Evidence map›Paper›PMID 33547244›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2021

Inositol hexakisphosphate kinase-2 determines cellular energy dynamics by regulating creatine kinase-B.

Latika Nagpal, Michael D Kornberg, Lauren K Albacarys, Solomon H Snyder

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.4field-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

7 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
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  7. 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
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 1 institution in 1 country.

Latika NagpalThe Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205.ORCID 0000-0003-0510-7299
Michael D KornbergThe Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205.ORCID 0000-0003-2588-7325
Lauren K AlbacarysThe Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205.
Solomon H SnyderThe Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205; ssnyder@jhmi.edu.
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 P50 DA000266NIMH NIH HHS R01 MH018501NIMH NIH HHS R37 MH018501
6 · The paper itself

Abstract

Inositol hexakisphosphate kinases (IP6Ks) regulate various biological processes. IP6Ks convert IP6 to pyrophosphates such as diphosphoinositol pentakisphosphate (IP7) and bis-diphosphoinositol tetrakisphosphate (IP8). IP7 is produced in mammals by a family of inositol hexakisphosphate kinases, IP6K1, IP6K2, and IP6K3, which have distinct biological functions. The inositol hexakisphosphate kinase 2 (IP6K2) controls cellular apoptosis. To explore roles for IP6K2 in brain function, we elucidated its protein interactome in mouse brain revealing a robust association of IP6K2 with creatine kinase-B (CK-B), a key enzyme in energy homeostasis. Cerebella of IP6K2-deleted mice (IP6K2-knockout [KO]) produced less phosphocreatine and ATP and generated higher levels of reactive oxygen species and protein oxidative damage. In IP6K2-KO mice, mitochondrial dysfunction was associated with impaired expression of the cytochrome-c1 subunit of complex III of the electron transport chain. We reversed some of these effects by combined treatment with

Indexed as

AcetylcysteineAdenosine TriphosphateAnimalsApoptosisCreatine KinaseCytochromes c1Electron Transport Complex IIIEnergy MetabolismHumansMiceMice, KnockoutMitochondriaPhosphocreatinePhosphotransferases (Phosphate Group Acceptor)AcetylcysteineAdenosine TriphosphateCreatine KinaseCytochromes c1Electron Transport Complex IIIIhpk1 protein, mouseinositol hexakisphosphate kinaseIp6k2 protein, mousePhosphocreatinePhosphotransferases (Phosphate Group Acceptor)creatine kinaseelectron transport chaininositol phosphatesmitochondrial dysfunctionoxidative stress

Identifiers

PMID33547244
PMCPMC8017945
OpenAlexW3126794722

What Socratic 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 Socratic graph.