Evidence map›Paper›PMID 17895383›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2007

Alterations in an inositol phosphate code through synergistic activation of a G protein and inositol phosphate kinases.

James C Otto, Patrick Kelly, Shean-Tai Chiou, John D York

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

31 citing papers in PubMed, 55 citations in OpenAlex.

  1. Review
  2. Article
  3. Human plasma inositol hexakisphosphate (InsPmicroPublication biology · 2024
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. The Key Role of IPMolecules (Basel, Switzerland) · 2020
    Review
  10. InsPProceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  11. Vip1 is a kinase and pyrophosphatase switch that regulates inositol diphosphate signaling.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  12. Article
  13. ITPK1 mediates the lipid-independent synthesis of inositol phosphates controlled by metabolism.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  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 3 institutions in 1 country.

James C OttoHoward Hughes Medical Institute, Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC 27710, USA.
Patrick Kelly
Shean-Tai Chiou
John D York
Howard Hughes Medical Institute · USDuke Medical Center · USDuke University Hospital · US

Funding

Oscilloscopes Spatio-Temporal Metabolomics (RMI)R33DK070272 · NIDDK · DUKE UNIVERSITY · PI YORK, JOHN D. · 2004 to 2006
$5.5M
The Role of Inositol Signaling in Human DiseaseR01HL055672 · NHLBI · WASHINGTON UNIVERSITY · PI YORK, JOHN D. · 1996 to 2012
$5.4M
NHLBI NIH HHS R01 HL055672NHLBI NIH HHS R01 HL-55672NIDDK NIH HHS R33 DK-070272NIDDK NIH HHS R33 DK070272
6 · The paper itself

Abstract

In mammals, many cellular stimuli evoke a response through G protein activation of phospholipase C, which results in the lipid-derived production of inositol 1,4,5-trisphosphate (IP(3)). Although it is well established that IP(3) is converted to numerous inositol phosphates (IPs) and pyrophosphates (PP-IPs) through the action of up to six classes of inositol phosphate kinases (IPKs), it is not clear that these metabolites are influenced by G protein signaling. Here we report that activation of Galpha(q) leads to robust stimulation of IP(3) to IP(8) metabolism. To expose flux through these pathways, genetic perturbation was used to alter IP homeostasis. Coupled expression of a constitutively active Galpha(q)QL and one or more IPK gene products synergistically generated dramatic changes in the patterns of intracellular IP messengers. Many distinct IP profiles were observed through the expression of different combinations of IPKs, including changes in previously unappreciated pools of IP(5) and IP(6), two molecules widely viewed as stable metabolites. Our data link the activation of a trimeric G protein to a plethora of metabolites downstream of IP(3) and provide a framework for suggesting that cells possess the machinery to produce an IPK-dependent IP code. We imply, but do not prove, that agonist-induced alterations in such a code would theoretically be capable of enhancing signaling complexity and specificity. The essential roles for IPKs in organism development and cellular adaptation are consistent with our hypothesis that such an IP code may be relevant to signaling pathways.

Indexed as

1-Phosphatidylinositol 4-KinaseCell LineEnzyme ActivationGTP-Binding ProteinsHumansInositol 1,4,5-TrisphosphateInositol PhosphatesKidneyKineticsPhosphatidylinositol 3-KinasesPhosphotransferases (Alcohol Group Acceptor)Phytic Acid1-Phosphatidylinositol 4-KinaseGTP-Binding ProteinsInositol 1,4,5-TrisphosphateInositol 1,4,5-trisphosphate 3-kinaseInositol PhosphatesPhosphatidylinositol 3-KinasesPhosphotransferases (Alcohol Group Acceptor)Phytic Acid

Identifiers

PMID17895383
PMCPMC1994134
OpenAlexW1976398980

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.