The DOI matches its Crossref record; 34 of the 34 references it cites were found in a registry or an index.
An Interleukin-4-Induced Transcription Factor: IL-4 Stat
Abstract
Interleukin-4 (IL-4) is an immunomodulatory cytokine secreted by activated T lymphocytes, basophils, and mast cells. It plays an important role in modulating the balance of T helper (Th) cell subsets, favoring expansion of the Th2 lineage relative to Th1. Imbalance of these T lymphocyte subsets has been implicated in immunological diseases including allergy, inflammation, and autoimmune disease. IL-4 may mediate its biological effects, at least in part, by activating a tyrosine-phosphorylated DNA binding protein. This protein has now been purified and its encoding gene cloned. Examination of the primary amino acid sequence of this protein indicates that it is a member of the signal transducers and activators of transcription (Stat) family of DNA binding proteins, hereby designated IL-4 Stat. Study of the inhibitory activities of phosphotyrosine-containing peptides derived from the intracellular domain of the IL-4 receptor provided evidence for direct coupling of receptor and transcription factor during the IL-4 Stat activation cycle. Such observations indicate that IL-4 Stat has the same functional domain for both receptor coupling and dimerization.
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Cites
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The JAK/STAT signaling pathway: from bench to clinic
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Metadata
- Authors
- Hou, J., Schindler, U., Henzel, W. J., Ho, T. C., Brasseur, M., & McKnight, S. L.
- Venue
- Science
- Published
- 1994-09-16
- Volume
- 265
- Issue
- 5179
- Pages
- 1701-1706
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W2052172628
- Cited by
- 854
- References
- 34
- FWCI
- 37.97
- Type
- journal article
- Language
- en
- Open access
- closed
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- Hou, J., Schindler, U., Henzel, W. J., Ho, T. C., Brasseur, M., & McKnight, S. L. (1994). An Interleukin-4-Induced Transcription Factor: IL-4 Stat. Science. https://doi.org/10.1126/science.8085155
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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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