The DOI matches its Crossref record; 44 of the 44 references it cites were found in a registry or an index.
Ras-Independent Growth Factor Signaling by Transcription Factor Tyrosine Phosphorylation
Abstract
Interferons induce transcriptional activation through tyrosine phosphorylation of the latent, cytoplasmic transcription factor interferon-stimulated gene factor-3 (ISGF-3). Growth factors and cytokines were found to use a similar pathway: The 91-kilodalton subunit of ISGF-3 was activated and tyrosine phosphorylated in response to epidermal growth factor (EGF), platelet-derived growth factor, and colony stimulating factor-1. The tyrosine phosphorylated factor acquired DNA binding activity and accumulated in nuclei. Activation required the major sites for autophosphorylation on the EGF receptor that bind Src homology region 2 domain-containing proteins implicated in Ras activation. However, activation of this factor was independent of the normal functioning of Ras.
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Cites
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Self-citationSH2 and SH3 Domains: Elements that Control Interactions of Cytoplasmic Signaling Proteins
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Self-citationGrowth factor signaling by receptor tyrosine kinases
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Self-citation
Cited by
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The STATs of cancer — new molecular targets come of age
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Metadata
- Authors
- Silvennoinen, O., Schindler, C., Schlessinger, J., & Levy, D. E.
- Venue
- Science
- Published
- 1993-09-24
- Volume
- 261
- Issue
- 5129
- Pages
- 1736-1739
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W1997935194
- Cited by
- 338
- References
- 44
- FWCI
- 23.23
- Type
- journal article
- Language
- en
- Open access
- closed
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- Silvennoinen, O., Schindler, C., Schlessinger, J., & Levy, D. E. (1993). Ras-Independent Growth Factor Signaling by Transcription Factor Tyrosine Phosphorylation. Science. https://doi.org/10.1126/science.8378775
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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.
