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Cited by 879

The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.

Bifunctional role of glycosphingolipids. Modulators for transmembrane signaling and mediators for cellular interactions.

Open access
Hakomori, S·1990·Journal of Biological Chemistry

Abstract

Glycosphingolipids (GSLs), or their modified catabolites, at the cell surface modulate transmembrane signal transduction by influencing protein kinases associated with growth factor receptors and protein kinase C. On the other hand, the same or different GSLs at the cell surface interact in highly specific fashion with other GSLs or with binding proteins, possibly at the surface of adjacent interacting cells or in the extracellular matrix. The GSL-GSL interaction apparently provides the basis for a specific cell recognition system independent of the fibronectin/integrin or surface lectin systems, occurring earlier during a cell recognition event.

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Crossref · 10.1016/s0021-9258(17)30565-3

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Metadata

Authors
Hakomori, S.
Venue
Journal of Biological Chemistry
Publisher
Elsevier BV
Published
1990-11
Volume
265
Issue
31
Pages
18713-18716
ISSN
0021-9258 (ISSN-L)
OpenAlex
W1680920356
Cited by
879
References
2
FWCI
15.53
Type
journal article
Language
en
Open access
hybrid

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CoChat. (2026). Citation check: Bifunctional role of glycosphingolipids. Modulators for transmembrane signaling and mediators for cellular interactions. https://app.cochat.ai/papers/10.1016/s0021-9258(17)30565-3
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Hakomori, S. (1990). Bifunctional role of glycosphingolipids. Modulators for transmembrane signaling and mediators for cellular interactions. Journal of Biological Chemistry. https://doi.org/10.1016/s0021-9258(17)30565-3

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.