Evidence map›Paper›PMID 24449917›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

PIKE is essential for oligodendroglia development and CNS myelination.

Chi Bun Chan, Xia Liu, Lixia Zhao, Guanglu Liu, Chi Wai Lee, Yue Feng, Keiqang Ye

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Genome research · 2024
    Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. [Mechanisms underlying remyelination with special focus on demyelination models of multiple sclerosis].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2020
    Review
  8. Article
  9. α-Synuclein binds and sequesters PIKE-L into Lewy bodies, triggering dopaminergic cell death via AMPK hyperactivation.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  10. Olig2-Targeted G-Protein-Coupled Receptor Gpr17 Regulates Oligodendrocyte Survival in Response to Lysolecithin-Induced Demyelination.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  11. Review
  12. Article
  13. 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

7 authors at 2 institutions in 2 countries.

Chi Bun ChanDepartment of Pathology and Laboratory Medicine, Department of Pharmacology, Emory University School of Medicine, Atlanta, GA 30322.
Xia Liu
Lixia Zhao
Guanglu Liu
Chi Wai Lee
Yue Feng
Keiqang Ye
Emory University · USNational University of Singapore · SG

Funding

Nuclear GTPase PIKE Regulation and FunctionsR01NS045627 · NINDS · EMORY UNIVERSITY · PI YE, KEQIANG · 2004 to 2013
$3.1M
Role of QKI in oligodendroglia and myelin developmentR01NS056097 · NINDS · EMORY UNIVERSITY · PI FENG, YUE · 2007 to 2011
$1.7M
NINDS NIH HHS R01 NS045627NINDS NIH HHS R01NS045627NINDS NIH HHS R01 NS056097NINDS NIH HHS R01NS056097
6 · The paper itself

Abstract

Oligodendrocyte (OL) differentiation and myelin development are complex events regulated by numerous signal transduction factors. Here, we report that phosphoinositide-3 kinase enhancer L (PIKE-L) is required for OL development and myelination. PIKE-L expression is up-regulated when oligodendrocyte progenitor cells commit to differentiation. Conversely, depleting phosphoinositide-3 kinase enhancer (PIKE) expression by shRNA prevents oligodendrocyte progenitor cell differentiation. In both conventional PIKE knockout (PIKE(-/-)) and OL-specific PIKE knockout mice, the number of OLs is reduced in the corpus callosum. PIKE(-/-) OLs also display defects when forming myelin sheath on neuronal axons during neonatal development, which is partially rescued when PTEN is ablated. In addition, Akt/mTOR signaling is impaired in OL-enriched tissues of the PIKE(-/-) mutant, leading to reduced expression of critical proteins for myelin development and hypomyelination. Moreover, myelin repair of lysolecithin-induced lesions is delayed in PIKE(-/-) brain. Thus, PIKE plays pivotal roles to advance OL development and myelinogenesis through Akt/mTOR activation.

Indexed as

AnimalsAxonsBrainCell CountCells, CulturedCentral Nervous SystemGTP PhosphohydrolasesMiceMice, KnockoutMonomeric GTP-Binding ProteinsMutationMyelin SheathNerve Tissue ProteinsOligodendrogliaProto-Oncogene Proteins c-aktRatsAgap2 protein, ratGTP PhosphohydrolasesMonomeric GTP-Binding ProteinsNerve Tissue ProteinsPIKE protein, mouseProto-Oncogene Proteins c-aktTOR Serine-Threonine Kinases

Identifiers

PMID24449917
PMCPMC3918755
OpenAlexW2011443140

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.