Evidence map›Paper›PMID 19666609›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2009

CK2 negatively regulates Galphas signaling.

Heike Rebholz, Akinori Nishi, Sabine Liebscher, Angus C Nairn, Marc Flajolet, Paul Greengard

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

25 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Splicing Interruption by Intron Variants inFrontiers in neuroscience · 2022
    Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. CK2 Oppositely Modulates l-DOPA-Induced Dyskinesia via Striatal Projection Neurons Expressing D1 or D2 Receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  16. Review
  17. CK2-An Emerging Target for Neurological and Psychiatric Disorders.Pharmaceuticals (Basel, Switzerland) · 2017
    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

6 authors at 3 institutions in 2 countries.

Heike RebholzLaboratory of Molecular and Cellular Neuroscience, The Rockefeller University, New York, NY 10065, USA.
Akinori Nishi
Sabine Liebscher
Angus C Nairn
Marc Flajolet
Paul Greengard
Rockefeller University · USConnecticut Mental Health Center · USKurume University · JP

Funding

THE ROLE OF DARPPS IN THE ACUTE AND CHRONIC EFFECTS OF COCAINE AND AMPHETAMINEP01DA010044 · NIDA · ROCKEFELLER UNIVERSITY · PI GREENGARD, PAUL · 1996 to 2015
$23.6M
Transgenic Core - Greengard (pgs. 218 - 235)P50MH074866 · NIMH · ROCKEFELLER UNIVERSITY · PI GREENGARD, PAUL · 2005 to 2009
$11.6M
NIDA NIH HHS DA10044NIDA NIH HHS P01 DA010044NIMH NIH HHS MH074886NIMH NIH HHS P50 MH074866
6 · The paper itself

Abstract

We present evidence, using biochemical and cellular approaches, that the kinase, CK2, negatively controls signaling via Galpha(s) (or Galpha(olf)) coupled to dopamine D1 and adenosine A2A receptors. Pharmacological inhibition of CK2 or CK2 knockdown by RNAi lead to elevated cAMP levels in dopamine D1 receptor-activated neuroblastoma cells. Phosphorylation levels of protein kinase A substrates were increased in the presence of CK2 inhibitors in mouse striatal slices. The effect of D1 receptor and A2A receptor agonists on the phosphorylation of protein kinase A sites was potentiated upon CK2 inhibition. Furthermore, in cell lines, we observed that reduction in CK2 activity, pharmacologically or genetically, reduced the amount of D1 receptor that was internalized in response to dopamine. Finally, the beta subunit of CK2 was found to interact specifically with the Galpha(s) subunit through protein interaction analyses. Thus CK2 can inhibit G protein-coupled receptor action by enabling faster receptor internalization, possibly through a direct association with Galpha(s).

Indexed as

Gene Expression RegulationAnimalsApigeninBrainCasein Kinase IICell LineCell Line, TumorCyclic AMPGTP-Binding Protein alpha SubunitsHumansKineticsMiceModels, BiologicalPhosphorylationSignal TransductionApigeninCasein Kinase IICyclic AMPGTP-Binding Protein alpha Subunits

Identifiers

PMID19666609
PMCPMC2729026
OpenAlexW1995864046

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.