Evidence map›Paper›PMID 21454696›Full record

ArticleThe Journal of biological chemistry2011

Functional activation of Src family kinase yes protein is essential for the enhanced malignant properties of human melanoma cells expressing ganglioside GD3.

Kazunori Hamamura, Momoko Tsuji, Hiroshi Hotta, Yuki Ohkawa, Masataka Takahashi, Hidenobu Shibuya, Hideyuki Nakashima, Yoshio Yamauchi, Noboru Hashimoto, Hisashi Hattori and 3 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

40 citing papers in PubMed, 75 citations in OpenAlex.

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  16. Gangliosides as Signaling Regulators in Cancer.International journal of molecular sciences · 2021
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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

13 authors at 2 institutions in 1 country.

Kazunori HamamuraDepartment of Biochemistry II, Nagoya University Graduate School of Medicine, 65 Tsurumai, Showa-ku, Nagoya 466-0065, USA.
Momoko Tsuji
Hiroshi Hotta
Yuki Ohkawa
Masataka Takahashi
Hidenobu Shibuya
Hideyuki Nakashima
Yoshio Yamauchi
Noboru Hashimoto
Hisashi Hattori
Minoru Ueda
Keiko Furukawa
Koichi Furukawa
Nagoya University · JPChubu University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The possible roles of Src family kinases in the enhanced malignant properties of melanomas related to GD3 expression were analyzed. Among Src family kinases only Yes, not Fyn or Src, was functionally involved in the increased cell proliferation and invasion of GD3-expressing transfectant cells (GD3+). Yes was located upstream of p130Cas and paxillin and at an equivalent level to focal adhesion kinase. Yes underwent autophosphorylation even before serum treatment and showed stronger kinase activity in GD3+ cells than in GD3- cells following serum treatment. Coimmunoprecipitation experiments revealed that Yes bound to focal adhesion kinase or p130Cas more strongly in GD3+ cells than in GD3- cells. As a possible mechanism for the enhancing effects of GD3 on cellular phenotypes, it was shown that majority of Yes was localized in glycolipid-enriched microdomain/rafts in GD3+ cells even before serum treatment, whereas it was scarcely detected in glycolipid-enriched microdomain/rafts in GD3- cells. An in vitro kinase assay of Yes revealed that coexistence of GD3 with Yes in membranous environments enhances the kinase activity of GD3- cell-derived Yes toward enolase, p125, and Yes itself. Knockdown of GD3 synthase resulted in the alleviation of tumor phenotypes and reduced activation levels of Yes. Taken together, these results suggest a role of GD3 in the regulation of Src family kinases.

Indexed as

Gene Expression Regulation, NeoplasticCell Line, TumorCrk-Associated Substrate ProteinEnzyme ActivationFocal Adhesion Protein-Tyrosine KinasesGangliosidesGene Knockdown TechniquesHumansMelanomaMembrane MicrodomainsPhosphopyruvate HydrataseProto-Oncogene Proteins c-yesSialyltransferasesalpha-N-acetylneuraminate alpha-2,8-sialyltransferaseCrk-Associated Substrate ProteinFocal Adhesion Protein-Tyrosine Kinasesganglioside, GD3GangliosidesPhosphopyruvate HydrataseProto-Oncogene Proteins c-yesSialyltransferasesYES1 protein, human

Identifiers

PMID21454696
PMCPMC3099669
OpenAlexW2003859883

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.