Evidence map›Paper›PMID 24198336›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2013

Interaction of ganglioside GD3 with an EGF receptor sustains the self-renewal ability of mouse neural stem cells in vitro.

Jing Wang, Robert K Yu

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

66 citing papers in PubMed, 109 citations in OpenAlex.

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  15. Gangliosides in Neurodegenerative Diseases.Advances in neurobiology · 2023
    Article
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6 more citing papers are in PubMed but not listed here.

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.

Jing WangInstitute of Molecular Medicine and Genetics and Institute of Neuroscience, Medical College of Georgia, Georgia Regents University, Augusta, GA 30912.
Robert K Yu
Augusta University · US

Funding

Spingoglycolipids of normal and pathological brainsR01NS011853 · NINDS · YALE UNIVERSITY · PI YU, ROBERT K. · 1985 to 2010
$3.5M
ROLE OF GLYCOLIPIDS IN EXPERIMENTAL NEUROPATHYR01NS026994 · NINDS · VIRGINIA COMMONWEALTH UNIVERSITY · PI YU, ROBERT K. · 1988 to 2012
$3.3M
Effects of Gangliosides on Neural Stem Cells: Role in NeuroregenerationI01BX001388 · VA · CHARLIE NORWOOD VA MEDICAL CENTER · PI YU, ROBERT K. · 2012 to 2015
–
BLRD VA I01 BX001388NINDS NIH HHS NS11853NINDS NIH HHS NS26994NINDS NIH HHS R01 NS011853NINDS NIH HHS R01 NS026994
6 · The paper itself

Abstract

Mounting evidence supports the notion that gangliosides serve regulatory roles in neurogenesis; little is known, however, about how these glycosphingolipids function in neural stem cell (NSC) fate determination. We previously demonstrated that ganglioside GD3 is a major species in embryonic mouse brain: more than 80% of the NSCs obtained by the neurosphere method express GD3. To investigate the functional role of GD3 in neurogenesis, we compared the properties of NSCs from GD3-synthase knockout (GD3S-KO) mice with those from their wild-type littermates. NSCs from GD3S-KO mice showed decreased self-renewal ability compared with those from the wild-type animals, and that decreased ability was accompanied by reduced expression of EGF receptor (EGFR) and an increased degradation rate of EGFR and EGF-induced ERK signaling. We also showed that EGFR switched from the low-density lipid raft fractions in wild-type NSCs to the high-density layers in the GD3S-KO NSCs. Immunochemical staining revealed colocalization of EGFR and GD3, and EGFR could be immunoprecipitated from the NSC lysate with an anti-GD3 antibody from the wild-type, but not from the GD3S-KO, mice. Tracking the localization of endocytosed EGFR with endocytosis pathway markers indicated that more EGFR in GD3S-KO NSCs translocated through the endosomal-lysosomal degradative pathway, rather than through the recycling pathway. Those findings support the idea that GD3 interacts with EGFR in the NSCs and that the interaction is responsible for sustaining the expression of EGFR and its downstream signaling to maintain the self-renewal capability of NSCs.

Indexed as

AnimalsCell MembraneCell ProliferationCells, CulturedEndocytosisEpidermal Growth FactorErbB ReceptorsGangliosidesImmunoblottingImmunoprecipitationMiceMice, KnockoutMicroscopy, ConfocalNeural Stem CellsReal-Time Polymerase Chain ReactionSignal TransductionEpidermal Growth FactorErbB Receptorsganglioside, GD3Gangliosides

Identifiers

PMID24198336
PMCPMC3839736
OpenAlexW2139443474

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.