Evidence map›Paper›PMID 30392847›Full record

ReviewAdvances in biological regulation2019

Inositol phosphate kinases: Expanding the biological significance of the universal core of the protein kinase fold.

Stephen B Shears, Huanchen Wang

Open access · greenAbstract readReview
In one paragraph

Review in Advances in biological regulation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

29 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Structural Rationalization of IPMK Inhibitor Potency.Journal of medicinal chemistry · 2025
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Synthesis and biological evaluation of flavonoid-based IP6K2 inhibitors.Journal of enzyme inhibition and medicinal chemistry · 2023
    Article
  13. Article
  14. Review
  15. Article
  16. Structural and catalytic analyses of the InsPFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    Article
  17. Article
  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

2 authors at 1 institution in 1 country.

Stephen B ShearsInositol Signaling Group, Signal Transduction Laboratory, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA. Electronic address: shears@niehs.nih.gov.
Huanchen WangInositol Signaling Group, Signal Transduction Laboratory, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA. Electronic address: Huanchen.wang@nih.gov.
National Institute of Environmental Health Sciences · US

Funding

Inositol SignallingZIAES080046 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI SHEARS, STEPHEN B · 2009 to 2023
$31.3M
REGULATION OF INOSITOL LIPID SIGNALLING MECHANISMSZ01ES080046 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI SHEARS, STEPHEN B · 1990 to 2008
$4.3M
Intramural NIH HHS Z01 ES080046
6 · The paper itself

Abstract

The protein kinase family is characterized by substantial conservation of architectural elements that are required for both ATP binding and phosphotransferase activity. Many of these structural features have also been identified in homologous enzymes that phosphorylate a variety of alternative, non-protein substrates. A comparative structural analysis of these different kinase sub-classes is a portal to a greater understanding of reaction mechanisms, enzyme regulation, inhibitor-development strategies, and superfamily-level evolutionary relationships. To serve such advances, we review structural elements of the protein kinase fold that are conserved in the subfamily of inositol phosphate kinases (InsPKs) that share a PxxxDxKxG catalytic signature: inositol 1,4,5-trisphosphate kinase (IP3K), inositol hexakisphosphate kinase (IP6K), and inositol polyphosphate multikinase (IPMK). We describe conservation of the fundamental two-lobe kinase architecture: an N-lobe constructed upon an anti-parallel β-strand scaffold, which is coupled to a largely helical C-lobe by a single, adenine-binding hinge. This equivalency also includes a G-loop that embraces the β/γ-phosphates of ATP, a transition-state stabilizing residue (Lys/His), and a Mg-positioning aspartate residue within a catalytic triad. Furthermore, we expand this list of conserved structural features to include some not previously identified in InsPKs: a 'gatekeeper' residue in the N-lobe, and an 'αF'-like helix in the C-lobe that anchors two structurally-stabilizing, hydrophobic spines, formed from non-consecutive residues that span the two lobes. We describe how this wide-ranging structural homology can be exploited to develop lead inhibitors of IP6K and IPMK, by using strategies similar to those that have generated ATP-competing inhibitors of protein-kinases. We provide several examples to illustrate how such an approach could benefit human health.

Indexed as

Phosphotransferases (Alcohol Group Acceptor)Phosphotransferases (Phosphate Group Acceptor)AnimalsBinding SitesHumansInositol PhosphatesPhosphorylationProtein KinasesProtein Structure, Secondaryinositol hexakisphosphate kinaseInositol Phosphatesinositol polyphosphate multikinasePhosphotransferases (Alcohol Group Acceptor)Phosphotransferases (Phosphate Group Acceptor)Protein Kinases

Identifiers

PMID30392847
PMCPMC9364425
OpenAlexW2898604408

What Socratic holds

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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 Socratic graph.