Evidence map›Paper›PMID 25486050›Full record

ArticlePrion2014

The cellular form of the prion protein guides the differentiation of human embryonic stem cells into neuron-, oligodendrocyte-, and astrocyte-committed lineages.

Young Jin Lee, Ilia V Baskakov

Open access · bronzeAbstract read
In one paragraph

Article in Prion, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

21 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. The Cellular Prion Protein: A Promising Therapeutic Target for Cancer.International journal of molecular sciences · 2020
    Review
  9. Review
  10. Review
  11. Prion Protein in Glioblastoma Multiforme.International journal of molecular sciences · 2019
    Review
  12. Cellular and Molecular Mechanisms Mediated by recPrPInternational journal of molecular sciences · 2019
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Physiological Functions of the Cellular Prion Protein.Frontiers in molecular biosciences · 2017
    Review
  20. Review
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 3 countries.

Young Jin Leea Center for Biomedical Engineering and; Technology Department of Anatomy and Neurobiology ; University of Maryland School of Medicine ; Baltimore , MD USA.
Ilia V Baskakov
University of Baltimore · US

Funding

Self-Propagating Mechanism of Prion DiseasesR01NS045585 · NINDS · UNIVERSITY OF MD BIOTECHNOLOGY INSTITUTE · PI Ilia V Baskakov · 2003 to 2026
$9.6M
NINDS NIH HHS NS045585NINDS NIH HHS R01 NS045585
6 · The paper itself

Abstract

Prion protein, PrP(C), is a glycoprotein that is expressed on the cell surface beginning with the early stages of embryonic stem cell differentiation. Previously, we showed that ectopic expression of PrP(C) in human embryonic stem cells (hESCs) triggered differentiation toward endodermal, mesodermal, and ectodermal lineages, whereas silencing of PrP(C) suppressed differentiation toward ectodermal but not endodermal or mesodermal lineages. Considering that PrP(C) might be involved in controlling the balance between cells of different lineages, the current study was designed to test whether PrP(C) controls differentiation of hESCs into cells of neuron-, oligodendrocyte-, and astrocyte-committed lineages. PrP(C) was silenced in hESCs cultured under three sets of conditions that were previously shown to induce hESCs differentiation into predominantly neuron-, oligodendrocyte-, and astrocyte-committed lineages. We found that silencing of PrP(C) suppressed differentiation toward all three lineages. Similar results were observed in all three protocols, arguing that the effect of PrP(C) was independent of differentiation conditions employed. Moreover, switching PrP(C) expression during a differentiation time course revealed that silencing PrP(C) expression during the very initial stage that corresponds to embryonic bodies has a more significant impact than silencing at later stages of differentiation. The current work illustrates that PrP(C) controls differentiation of hESCs toward neuron-, oligodendrocyte-, and astrocyte-committed lineages and is likely involved at the stage of uncommitted neural progenitor cells rather than lineage-committed neural progenitors.

Indexed as

AstrocytesEmbryonic Stem CellsGene SilencingHumansNeurogenesisNeuronsOligodendrogliaPrPC ProteinsPrPC ProteinsbFGF, basic fibroblast growth factorCNTF, ciliary neurotrophic factorEBs, embryoid bodiesEFG, epidermal growth factorESCs, embryonic stem cellsGFAP, glial fibrillary acidic proteinGRM, glial restrictive mediumhESCs, human ESCshES+TetR+ShPrPC, hESCs transfected with Lenti-TetR and Lenti-ShPrPChES+TetR+ShScram, hESCs transfected with Lenti-TetR and Lenti-ShScramhuman embryonic stem cellsLenti-ShPrPC, lentiviral vector expressing short hairpin RNA against PrPCLenti-ShScram, lentiviral vector expressing scrambled shRNALenti-TetR, lentiviral vector expressing tetracycline repressorMEF-CM, mouse embryonic feeder-conditioned mediumMEFs, mouse embryonic fibroblastsNDM, neuronal differentiation mediumneural progenitor cellsneuron-committed lineagesNIM, neural induction mediumNPM, neural proliferation mediumOlig1, a marker of oligodendrocyte-committed lineagesprion proteinPrPC, normal, cellular isoform of the prion proteinRA, retinoic acidstem cell differentiationSyn, synapsin ITetR, tetracycline repressorTet, tetracyclineTH, tyrosine hydroxylase

Identifiers

PMID25486050
PMCPMC4601225
OpenAlexW1990952979

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.