Evidence map›Paper›PMID 9819386›Full record

ArticleMolecular and cellular biology1998

Cyclic-GMP-dependent protein kinase inhibits the Ras/Mitogen-activated protein kinase pathway.

M Suhasini, H Li, S M Lohmann, G R Boss, R B Pilz

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 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

26 citing papers in PubMed, 111 citations in OpenAlex.

  1. Article
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  5. Guanylyl cyclase-A phosphorylation decreases cardiac hypertrophy and improves systolic function in male, but not female, mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
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  19. Inhibition of calcineurin-NFAT hypertrophy signaling by cGMP-dependent protein kinase type I in cardiac myocytes.Proceedings of the National Academy of Sciences of the United States of America · 2002
    Article
  20. Article
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 2 institutions in 2 countries.

M SuhasiniDepartment of Medicine, University of California, San Diego, La Jolla, California 92093-0652, USA.
H Li
S M Lohmann
G R Boss
R B Pilz
University of California San Diego · USFreie Universität Berlin · DE

Funding

VOLUMETRIC CONTOUR-BASED SURFACE RECONSTRUCTIONP41RR004050 · NCRR · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI PASQUALE, ELENA B · 1989 to 2011
$28.0M
NCRR NIH HHS P41 RR004050NCRR NIH HHS RR04050NIGMS NIH HHS GM4960
6 · The paper itself

Abstract

Agents which increase the intracellular cyclic GMP (cGMP) concentration and cGMP analogs inhibit cell growth in several different cell types, but it is not known which of the intracellular target proteins of cGMP is (are) responsible for the growth-suppressive effects of cGMP. Using baby hamster kidney (BHK) cells, which are deficient in cGMP-dependent protein kinase (G-kinase), we show that 8-(4-chlorophenylthio)guanosine-3', 5'-cyclic monophosphate and 8-bromoguanosine-3',5'-cyclic monophosphate inhibit cell growth in cells stably transfected with a G-kinase Ibeta expression vector but not in untransfected cells or in cells transfected with a catalytically inactive G-kinase. We found that the cGMP analogs inhibited epidermal growth factor (EGF)-induced activation of mitogen-activated protein (MAP) kinase and nuclear translocation of MAP kinase in G-kinase-expressing cells but not in G-kinase-deficient cells. Ras activation by EGF was not impaired in G-kinase-expressing cells treated with cGMP analogs. We show that activation of G-kinase inhibited c-Raf kinase activation and that G-kinase phosphorylated c-Raf kinase on Ser43, both in vitro and in vivo; phosphorylation of c-Raf kinase on Ser43 uncouples the Ras-Raf kinase interaction. A mutant c-Raf kinase with an Ala substitution for Ser43 was insensitive to inhibition by cGMP and G-kinase, and expression of this mutant kinase protected cells from inhibition of EGF-induced MAP kinase activity by cGMP and G-kinase, suggesting that Ser43 in c-Raf is the major target for regulation by G-kinase. Similarly, B-Raf kinase was not inhibited by G-kinase; the Ser43 phosphorylation site of c-Raf is not conserved in B-Raf. Activation of G-kinase induced MAP kinase phosphatase 1 expression, but this occurred later than the inhibition of MAP kinase activation. Thus, in BHK cells, inhibition of cell growth by cGMP analogs is strictly dependent on G-kinase and G-kinase activation inhibits the Ras/MAP kinase pathway (i) by phosphorylating c-Raf kinase on Ser43 and thereby inhibiting its activation and (ii) by inducing MAP kinase phosphatase 1 expression.

Indexed as

Cell Cycle ProteinsPhosphoprotein PhosphatasesAnimalsCalcium-Calmodulin-Dependent Protein KinasesCell DivisionCells, CulturedCricetinaeCyclic GMPCyclic GMP-Dependent Protein KinasesDual Specificity Phosphatase 1Enzyme ActivationEpidermal Growth FactorGenes, rasImmediate-Early ProteinsPhosphorylationProtein Phosphatase 18-((4-chlorophenyl)thio)cyclic-3',5'-GMPCalcium-Calmodulin-Dependent Protein KinasesCell Cycle ProteinsCyclic GMPCyclic GMP-Dependent Protein KinasesDual Specificity Phosphatase 1Epidermal Growth FactorImmediate-Early ProteinsPhosphoprotein PhosphatasesProtein Phosphatase 1Protein Tyrosine PhosphatasesProto-Oncogene Proteins c-rafThionucleotides

Identifiers

PMID9819386
PMCPMC109281
OpenAlexW1944726467

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.