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At least 127 records · Page 7Linked to original sources
PubMed1994

Dual control of myc expression through a single DNA binding site targeted by ets family proteins and E2F-1.

NIH3T3 cells expressing a mutant colony-stimulating factor-1 receptor (CSF-1R) containing a phenylalanine for tyrosine substitution in the tyrosine kinase domain at codon 809 exhibit defective myc regulation and do not enter S phase when stimulated by CSF-1. Enforced expression of either ets-1 or ets-2 in these cells restores their mitogenic response, albeit less efficiently than myc itself, suggesting that ets proteins may regulate c-myc expression. Ets-1 transactivates reporter genes driven by the human and mouse c-myc promoters through the binding site for the transcription factor E2F, the latter being required for E1A- and serum-induced c-myc expression. Analysis of E2F-1 sequences identified a minimal DNA binding domain that is related to those of ets proteins. Although E2F and ets proteins interact with similar consensus DNA binding sites, in vitro binding assays revealed that E2F can bind DNA as a homodimer, whereas ets proteins bind these sites as monomers. E2F and ets proteins do not form heterodimers in vitro and do not transactivate c-myc synergistically. Thus, E2F-1 and ets family members may independently regulate c-myc transcription through the same binding site at different times following growth factor stimulation.

Amino Acid Sequence↗
PubMed1994

Dual control of inositol transport in Saccharomyces cerevisiae by irreversible inactivation of permease and regulation of permease synthesis by INO2, INO4, and OPI1.

Uptake of inositol by Saccharomyces cerevisiae is regulated through transcriptional control of the gene that encodes the major inositol permease, ITR1 (Nikawa, J., Tsukagoshi, Y., and Yamashita, S. (1991) J. Biol. Chem. 266, 11184-11191). ITR1 mRNA abundance decreases when cells are transferred from medium without inositol to medium with inositol. Here we demonstrate that the mechanism of transcriptional regulation of ITR1 is through the action of the INO2, INO4 and OPI1 genes. INO2 and INO4 are required for derepressed levels of ITR1 mRNA, and OPI1 is necessary for repression of transcript levels in response to inositol. The INO2, INO4, and OPI1 genes thus coordinate uptake of inositol to endogenous inositol biosynthesis and to phospholipid biosynthesis. Repression of transcription of ITR1 also requires ongoing synthesis of phosphatidylcholine, defining an additional link between synthesis of phospholipids and regulation of inositol uptake. Analysis showed that the INO1 gene, encoding a key enzyme in the inositol biosynthetic pathway, responded to decreases in permease activity with a graduated increase in the level of INO1 mRNA. We also found that, in addition to the transcriptional regulation, inositol permease activity is regulated by irreversible inactivation. Inactivation of the ITR1 permease occurs in response to the presence of inositol and involves a change in the functional half-life of the protein.

Biological Transport↗
PubMed1998

Endogenous basic fibroblast growth factor is essential for cyclin E-CDK2 activity in multiple external cytokine-induced proliferation of AIDS-associated Kaposi's sarcoma cells: dual control of AIDS-associated Kaposi's sarcoma cell growth and cyclin E-CDK2 activity by endogenous and external signals.

AIDS-associated Kaposi's sarcoma (KS) cell, a key element for development of KS lesions, proliferates in response to external cytokines, such as oncostatin M, the soluble IL-6R-IL-6 complex, TNF-alpha, and IL-1beta. In addition, the KS cell-produced basic fibroblast growth factor (bFGF) was reported to function as an autocrine growth factor. However, little is known of the exact roles of these external growth factors and endogenous bFGF on proliferation of KS cells, and underlying intracellular events have remained to be defined. We obtained evidence that anti-bFGF Ab abolished growth of KS cells by preventing S phase entry of the cell cycle, even in the presence of the external growth factors. Blockade of the FGF action profoundly inhibited cyclin E expression and cyclin-dependent kinase-2 (CDK2) activity, but not D-type cyclin expression and CDK4 activity. Exogenously added acidic FGF (aFGF), which generated a rapid tyrosine phosphorylation of FGFR1 and FGFR2 on KS cells, reversed the inhibitory effects of anti-bFGF Ab. Thus, FGF actions are essential for cyclin E-CDK2 activity and S phase entry. We also observed that the presence of external growth factors markedly induced cyclin E-CDK2 activity and S phase entrance, while the addition of aFGF or bFGF alone was insufficient to induce these responses. All this evidence shows that integration of the activities of external growth factors and endogenous bFGF is required for full activation of cyclin E-CDK2 activity and KS cell proliferation.

