Evidence map›Paper›PMID 9632754›Full record

ArticleMolecular and cellular biology1998

Differential effects of protein kinase A on Ras effector pathways.

M J Miller, L Rioux, G V Prendergast, S Cannon, M A White, J L Meinkoth

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
4.1field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 72 citations in OpenAlex.

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  9. On the mitogenic properties of Rap1b: cAMP-induced G(1)/S entry requires activated and phosphorylated Rap1b.Proceedings of the National Academy of Sciences of the United States of America · 2002
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 2 countries.

M J MillerDepartment of Pharmacology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104-6084, USA.
L Rioux
G V Prendergast
S Cannon
M A White
J L Meinkoth
University of Pennsylvania · USThe University of Texas Southwestern Medical Center · US

Funding

CYCLIC AMP, RAS, AND ENDOCRINE CELL PROLIFERATIONR01DK045696 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI MEINKOTH, JUDY L · 1993 to 2004
$1.4M
CROSSTALK BETWEEN CAMP AND RAS IN ENDOCRINE CELLSK02DK002494 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI MEINKOTH, JUDY L · 1997 to 2001
$212k
NIDDK NIH HHS DK 02494NIDDK NIH HHS DK45696NIDDK NIH HHS R01 DK045696
6 · The paper itself

Abstract

Ras mutants with the ability to interact with different effectors have played a critical role in the identification of Ras-dependent signaling pathways. We used two mutants, RasS35 and RasG37, which differ in their ability to bind Raf-1, to examine Ras-dependent signaling in thyroid epithelial cells. Wistar rat thyroid cells are dependent upon thyrotropin (TSH) for growth. Although TSH-stimulated mitogenesis requires Ras, TSH activates protein kinase A (PKA) and downregulates signaling through Raf and the mitogen-activated protein kinase (MAPK) cascade. Cells expressing RasS35, a mutant which binds Raf, or RasG37, a mutant which binds RalGDS, exhibited TSH-independent proliferation. RasS35 stimulated morphological transformation and anchorage-independent growth. RasG37 stimulated proliferation but not transformation as measured by these indices. TSH exerted markedly different effects on the Ras mutants and transiently repressed MAPK phosphorylation in RasS35-expressing cells. In contrast, TSH stimulated MAPK phosphorylation and growth in cells expressing RasG37. The Ras mutants, in turn, exerted differential effects on TSH signaling. RasS35 abolished TSH-stimulated changes in cell morphology and thyroglobulin expression, while RasG37 had no effect on these activities. Together, the data indicate that cross talk between Ras and PKA discriminates between distinct Ras effector pathways.

Indexed as

Signal TransductionAnimalsCalcium-Calmodulin-Dependent Protein KinasesCell DivisionCell LineCyclic AMPCyclic AMP-Dependent Protein KinasesGene Expression RegulationMutagenesis, Site-DirectedPhosphorylationras ProteinsRatsRats, WistarThyroglobulinThyroid GlandCalcium-Calmodulin-Dependent Protein KinasesCyclic AMPCyclic AMP-Dependent Protein Kinasesras ProteinsThyroglobulin

Identifiers

PMID9632754
PMCPMC108954
OpenAlexW2143660761

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.