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Cited by 367

The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.

Newest findings on the oldest oncogene; how activated src does it

Frame, Margaret C.·2004·Journal of Cell Science

Abstract

Oncogenic forms of the non-receptor tyrosine kinase Src alter cell structure, in particular the actin cytoskeleton and the adhesion networks that control cell migration, and also transmit signals that regulate proliferation and cell survival. Recent work indicates that they do so by influencing the RhoA-ROCK pathway that controls contractile actin filament assembly, the STAT family of transcription factors needed for transformation, and the Cbl ubiquitin ligase that controls Src protein levels. These studies also shed light on the role of focal adhesion kinase (FAK) downstream of v-Src and other signalling pathways in controlling migration, invasion and survival of transformed cells. Src directly phosphorylates integrins and can also modulate R-Ras activity. Moreover, it stimulates the E-cadherin regulator Hakai, interacts with and phosphorylates the novel podosome-linked adaptor protein Fish, and progressively phosphorylates the gap junction component connexion 43. A recurring theme is the identification of novel and important Src substrates that mediate key biological events associated with transformation.

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Metadata

Authors
Frame, M. C.
Venue
Journal of Cell Science
Published
2004-03-01
Volume
117
Issue
7
Pages
989-998
ISSN
  • 0021-9533 (ISSN-L)
  • 1477-9137
OpenAlex
W1965878299
Cited by
367
References
8
FWCI
10.28
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Newest findings on the oldest oncogene; how activated src does it. https://app.cochat.ai/papers/10.1242/jcs.01111
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Frame, M. C. (2004). Newest findings on the oldest oncogene; how activated src does it. Journal of Cell Science. https://doi.org/10.1242/jcs.01111

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

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