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40
Characterization of E2F8, a novel E2F-like cell-cycle regulated repressor of E2F-activated transcription
- Nucleic Acids Res
, 2005
"... regulated repressor of E2F-activated transcription ..."
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regulated repressor of E2F-activated transcription
E2F1 and E2F2 Determine Thresholds for Antigen-Induced T-Cell Proliferation and Suppress Tumorigenesis
, 2001
"... E2F activity is critical for the control of the G 1 to S phase transition. We show that the combined loss of E2F1 and E2F2 results in profound effects on hematopoietic cell proliferation and differentiation, as well as increased tumorigenesis and decreased lymphocyte tolerance. The loss of E2F1 and ..."
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E2F activity is critical for the control of the G 1 to S phase transition. We show that the combined loss of E2F1 and E2F2 results in profound effects on hematopoietic cell proliferation and differentiation, as well as increased tumorigenesis and decreased lymphocyte tolerance. The loss of E2F1 and E2F2 impedes B-cell differentiation, and hematopoietic progenitor cells in the bone marrow of mice lacking E2F1 and E2F2 exhibit increased cell cycling. Importantly, we show that E2F1 and E2F2 double-knockout T cells exhibit more rapid entry into S phase following antigenic stimulation. Furthermore, T cells lacking E2F1 and E2F2 proliferate much more extensively in response to subthreshold antigenic stimulation. Consistent with these observations, E2F1/E2F2 mutant mice are highly predisposed to the development of tumors, and some mice exhibit signs of autoimmunity. E2F activity controls the transcription of a group of genes that are normally regulated at the G 1/S transition and that encode proteins important for S-phase events, including cyclin E, B-Myb, dihydrofolate reductase, DNA polymerase �, and Cdc6, a limiting component of the prereplication complex (12). E2F transcriptional activity is composed of a variety of heterodimers
Y: Robustness and backbone motif of a cancer network regulated by miR-17-92 cluster during the G1/S transition. PLoS One 2013
"... Based on interactions among transcription factors, oncogenes, tumor suppressors and microRNAs, a Boolean model of cancer network regulated by miR-17-92 cluster is constructed, and the network is associated with the control of G1/S transition in the mammalian cell cycle. The robustness properties of ..."
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Based on interactions among transcription factors, oncogenes, tumor suppressors and microRNAs, a Boolean model of cancer network regulated by miR-17-92 cluster is constructed, and the network is associated with the control of G1/S transition in the mammalian cell cycle. The robustness properties of this regulatory network are investigated by virtue of the Boolean network theory. It is found that, during G1/S transition in the cell cycle process, the regulatory networks are robustly constructed, and the robustness property is largely preserved with respect to small perturbations to the network. By using the unique process-based approach, the structure of this network is analyzed. It is shown that the network can be decomposed into a backbone motif which provides the main biological functions, and a remaining motif which makes the regulatory system more stable. The critical role of miR-17-92 in suppressing the G1/S cell cycle checkpoint and increasing the uncontrolled proliferation of the cancer cells by targeting a genetic network of interacting proteins is displayed with our model.
Transforming growth factor �-mediated transcriptional repression of c-myc is dependent on direct binding of Smad3 to a novel repressive Smad binding element
, 2004
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Elevated expression of miR-210 predicts poor survival of cancer patients: a systematic review and meta-analysis. PloS one
, 2014
"... Background: MiRNAs are important regulators of different biological processes, including tumorigenesis. MiR-210 is a potential prognostic factor for survival in patients with cancer according to previous clinical researches. We conducted a systematic review and meta-analysis to summarize the signifi ..."
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Background: MiRNAs are important regulators of different biological processes, including tumorigenesis. MiR-210 is a potential prognostic factor for survival in patients with cancer according to previous clinical researches. We conducted a systematic review and meta-analysis to summarize the significance of increased miR-210 expression in the prognosis of indicated cancers. Methodology/Principal Findings: The present systematic review and meta-analysis of 16 researches included 1809 patients with 7 different types of cancers from 7 countries, and aimed to explore the association between miR-210 expression and the survival of cancer patients. Over-expression of miR-210 may predict poor overall survival (OS, HR = 1.33, 95 % CI: 0.85– 2.09, P = 0.210), but the effect was not significant. While the predictive effect on disease-free survival (DFS, HR = 1.89, 95 % CI: 1.30–2.74, P = 0.001), progression-free survival (PFS, HR = 1.20, 95 % CI: 1.05–1.38, P = 0.007) and relapse-free survival(RFS, HR = 4.42, 95 % CI: 2.14–9.15, P = 0.000) for patients with breast cancer, primary head and neck squamous cell carcinoma (HNSCC), renal cancer, soft-tissue sarcoma, pediatric osteosarcoma, bladder cancer or glioblastoma was certain. Subgroup analysis showed the limited predictive effect of over-expressed miR-210 on breast cancer OS (HR = 1.63, 95 % CI: 0.47–5.67,
Estrogen regulation of cyclin E2 requires cyclin D1 but not c-Myc
- Mol. Cell. Biol
, 2009
"... During estrogen-induced proliferation, c-Myc and cyclin D1 initiate independent pathways that activate cyclin E1-Cdk2 by sequestration and/or downregulation of the CDK inhibitor p21Waf1/Cip1, without significant increases in cyclin E1 protein levels. In contrast, cyclin E2 undergoes a marked increas ..."