Acquired Immunodeficiency Syndrome↗
PubMed2002

Dual adrenergic control of in vivo choline levels in the mouse major salivary glands.

1. The purpose of this study was to demonstrate that the adrenergic nervous system regulates the in vivo choline levels in the mouse major salivary glands. 2. Methoxamine (alpha1-adrenoceptor agonist, 2.5-20 mg kg-1, s.c.) elevated choline levels dose-dependently and the effect of methoxamine (10 mg kg-1) was completely inhibited by the alpha-adrenoceptor antagonist phentolamine (5 mg kg-1, i.p.) but not by the beta-adrenoceptor antagonist propranolol (3 mg kg-1, i.p.). 3. In contrast, isoprenaline (beta-adrenoceptor agonist 0.25-20 mg kg-1, s.c.) lowered choline levels and the effect of isoprenaline (2 mg kg-1) was inhibited by propranolol, but not by phentolamine. 4 Noradrenaline (1-4 mg kg-1, s.c.) manifested both the alpha- and beta-adrenergic actions depending on its dose. Noradrenaline at 1-2 mg kg-1, lowered choline levels and the effect of noradrenaline (1 mg kg-1) was inhibited by propranolol, but not by phentolamine. On the other hand, noradrenaline (4 mg kg-1) elevated choline levels and the effect was blocked by phentolamine, but not by propranolol. 5. Tyramine (5-80 mg kg-1, s.c.) elicited the release of noradrenaline from sympathetic nerve terminals and induced essentially the same effects on the choline levels as noradrenaline. Tyramine (10 mg kg-1) lowered choline levels and the effect was inhibited by propranolol, but not by phentolamine. However, tyramine (80 mg kg-1) elevated choline levels and the effect was inhibited by phentolamine, but not by propranolol. 6. These results suggest that choline levels in the salivary glands may be under separate alpha- and beta-adrenergic control and suggest a possibility that the neurotransmitter noradrenaline released for sympathetic nerve terminals can manage the dual control of choline levels in some autonomic organs in a characteristic dose-dependent manner.

Adrenergic Agonists↗
PubMed2004

A gene expression system offering multiple levels of regulation: the Dual Drug Control (DDC) system.

BACKGROUND: Whether for cell culture studies of protein function, construction of mouse models to enable in vivo analysis of disease epidemiology, or ultimately gene therapy of human diseases, a critical enabling step is the ability to achieve finely controlled regulation of gene expression. Previous efforts to achieve this goal have explored inducible drug regulation of gene expression, and construction of synthetic promoters based on two-hybrid paradigms, among others. RESULTS: In this report, we describe the combination of dimerizer-regulated two-hybrid and tetracycline regulatory elements in an ordered cascade, placing expression of endpoint reporters under the control of two distinct drugs. In this Dual Drug Control (DDC) system, a first plasmid expresses fusion proteins to DBD and AD, which interact only in the presence of a small molecule dimerizer; a second plasmid encodes a cassette transcriptionally responsive to the first DBD, directing expression of the Tet-OFF protein; and a third plasmid encodes a reporter gene transcriptionally responsive to binding by Tet-OFF. We evaluate the dynamic range and specificity of this system in comparison to other available systems. CONCLUSION: This study demonstrates the feasibility of combining two discrete drug-regulated expression systems in a temporally sequential cascade, without loss of dynamic range of signal induction. The efficient layering of control levels allowed by this combination of elements provides the potential for the generation of complex control circuitry that may advance ability to regulate gene expression in vivo.

Animals↗
PubMedDate not supplied

Analysis and design of DSP-based dual-loop controlled UPS inverters.

This paper presents a novel digital dual-loop control scheme of the PWM (Pulse width modulate) inverter. Deadbeat control technique are employed to enhance the performance. Half switching period delayed sampling and control tining strategy is used to improve the system dynamic response. Simulation and experimental results presented in the paper verified the validity of the proposed control scheme.

Computer Simulation↗