Evidence map›Paper›PMID 21878680›Full record

ReviewScience signaling2011

Inositol pyrophosphates as mammalian cell signals.

Anutosh Chakraborty, Seyun Kim, Solomon H Snyder

Abstract readReview
In one paragraph

Review in Science signaling, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed
8.4field-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

104 citing papers in PubMed, 151 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Synthesis and biological evaluation of flavonoid-based IP6K2 inhibitors.Journal of enzyme inhibition and medicinal chemistry · 2023
    Article
  11. The human milk componentProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  12. Review
  13. Article
  14. TNP and its analogs: Modulation of IP6K and CYP3A4 inhibition.Journal of enzyme inhibition and medicinal chemistry · 2022
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

44 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Anutosh ChakrabortyThe Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Seyun Kim
Solomon H Snyder
Johns Hopkins University · US

Funding

UNDERSTANDING NO SIGNALING RESULTING IN NEUROPROTECTION.P50DA000266 · NIDA · JOHNS HOPKINS UNIVERSITY · PI WORLEY, PAUL F · 1985 to 2017
$45.2M
NEUROCHEMICAL ACTIONS OF PSYCHOTROPIC DRUGSR37MH018501 · NIMH · JOHNS HOPKINS UNIVERSITY · PI SNYDER, SOLOMON H. · 1990 to 2009
$11.5M
NEUROCHEMICAL ACTIONS OF PSYCHOTROPIC DRUGSR01MH018501 · NIMH · JOHNS HOPKINS UNIVERSITY · PI SNYDER, SOLOMON H. · 1985 to 2019
$10.8M
NIDA NIH HHS DA-000266NIDA NIH HHS P50 DA000266NIMH NIH HHS MH18501NIMH NIH HHS R01 MH018501NIMH NIH HHS R37 MH018501
6 · The paper itself

Abstract

Inositol pyrophosphates are highly energetic inositol polyphosphate molecules present in organisms from slime molds and yeast to mammals. Distinct classes of enzymes generate different forms of inositol pyrophosphates. The biosynthesis of these substances principally involves phosphorylation of inositol hexakisphosphate (IP₆) to generate the pyrophosphate IP₇. Initial insights into functions of these substances derived primarily from yeast, which contain a single isoform of IP₆ kinase (yIP₆K), as well as from the slime mold Dictyostelium. Mammalian functions for inositol pyrophosphates have been investigated by using cell lines to establish roles in various processes, including insulin secretion and apoptosis. More recently, mice with targeted deletion of IP₆K isoforms as well as the related inositol polyphosphate multikinase (IPMK) have substantially enhanced our understanding of inositol polyphosphate physiology. Phenotypic alterations in mice lacking inositol hexakisphosphate kinase 1 (IP₆K1) reveal signaling roles for these molecules in insulin homeostasis, obesity, and immunological functions. Inositol pyrophosphates regulate these processes at least in part by inhibiting activation of the serine-threonine kinase Akt. Similar studies of IP₆K2 establish this enzyme as a cell death inducer acting by stimulating the proapoptotic protein p53. IPMK is responsible for generating the inositol phosphate IP₅ but also has phosphatidylinositol 3-kinase activity--that participates in activation of Akt. Here, we discuss recent advances in understanding the physiological functions of the inositol pyrophosphates based in substantial part on studies in mice with deletion of IP₆K isoforms. These findings highlight the interplay of IPMK and IP₆K in regulating growth factor and nutrient-mediated cell signaling.

Indexed as

Signal TransductionAnimalsCarbohydrate SequenceHomeostasisHumansInositol PhosphatesInsulinMiceMolecular Sequence DataPhenotypePhosphotransferases (Alcohol Group Acceptor)Inositol Phosphatesinositol polyphosphate multikinaseInsulinPhosphotransferases (Alcohol Group Acceptor)

Identifiers

PMID21878680
PMCPMC3667551
OpenAlexW2053940277

What OpenQuestion holds

Textmetadata
LicenceTDM
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.