FCS 9013 PDF

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Zulkigul Fuel Activator Chemical Corporation. Advanced America PetroProducts Inc. Apex Oil Company, Inc. LY did not inhibit induction of the Glut1 promoter by V12Ras.

In response to treatment with a variety of different agonists, primary cultures of ventricular myocytes isolated from neonatal rat hearts display many of the associated with hypertrophy in vivo and provide a useful model to study this nonproliferative growth response Global Power in Motion.

American Technologies Group, Inc. List of Registered Gasoline Additives The expression of this reporter in response to the hypertrophic agonists O -tetradecanoylphorbolacetate TPA 1 and phenylephrine was assessed, and the signaling pathways responsible for fcz expression of GLUT1 were investigated. Green Auto Solutions Inc. BP Amoco Chemical Company. Enron Gas Liquids Incorporated. TPA and phenylephrine induce hypertrophy of rat neonatal ventricular myocytes.

Industrial Parts Supply, Inc. Hygeia Coca-Cola Bottling Company. Although this study used pharmacological agonists to study the in vitro hypertrophic response of glucose transporters, it has implications for the understanding of glucose metabolism in pathophysiological situations. Lifetime Energy Solutions, Corp. Beta Strategy Group Ltd. Stimulation of the cells with O -tetradecanoylphorbolacetate or phenylephrine induced transcription from the Glut1 promoter, which was inhibited by cotransfection with the mitogen-activated kinase phosphatases CL and MKP Myocardial hypertrophy is associated with increased basal glucose metabolism.

For transfection experiments, cells were plated at a density of 2. Therefore, it was a potential concern that the effect of TPA, a non-tissue-specific protein C agonist, could be due to increased expression of the Glut1 promoter in contaminating non-myocyte cardiac cells, mainly cardiac fibroblasts.

GLUT1 is the principal isoform expressed in the fetal heart, and its expression is down-regulated following birth in normal myocardium concomitantly with the shift from glycolytic to oxidative metabolism 1. Interestingly rcs signaling pathways that are used in different cell types in the heart to activate the ERK molecules are different. Eastern Greenway Oils Inc.

The results shown in Fig. However, treatment with PD markedly reduced expression of the Glut1 gene induced by either TPA or phenylephrine, without affecting expression of the Glut4 gene Fig.

Articles by Thorburn, A. However, Marais et al. The plasmid containing 1. These results suggest that PI3K activation contributes to the induction of the Glut1 promoter in response to TPA and phenylephrine and that it acts upstream of Ras.

The present study does not allow us to draw firm conclusions on this issue. We therefore assessed the involvement of MAP kinase pathways in the overexpression of Glut1.

These results suggest that Ras does not participate in signal transduction activated by TPA in cardiac fibroblasts, although it does participate in induction by TPA in cardiac myocytes. Apex International Group, Inc. CrossRef Medline Google Scholar. In addition, active MAP kinase is required for induction of the c- fos and atrial natriuretic factor promoters by phenylephrine and expression of constitutively active MEK1 results in overexpression of hypertrophic genes Bright Star Industries, Inc.

GO KIFU PDF Transient transfection experiments with a luciferase reporter under the control of the mouse Glut1 promoter indicated that treatment of myocytes with hypertrophic agonists resulted in increased transcription from the Glut1 promoter occurring between 6 and 48 h following addition of the agonist.

Gasolines are required to contain detergent additives which have been certified in accordance with the regulations at 40 CFR 80, Subpart G. Hypertrophic induction of the Glut1 promoter was also partially sensitive to inhibition of the phosphatidylinositol 3-kinase pathway and was strongly inhibited by cotransfection with dominant-negative Ras.

Epoch Energy Technology Corp. ER-transfected cells were then treated with either 0. Thus, the modes of action of both agonists may converge onto Raf. Because of the low transfection efficiency in primary myocytes, it was not possible to assess the effect of transfection with these molecules on expression of endogenous Glut1 mRNA. As shown in Fig. TPA belongs to the phorbol ester family, a class of compounds able to directly stimulate the classical and novel protein kinase C PKC isoforms.

International Fuel Technology, Inc. These results therefore suggest that Ras-mediated Raf activation, rather than PKC-mediated Raf phosphorylation, is the main pathway leading to stimulation of ERK activity in myocytes treated with phorbol esters.

Crown Central Petroleum Corporation. Cells for morphological analysis were plated on glass coverslips ccs with gelatin and laminin. Dae Yang Industrial Co.


9013 Datasheet, Equivalent, Cross Reference Search

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FCS 9013 PDF

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