ArticleProceedings of the National Academy of Sciences of the United States of America1992
A human interleukin 3 analog with increased biological and binding activities.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 49 citations in OpenAlex.
- Cardiovascular Toxicity of Antineoplastic Treatments in Hematological Diseases: Focus on Molecular Mechanisms to Improve Therapeutic Management.Journal of clinical medicine · 2024Review
- Structural and evolutionary exploration of the IL-3 family and its alpha subunit receptors.Amino acids · 2021Article
- Review
- In silico mutational analysis and identification of stability centers in human interleukin-4.Molecular biology research communications · 2018Article
- A dual role for the N-terminal domain of the IL-3 receptor in cell signalling.Nature communications · 2018Article
- AntiCD3Fv fused to human interleukin-3 deletion variant redirected T cells against human acute myeloid leukemic stem cells.Journal of hematology & oncology · 2015Article
- A cytokine-cytokine interaction in the assembly of higher-order structure and activation of the interleukine-3:receptor complex.PloS one · 2009Article
- Binding in the growth hormone receptor complex.Proceedings of the National Academy of Sciences of the United States of America · 1996Review
- Molecular modeling of the GM-CSF and IL-3 receptor complexes.Protein science : a publication of the Protein Society · 1995Article
- Identification of receptor-binding domains on human interleukin 5 and design of an interleukin 5-derived receptor antagonist.Proceedings of the National Academy of Sciences of the United States of America · 1995Article
- Homology model of human interferon-alpha 8 and its receptor complex.Protein science : a publication of the Protein Society · 1995Article
- Molecular evolution of interleukin-3.Journal of molecular evolution · 1994Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Human interleukin 3 (IL-3) variants generated by site-directed mutagenesis were analyzed in multiple biological and binding assays to identify residues critical for IL-3 activity. Two mutants carrying substitutions in the predicted hydrophilic region within the first alpha-helix, [Ala21,Leu22]IL-3 and [Ala21,Leu22,Ala25]IL-3 showed loss of biological activity and high-affinity binding. Mutants in a second predicted hydrophilic region, [Ala44,Leu45,Ala46]IL-3 and [Ala44,Ala46]IL-3, however, showed similar biological and binding activities to wild-type IL-3. Mutations in a C-terminal hydrophilic region that overlaps the fourth predicted alpha-helix led to either loss or gain of function. IL-3 analogs [Glu104,Asp105]-, [Leu108]-, [Asn108]-, [Thr108]-, and [Ala101,Leu108]IL-3 were less active than wild-type IL-3, whereas [Ala101]IL-3 and [Val116]IL-3 were 2- to 3-fold more potent. Significantly, the double mutant [Ala101,Val116]IL-3 exhibited a 15-fold greater potency than native IL-3. Receptor binding studies showed that [Ala101,Val116]IL-3 exhibited increased binding to the high- and low-affinity receptors of monocytes. These results show the generation of an IL-3 analog with increased biological and binding activities and support a model where the C terminus of IL-3 interacts with the alpha chain of the IL-3 receptor, making this region a useful focus for the development of more potent IL-3 agonists or antagonists.
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