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Institution

Parke-Davis

About: Parke-Davis is a based out in . It is known for research contribution in the topics: Receptor & Alkyl. The organization has 4140 authors who have published 4596 publications receiving 182248 citations. The organization is also known as: Parke, Davis & Company.
Topics: Receptor, Alkyl, Agonist, Atorvastatin, Population


Papers
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Journal ArticleDOI
TL;DR: The results indicate that the activation of Raf is suppressed and that its inactivation is accelerated by a downstream component(s) of the MAP kinase pathway.

3,444 citations

Journal ArticleDOI
TL;DR: Results indicate that the MAPK pathway is essential for growth and maintenance of the ras-transformed phenotype and PD 098059 is an invaluable tool that will help elucidate the role of theMAPK cascade in a variety of biological settings.
Abstract: Treatment of cells with a variety of growth factors triggers a phosphorylation cascade that leads to activation of mitogen-activated protein kinases (MAPKs, also called extracellular signal-regulated kinases, or ERKs). We have identified a synthetic inhibitor of the MAPK pathway. PD 098059 [2-(2'-amino-3'-methoxyphenyl)-oxanaphthalen-4-one] selectively inhibited the MAPK-activating enzyme, MAPK/ERK kinase (MEK), without significant inhibitory activity of MAPK itself. Inhibition of MEK by PD 098059 prevented activation of MAPK and subsequent phosphorylation of MAPK substrates both in vitro and in intact cells. Moreover, PD 098059 inhibited stimulation of cell growth and reversed the phenotype of ras-transformed BALB 3T3 mouse fibroblasts and rat kidney cells. These results indicate that the MAPK pathway is essential for growth and maintenance of the ras-transformed phenotype. Further, PD 098059 is an invaluable tool that will help elucidate the role of the MAPK cascade in a variety of biological settings.

2,697 citations

Journal ArticleDOI
17 Apr 1998-Cell
TL;DR: It is shown that cardiac hypertrophy is induced by the calcium-dependent phosphatase calcineurin, which dephosphorylates the transcription factor NF-AT3, enabling it to translocate to the nucleus.

2,596 citations

Journal ArticleDOI
01 Mar 1996-Neuron
TL;DR: It is suggested that glial glutamate transporters provide the majority of functional glutamate transport and are essential for maintaining low extracellular glutamate and for preventing chronic glutamate neurotoxicity.

2,482 citations

Journal ArticleDOI
24 Oct 1997-Science
TL;DR: The proapoptotic function of BAD is regulated by the PI 3-kinase-Akt pathway, and active, but not inactive, forms of Akt were found to phosphorylate BAD in vivo and in vitro at the same residues that are phosphorylated in response to IL-3.
Abstract: BAD is a distant member of the Bcl-2 family that promotes cell death. Phosphorylation of BAD prevents this. BAD phosphorylation induced by interleukin-3 (IL-3) was inhibited by specific inhibitors of phosphoinositide 3-kinase (PI 3-kinase). Akt, a survival-promoting serine-threonine protein kinase, was activated by IL-3 in a PI 3-kinase-dependent manner. Active, but not inactive, forms of Akt were found to phosphorylate BAD in vivo and in vitro at the same residues that are phosphorylated in response to IL-3. Thus, the proapoptotic function of BAD is regulated by the PI 3-kinase-Akt pathway.

2,321 citations


Authors

Showing all 4140 results

NameH-indexPapersCitations
Gabriel Núñez148466105724
Charles Taylor12674177626
Nicholas J. Schork12558762131
Bertram Pitt10775478458
Robert J. Coffey10340242409
Richard J. Whitley10351644049
Robert W. Schrier9958638996
Alan R. Saltiel9933649325
Emilio Ros9555437490
Michael Aviram9447931141
Joseph A. Loo8941326162
Rainer Schulz8748227135
Gordon L. Amidon8646635880
Kevin K.W. Wang7938420510
David Ginsburg7626619779
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
20131
20121
201118
201017
200915
20085