Evidence map›Paper›PMID 9774335›Full record

ArticleThe EMBO journal1998

Extracellular signal-regulated activation of Rap1 fails to interfere in Ras effector signalling.

F J Zwartkruis, R M Wolthuis, N M Nabben, B Franke, J L Bos

Abstract read
In one paragraph

Article in The EMBO journal, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
9.6field-weighted citation impact, top 1% 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

71 citing papers in PubMed, 217 citations in OpenAlex.

  1. Sphingomyelin as a key negative mediator in atrial fibrillation via lipid profiling analysis and functional identification.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2026
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  2. Review
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  6. Integration of Rap1 and Calcium Signaling.International journal of molecular sciences · 2020
    Review
  7. Review
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  9. From Ras to Rap and Back, a Journey of 35 Years.Cold Spring Harbor perspectives in medicine · 2018
    Review
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11 more citing papers are in PubMed but not listed here.

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

5 authors at 1 institution in 1 country.

F J ZwartkruisLaboratory for Physiological Chemistry, Utrecht University, Universiteitsweg 100, 2584 CG Utrecht, The Netherlands.
R M Wolthuis
N M Nabben
B Franke
J L Bos
Utrecht University · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The small GTPase Rap1 has been implicated in both negative and positive control of Ras-mediated signalling events. We have investigated which extracellular signals can activate Rap1 and whether this activation leads to a modulation of Ras effector signalling, i.e. the activation of ERK and the small GTPase Ral. We found that Rap1 is rapidly activated following stimulation of a large variety of growth factor receptors. These receptors include receptor tyrosine kinases for platelet-derived growth factor (PDGF) and epithelial growth factor (EGF), and G protein-coupled receptors for lysophosphatidic acid (LPA), thrombin and endothelin. At least three distinct pathways may transduce a signal towards Rap1 activation: increase in intracellular calcium, release of diacylglycerol and cAMP synthesis. Surprisingly, activation of endogenous Rap1 fails to affect Ras-dependent ERK activation. In addition, we found that although overexpression of active Rap1 is able to activate the Ral pathway, activation of endogenous Rap1 in fibroblasts does not result in Ral activation. Rap1 also does not negatively influence Ras-mediated Ral activation. We conclude that activation of Rap1 is a common event upon growth factor treatment and that the physiological function of Rap1 is likely to be different from modulation of Ras effector signalling.

Indexed as

3T3 CellsAnimalsBlotting, WesternCells, CulturedCOS CellsEpidermal Growth FactorGTP-Binding ProteinsLysophospholipidsMiceMitogen-Activated Protein KinasesPC12 CellsPlatelet-Derived Growth FactorProto-Oncogene Proteinsral GTP-Binding Proteinsrap GTP-Binding Proteinsras ProteinsEpidermal Growth FactorGTP-Binding ProteinsLysophospholipidsMitogen-Activated Protein KinasesPlatelet-Derived Growth FactorProto-Oncogene Proteinsral GTP-Binding Proteinsrap GTP-Binding Proteinsras ProteinsType C Phospholipases

Identifiers

PMID9774335
PMCPMC1170918
OpenAlexW2070564840

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.