have been identified (reviewed in 130), all being dramatically induced by growth stimulation of serum-starved human fibroblast KD cells and rat fibroblast REF52 cells, with peaks at the G1/S boundary (91,131). Cell cycle-dependent fluctuation has been demonstrated at the mRNA level with MCM2, 4, 5 and 6, and at the protein level with Mcm6 in human epithelial HeLa and REF52 cells (91,132).…”

Section: Regulatory Machinery For Dna Replicationmentioning

confidence: 99%

“…Cell cycle-dependent fluctuation has been demonstrated at the mRNA level with MCM2, 4, 5 and 6, and at the protein level with Mcm6 in human epithelial HeLa and REF52 cells (91,132). Human MCM5, MCM6 and MCM7, and murine MCM3 have been shown to contain E2F sites in their promoters, and at least for human MCM5 and MCM6 these E2F sites are primarily responsible for the cell cycleregulated expression (67,(131)(132)(133)(134). Considering the fact that overexpression of E2F causes induction of all endogenous MCM family mRNAs in REF52 cells (67,91), it is likely that there is a common regulation by E2F.…”

Section: Regulatory Machinery For Dna Replicationmentioning

confidence: 99%

Implication of transcription factor E2F in regulation of DNA replication

Ohtani¹

1999

Front Biosci

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The transcription factor E2F plays crucial roles in induction of S phase in mammalian cells by regulating the expression of genes that encode molecules involved in cell cycle progression. E2F exerts a repressive effect on E2F-responsive genes in G0/G1 phase by associating with the retinoblastoma tumor suppressor gene product pRb and the related protein p130. This repression is relieved by phosphorylation of the pRb family proteins by G1 cyclin (cyclin D and cyclin E) -dependent kinases, resulting in expression of E2F-responsive genes in late G1 with a peak at the G1/S boundary. One group of genes influenced by E2F encode cell cycle regulatory molecules, including members of the E2F family and cyclin E, demonstrating a loop-type regulation of activities of E2F and cyclin E-dependent kinase at this stage in the cell cycle. Another group is involved in DNA replication, including genes for molecules regulating initiation of DNA replication. Overexpression of E2F is sufficient to induce DNA synthesis in serum starved fibroblasts. In addition, overexpression of cyclin E, which is essential for entry into S phase, overcomes G1 arrest caused by inhibition of E2F activity without resuming E2F mediated transcription, suggesting the mergence of the two pathways. Thus, E2F target-gene products and cyclin E-dependent kinase activity apparently co-operate to initiate replication of DNA.

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Discovery of transcription factors and other candidate regulators of neural crest development

Adams

Gammill

Bronner‐Fraser

2008

Developmental Dynamics

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Neural crest cells migrate long distances and form divergent derivatives in vertebrate embryos. Despite previous efforts to identify genes up-regulated in neural crest populations, transcription factors have proved to be elusive due to relatively low expression levels and often transient expression. We screened newly induced neural crest cells for early target genes with the aim of identifying transcriptional regulators and other developmentally important genes. This yielded numerous candidate regulators, including 14 transcription factors, many of which were not previously associated with neural crest development. Quantitative real-time polymerase chain reaction confirmed up-regulation of several transcription factors in newly induced neural crest populations in vitro. In a secondary screen by in situ hybridization, we verified the expression of >100 genes in the neural crest. We note that several of the transcription factors and other genes from the screen are expressed in other migratory cell populations and have been implicated in diverse forms of cancer.

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Expression, Nuclear Localization and Interactions of Human MCM/P1 Proteins

Cited by 53 publications

References 22 publications

Cell growth-regulated expression of mammalian MCM5 and MCM6 genes mediated by the transcription factor E2F

Cell growth-regulated expression of mammalian MCM5 and MCM6 genes mediated by the transcription factor E2F

Implication of transcription factor E2F in regulation of DNA replication

Discovery of transcription factors and other candidate regulators of neural crest development

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