Evidence map›Paper›PMID 20066467›Full record

ReviewCellular and molecular life sciences : CMLS2010

Inositol trisphosphate 3-kinases: focus on immune and neuronal signaling.

Michael J Schell

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2010. 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
1.6field-weighted citation impact, top 19% 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, 38 citations in OpenAlex.

  1. Review
  2. Article
  3. Itpka depletion implicates defects in anterior neural development ofFrontiers in cell and developmental biology · 2025
    Article
  4. Inositol 1,3,4,5-tetrakisphosphate: a remarkable second messenger in platelet signaling.Research and practice in thrombosis and haemostasis · 2024
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Inositol phosphate kinases in the eukaryote landscape.Advances in biological regulation · 2021
    Article
  10. Article
  11. Review
  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. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. The Concise Guide to PHARMACOLOGY 2013/14: enzymes.British journal of pharmacology · 2013
    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

1 author at 1 institution in 2 countries.

Michael J SchellDepartment of Pharmacology, Uniformed Services University, 4301 Jones Bridge Rd, Bethesda, MD 20814, USA. mschell@usuhs.mil
Uniformed Services University of the Health Sciences · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The localized control of second messenger levels sculpts dynamic and persistent changes in cell physiology and structure. Inositol trisphosphate [Ins(1,4,5)P(3)] 3-kinases (ITPKs) phosphorylate the intracellular second messenger Ins(1,4,5)P(3). These enzymes terminate the signal to release Ca(2+) from the endoplasmic reticulum and produce the messenger inositol tetrakisphosphate [Ins(1,3,4,5)P(4)]. Independent of their enzymatic activity, ITPKs regulate the microstructure of the actin cytoskeleton. The immune phenotypes of ITPK knockout mice raise new questions about how ITPKs control inositol phosphate lifetimes within spatial and temporal domains during lymphocyte maturation. The intense concentration of ITPK on actin inside the dendritic spines of pyramidal neurons suggests a role in signal integration and structural plasticity in the dendrite, and mice lacking neuronal ITPK exhibit memory deficits. Thus, the molecular and anatomical features of ITPKs allow them to regulate the spatiotemporal properties of intracellular signals, leading to the formation of persistent molecular memories.

Indexed as

AnimalsHumansInositol 1,4,5-TrisphosphateMiceMice, KnockoutModels, ImmunologicalModels, MolecularModels, NeurologicalNeuronal PlasticityNeuronsPhosphorylationPhosphotransferases (Alcohol Group Acceptor)Second Messenger SystemsSignal TransductionInositol 1,4,5-TrisphosphateInositol 1,4,5-trisphosphate 3-kinasePhosphotransferases (Alcohol Group Acceptor)

Identifiers

PMID20066467
PMCPMC11115942
OpenAlexW1965516537

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.