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During estrogen-induced proliferation, c-Myc and cyclin D1 initiate independent pathways that activate cyclin E1-Cdk2 by sequestration and/or downregulation of the CDK inhibitor p21Waf1/Cip1, without significant increases in cyclin E1 protein levels. In contrast, cyclin E2 undergoes a marked increase in expression, which occurs within 9 to 12 h of estrogen treatment of antiestrogen-pretreated MCF-7 breast cancer cells. Both E cyclins are important to estrogen action, as small interfering RNA (siRNA)-mediated knockdown of either cyclin E1 or cyclin E2 attenuated estrogen-mediated proliferation. Inducible expression of cyclin D1 upregu-lated cyclin E2, while siRNA-mediated knockdown of cyclin D1 attenuated estrogen effects on cyclin E2. However, manipulation of c-Myc levels did not profoundly affect cyclin E2. Cyclin E2 induction by estrogen was accompanied by recruitment of E2F1 to the cyclin E1 and E2 promoters, and cyclin D1 induction was sufficient for E2F1 recruitment. siRNA-mediated knockdown of the chromatin remodelling factor CHD8 prevented cyclin E2 upregulation. Together, these data indicate that cyclin E2-Cdk2 activation by estrogen occurs via E2F- and CHD8-mediated transcription of cyclin E2 downstream of cyclin D1. This contrasts with the predominant regulation of cyclin E1-Cdk2 activity via CDK inhibitor association downstream of both c-Myc and cyclin D1 and indicates that cyclins E1 and E2 are not always coordinately regulated. In mammalian cells, there are two E-type cyclins, cyclins E1
Liang Z. Contribution of CDP/Cux, a transcription factor, to cell cycle progression
- Acta Biochim Biophys Sin. (Shanghai
, 2007
"... Abstract CCAAT-displacement protein/Cut homeobox (CDP/Cux) was initially identified as a transcrip-tional repressor. However, a number of studies have now suggested that CDP/Cux is a transcriptional activator as well. Stable DNA binding activity of CDP/Cux is up-regulated at the G1/S transition by t ..."
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Abstract CCAAT-displacement protein/Cut homeobox (CDP/Cux) was initially identified as a transcrip-tional repressor. However, a number of studies have now suggested that CDP/Cux is a transcriptional activator as well. Stable DNA binding activity of CDP/Cux is up-regulated at the G1/S transition by two mechanisms, dephosphorylation by the Cdc25A phosphatase and proteolytic processing to generate a 110 kDa amino-truncated isoform, CDP/Cux p110. The generation of CDP/Cux p110 stimulates the expression of reporter plasmid containing the promoter sequences of some S phase-specific-genes such as DNA polymerase α gene, dihydrofolate reductase gene, carbamoyl-phosphate synthase/aspartate carbamoyl-transferase/dihydroorotase gene, and cyclin A gene. However, DNA binding activity of CDP/Cux is down-regulated at G2 phase through a binding of cyclin A-cyclin-dependent kinases1 (Cdk1) to CDP/Cux. Furthermore, another CDP/Cux isoform, CDP/Cux p75, has been found to be associated with breast tumors indicating this isoform is involved in the abnormal proliferation of tumor cells. The differences in DNA binding of CDP/Cux isoforms in S and G2 phases suggest important roles of CDP/Cux in cell cycle progression. In this review, we discuss the functions of CDP/Cux with a focus on its roles in cell cycle
iTRAQ Isobaric Tagging for Relative and Absolute
"... proteomic analysis demonstrates post-transcriptional regulation of embryonic stem cell differentiation to hematopoiesis. ..."
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proteomic analysis demonstrates post-transcriptional regulation of embryonic stem cell differentiation to hematopoiesis.
4. TITLE AND SUBTITLE Role of cdc25 Phosphatases in Cellular Immortalization
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EMBO reports
, 2000
"... S phase inhibition and its role in preventing premature mitosis ..."
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