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פותח על ידי קלירמאש פתרונות בע"מ -
Interleukin (IL)-2 and IL-3 induce distinct but overlapping responses in murine IL-3-dependent 32D cells transduced with human IL-2 receptor β chain: Involvement of tyrosine kinase(s) other than p56lck
Year:
1992
Authors :
שרון, מיכל
;
.
Volume :
89
Co-Authors:
Otani, H., Cell Biology and Metabolism Branch, Natl. Inst. Child Hlth. Hum. Devmt., Bethesda, MD 20892, United States
Siegel, J.P., Laboratory of Cellular Immunology, Division of Cytokine Biology, Ctr. for Biologies Eval./Research, Bethesda, MD 20892, United States
Erdos, M., Cell Biology and Metabolism Branch, Natl. Inst. Child Hlth. Hum. Devmt., Bethesda, MD 20892, United States, Intramural Research Program, Natl. Heart Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892, United States
Gnarra, J.R., Cell Biology and Metabolism Branch, Natl. Inst. Child Hlth. Hum. Devmt., Bethesda, MD 20892, United States
Toledano, M.B., Cell Biology and Metabolism Branch, Natl. Inst. Child Hlth. Hum. Devmt., Bethesda, MD 20892, United States
Sharon, M., Cell Biology and Metabolism Branch, Natl. Inst. Child Hlth. Hum. Devmt., Bethesda, MD 20892, United States
Mostowski, H., Laboratory of Cellular Immunology, Division of Cytokine Biology, Ctr. for Biologies Eval./Research, Bethesda, MD 20892, United States
Feinberg, M.B., Whitehead Inst. for Biomed. Research, Cambridge, MA 02142, United States
Pierce, J.H., Lab. of Cell. and Molecular Biology, National Cancer Institute, Bethesda, MD 20892, United States
Leonard, W.J., Cell Biology and Metabolism Branch, Natl. Inst. Child Hlth. Hum. Devmt., Bethesda, MD 20892, United States, Intramural Research Program, Natl. Heart Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892, United States
Facilitators :
From page:
2789
To page:
2793
(
Total pages:
5
)
Abstract:
We have established IL-3-dependent 32D my id progenitor cells stably expressing the human IL-2 receptor β chain (IL-2Rβ). Whereas parental 32D cells proliferated only in response to IL-3, the transduced cells also proliferated in response to IL-2. Transduced cells expressed high- and intermediate-affinity IL-2Rs, resulting from expression of human IL-2Rβ and murine IL-2R α chain (IL-2Rα). IL-2 induced phenotypic changes not induced by IL-3, including the upregulated expression of endogenous murine IL-2Rα and IL-2Rβ and an increase in cell size. Therefore, the transduced IL-2Rβ was not merely coupling with the IL-3 signaling pathway. IL-3 augmented several IL-2-induced responses including the upregulation of IL-2Rα. Both IL-2- and IL-3-induced proliferation and IL-2 induced IL-2Rα expression were inhibited by the tyrosine kinase inhibitor herbimycin A. Thus, both IL-2- and IL-3-mediated effects required tyrosine kinase activity. The identity of the tyrosine kinase(s) mediating the IL-2 signals in these cells is not known but cannot be p56lck, a tyrosine kinase Sound in T cells, since 32D-IL-2Rβ cells do not express p56lck.
Note:
Related Files :
alpha chain
Animal
animal cell
Cell Division
enzyme activity
Hematopoietic Stem Cells
mice
Murinae
Quinones
עוד תגיות
תוכן קשור
More details
DOI :
Article number:
Affiliations:
Database:
סקופוס
Publication Type:
מאמר
;
.
Language:
אנגלית
Editors' remarks:
ID:
27082
Last updated date:
02/03/2022 17:27
Creation date:
17/04/2018 00:28
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Scientific Publication
Interleukin (IL)-2 and IL-3 induce distinct but overlapping responses in murine IL-3-dependent 32D cells transduced with human IL-2 receptor β chain: Involvement of tyrosine kinase(s) other than p56lck
89
Otani, H., Cell Biology and Metabolism Branch, Natl. Inst. Child Hlth. Hum. Devmt., Bethesda, MD 20892, United States
Siegel, J.P., Laboratory of Cellular Immunology, Division of Cytokine Biology, Ctr. for Biologies Eval./Research, Bethesda, MD 20892, United States
Erdos, M., Cell Biology and Metabolism Branch, Natl. Inst. Child Hlth. Hum. Devmt., Bethesda, MD 20892, United States, Intramural Research Program, Natl. Heart Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892, United States
Gnarra, J.R., Cell Biology and Metabolism Branch, Natl. Inst. Child Hlth. Hum. Devmt., Bethesda, MD 20892, United States
Toledano, M.B., Cell Biology and Metabolism Branch, Natl. Inst. Child Hlth. Hum. Devmt., Bethesda, MD 20892, United States
Sharon, M., Cell Biology and Metabolism Branch, Natl. Inst. Child Hlth. Hum. Devmt., Bethesda, MD 20892, United States
Mostowski, H., Laboratory of Cellular Immunology, Division of Cytokine Biology, Ctr. for Biologies Eval./Research, Bethesda, MD 20892, United States
Feinberg, M.B., Whitehead Inst. for Biomed. Research, Cambridge, MA 02142, United States
Pierce, J.H., Lab. of Cell. and Molecular Biology, National Cancer Institute, Bethesda, MD 20892, United States
Leonard, W.J., Cell Biology and Metabolism Branch, Natl. Inst. Child Hlth. Hum. Devmt., Bethesda, MD 20892, United States, Intramural Research Program, Natl. Heart Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892, United States
Interleukin (IL)-2 and IL-3 induce distinct but overlapping responses in murine IL-3-dependent 32D cells transduced with human IL-2 receptor β chain: Involvement of tyrosine kinase(s) other than p56lck
We have established IL-3-dependent 32D my id progenitor cells stably expressing the human IL-2 receptor β chain (IL-2Rβ). Whereas parental 32D cells proliferated only in response to IL-3, the transduced cells also proliferated in response to IL-2. Transduced cells expressed high- and intermediate-affinity IL-2Rs, resulting from expression of human IL-2Rβ and murine IL-2R α chain (IL-2Rα). IL-2 induced phenotypic changes not induced by IL-3, including the upregulated expression of endogenous murine IL-2Rα and IL-2Rβ and an increase in cell size. Therefore, the transduced IL-2Rβ was not merely coupling with the IL-3 signaling pathway. IL-3 augmented several IL-2-induced responses including the upregulation of IL-2Rα. Both IL-2- and IL-3-induced proliferation and IL-2 induced IL-2Rα expression were inhibited by the tyrosine kinase inhibitor herbimycin A. Thus, both IL-2- and IL-3-mediated effects required tyrosine kinase activity. The identity of the tyrosine kinase(s) mediating the IL-2 signals in these cells is not known but cannot be p56lck, a tyrosine kinase Sound in T cells, since 32D-IL-2Rβ cells do not express p56lck.
Scientific Publication
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