Evidence map›Paper›PMID 30006360›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2018

Inositol Hexakisphosphate Kinase-2 in Cerebellar Granule Cells Regulates Purkinje Cells and Motor Coordination via Protein 4.1N.

Latika Nagpal, Chenglai Fu, Solomon H Snyder

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.6field-weighted citation impact, top 36% 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

12 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Inositol hexakisphosphate kinase-2 non-catalytically regulates mitophagy by attenuating PINK1 signaling.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  9. Inositol hexakisphosphate kinase-2 determines cellular energy dynamics by regulating creatine kinase-B.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  10. Review
  11. Review
  12. 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

3 authors at 2 institutions in 2 countries.

Latika NagpalThe Solomon H. Snyder Department of Neuroscience, and.
Chenglai FuThe Solomon H. Snyder Department of Neuroscience, and.
Solomon H SnyderThe Solomon H. Snyder Department of Neuroscience, and ssnyder@jhmi.edu.
H. L. Snyder Medical Foundation · USLaboratory of Molecular Genetics · PL

Funding

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
NIMH NIH HHS R01 MH018501NIMH NIH HHS R37 MH018501
6 · The paper itself

Abstract

Inositol hexakisphosphate kinases (IP6Ks) regulate various biological processes. Among pyrophosphates generated by IP6Ks, diphosphoinositol pentakisphosphate (IP7), and bis-diphosphoinositol tetrakisphosphate have been extensively characterized. IP7 is produced in mammals by a family of inositol hexakisphosphate kinases, IP6K1, IP6K2, and IP6K3, which have distinct biological functions. We report that IP6K2 binds protein 4.1.N with high affinity and specificity. Nuclear translocation of 4.1N, which is required for its principal functions, is dependent on IP6K2. Both of these proteins are highly expressed in granule cells of the cerebellum where their interaction regulates Purkinje cell morphology and cerebellar synapses. The deletion of IP6K2 in male/female mice elicits substantial defects in synaptic influences of granule cells upon Purkinje cells as well as notable impairment of locomotor function. Moreover, the disruption of IP6K2-4.1N interactions impairs cell viability. Thus, IP6K2 and its interaction with 4.1N appear to be major determinants of cerebellar disposition and psychomotor behavior.

Indexed as

Active Transport, Cell NucleusAnimalsCell LineCell SurvivalCerebellumCytoskeletal ProteinsExploratory BehaviorFemaleMaleMembrane ProteinsMiceMice, Inbred C57BLMice, KnockoutMotor ActivityNerve Tissue ProteinsNeuronsCytoskeletal Proteinserythrocyte membrane protein band 4.1-like 1Ip6k2 protein, mouseMembrane ProteinsNerve Tissue ProteinsNeuropeptidesPhosphotransferases (Phosphate Group Acceptor)4.1NcerebellumIP6K2synapse

Identifiers

PMID30006360
PMCPMC6596132
OpenAlexW2884812018

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.