Evidence map›Paper›PMID 9564040›Full record

ArticleThe EMBO journal1998

Angiotensin II stimulates ERK via two pathways in epithelial cells: protein kinase C suppresses a G-protein coupled receptor-EGF receptor transactivation pathway.

X Li, J W Lee, L M Graves, H S Earp

Open access · bronzeAbstract 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 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
8.3field-weighted citation impact, top 2% 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

28 citing papers in PubMed, 152 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. NADPH oxidase-derived reactive oxygen species in cardiac pathophysiology.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2005
    Review
  9. Article
  10. Article
  11. Article
  12. Angiotensin II-mediated signal transduction pathways.Current hypertension reports · 2002
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. 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

4 authors at 1 institution in 1 country.

X LiLineberger Comprehension Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
J W Lee
L M Graves
H S Earp
University of North Carolina at Chapel Hill · US

Funding

MITOGEN-ACTIVATED PROTEIN KINASES--REGULATION BY CAMPR29GM054010 · NIGMS · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI GRAVES, LEE M · 1996 to 2000
$107k
NIGMS NIH HHS GM54010
6 · The paper itself

Abstract

In GN4 rat liver epithelial cells, angiotensin II (Ang II) produces intracellular calcium and protein kinase C (PKC) signals and stimulates ERK and JNK activity. JNK activation appears to be mediated by a calcium-dependent tyrosine kinase (CADTK). To define the ERK pathway, we established GN4 cells expressing an inhibitory Ras(N17). Induction of Ras(N17) blocked EGF- but not Ang II- or phorbol ester (TPA)-dependent ERK activation. In control cells, Ang II and TPA produced minimal increases in Ras-GTP level and Raf kinase activity. PKC depletion by chronic TPA exposure abolished TPA-dependent ERK activation but failed to diminish the effect of Ang II. In PKC-depleted cells, Ang II increased Ras-GTP level and activated Raf and ERK in a Ras-dependent manner. In PKC depleted cells, Ang II stimulated Shc and Cbl tyrosine phosphorylation, suggesting that without PKC, Ang II activates another tyrosine kinase. PKC-depletion did not alter Ang II-dependent tyrosine phosphorylation or activity of p125(FAK), CADTK, Fyn or Src, but PKC depletion or incubation with GF109203X resulted in Ang II-dependent EGF receptor tyrosine phosphorylation. In PKC-depleted cells, EGF receptor-specific tyrosine kinase inhibitors blocked Ang II-dependent EGF receptor and Cbl tyrosine phosphorylation, and ERK activation. In summary, Ang II can activate ERK via two pathways; the latent EGF receptor, Ras-dependent pathway is equipotent to the Ras-independent pathway, but is masked by PKC action. The prominence of this G-protein coupled receptor to EGF receptor pathway may vary between cell types depending upon modifiers such as PKC.

Indexed as

Angiotensin IIAnimalsCell LineEnzyme ActivationEnzyme InhibitorsEpidermal Growth FactorEpithelial CellsErbB ReceptorsGTP-Binding ProteinsHumansLiverProtein Kinase CProtein-Tyrosine KinasesQuinazolinesRatsRecombinant Proteins4-((3-bromophenyl)amino)-6,7-dimethoxyquinazolineAngiotensin IIEnzyme InhibitorsEpidermal Growth FactorErbB ReceptorsGTP-Binding ProteinsProtein Kinase CProtein-Tyrosine KinasesQuinazolinesRecombinant ProteinsTetradecanoylphorbol Acetate

Identifiers

PMID9564040
PMCPMC1170599
OpenAlexW1992610215

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.