Evidence map›Paper›PMID 10742305›Full record

ArticleBritish journal of pharmacology2000

P2Y(2) receptor-mediated proliferation of C(6) glioma cells via activation of Ras/Raf/MEK/MAPK pathway.

M T Tu, S F Luo, C C Wang, C S Chien, C T Chiu, C C Lin, C M Yang

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.1field-weighted citation impact, top 10% 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

27 citing papers in PubMed, 92 citations in OpenAlex.

  1. Trial
  2. Purinergic Receptor P2Y2 Regulates Neurogenesis and Functional Recovery Following Spinal Cord Injury in Zebrafish.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  3. Article
  4. Review
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  8. Article
  9. Article
  10. KScientific reports · 2017
    Article
  11. Article
  12. Review
  13. Article
  14. Purinergic signalling and cancer.Purinergic signalling · 2013
    Review
  15. Review
  16. Article
  17. Article
  18. Review
  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

7 authors at 1 institution in 1 country.

M T TuDepartment of Physiology and Pharmacology, College of Medicine, Chang Gung University, Kwei-San, Tao-Yuan, Taiwan.
S F Luo
C C Wang
C S Chien
C T Chiu
C C Lin
C M Yang
Chang Gung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1. Extracellular purine and pyrimidine nucleotides have been implicated in the regulation of several cellular functions including mitogenesis. In this study, experiments were conducted to characterize the P2Y receptor on C(6) glioma cells responsible for stimulating cell proliferation associated with mitogen-activated protein kinase (MAPK) activation. 2. UTP and ATP produced a similar effect on [(3)H]-thymidine incorporation in a time- and concentration-dependent manner, suggesting the involvement of P2Y(2) receptor in mediating proliferation of C(6) glioma cells. 3. In response to UTP, both p42 and p44 MAPK were activated in a time- and concentration-dependent manner using Western blot analysis with an anti-phospho-p42/p44 MAPK antibody. The phosphorylation reached maximal levels after 5 min and declining by 30 min. 4. Pretreatment with pertussis toxin (PTX) did not change these responses to UTP. Both DNA synthesis and phosphorylation of MAPK in response to UTP were attenuated by tyrosine kinase inhibitors, genistein and herbimycin A, protein kinase C (PKC) inhibitors, staurosporine and GF109203X, and removal of Ca(2+) by addition of BAPTA/AM plus EGTA. 5. UTP-induced [(3)H]-thymidine incorporation and p42/p44 MAPK phosphorylation was completely inhibited by PD98059 (an inhibitor of MEK1/2). Furthermore, we showed that overexpression of dominant negative mutants of Ras (RasN17) and Raf (Raf-301) completely suppressed MEK1/2 and p42/p44 MAPK activation induced by ATP and UTP. 6. These results conclude that the mitogenic effect of UTP mediated through a P2Y(2) receptor that involves the activation of Ras/Raf/MEK/MAPK pathway. UTP-mediated MAPK activation was modulated by Ca(2+), PKC, and tyrosine kinase associated with cell proliferation in cultured C(6) glioma cells.

Indexed as

Adenosine TriphosphateAnimalsCalciumCell DivisionDNAEnzyme ActivationEnzyme InhibitorsFlavonoidsGliomaIndolesIsoenzymesMaleimidesMAP Kinase Signaling SystemMitogen-Activated Protein Kinase KinasesMitogen-Activated Protein KinasesPertussis Toxin2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-oneAdenosine Triphosphatebisindolylmaleimide ICalciumDNAEnzyme InhibitorsFlavonoidsIndolesIsoenzymesMaleimidesMitogen-Activated Protein Kinase KinasesMitogen-Activated Protein KinasesPertussis ToxinProtein Kinase CProtein Serine-Threonine KinasesProto-Oncogene Proteins c-rafras ProteinsReceptors, Purinergic P2Receptors, Purinergic P2Y2StaurosporineUridine TriphosphateVirulence Factors, Bordetella

Identifiers

PMID10742305
PMCPMC1571966
OpenAlexW1986153986

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.