Contrasting Signaling Pathways of α1A- and α1B-Adrenergic Receptor Subtype Activation of Phosphatidylinositol 3-Kinase and Ras in Transfected NIH3T3 Cells
| العنوان: | Contrasting Signaling Pathways of α1A- and α1B-Adrenergic Receptor Subtype Activation of Phosphatidylinositol 3-Kinase and Ras in Transfected NIH3T3 Cells |
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| المؤلفون: | Xiao-You Shi, Zhuo-Wei Hu, Brian B. Hoffman, Richard Z. Lin |
| المصدر: | Molecular Endocrinology. 13:3-14 |
| بيانات النشر: | The Endocrine Society, 1999. |
| سنة النشر: | 1999 |
| مصطلحات موضوعية: | GTPase-activating protein, G protein, Biology, Transfection, Proto-Oncogene Proteins p21(ras), Mice, Norepinephrine, Phosphatidylinositol 3-Kinases, chemistry.chemical_compound, Endocrinology, GTP-binding protein regulators, GTP-Binding Proteins, Receptors, Adrenergic, alpha-1, Animals, Humans, Virulence Factors, Bordetella, Phosphatidylinositol, Protein kinase A, Molecular Biology, G protein-coupled receptor kinase, Kinase, 3T3 Cells, General Medicine, Cyclic AMP-Dependent Protein Kinases, Molecular biology, Recombinant Proteins, Cell biology, Enzyme Activation, Pertussis Toxin, chemistry, beta-Adrenergic Receptor Kinases, Calcium-Calmodulin-Dependent Protein Kinases, Mutation, Signal transduction, Adrenergic alpha-Agonists, Signal Transduction |
| الوصف: | Activation of protein kinases is an important intermediate step in signaling pathways of many G protein-coupled receptors including alpha1-adrenergic receptors. The present study was designed to investigate the capacity of the three cloned subtypes of human alpha1-receptors, namely, alpha1A, alpha1B and alpha1D to activate phosphatidylinositol 3-kinase (PI 3-kinase) and p21ras in transfected NIH3T3 cells. Norepinephrine activated PI 3-kinase in cells expressing human alpha1A and alpha1B via pertussis toxin-insensitive G proteins; alpha1D-receptors did not detectably activate this kinase. Transient transfection of NIH 3T3 cells with the alpha-subunit of the G protein transducin (alpha(t)) a scavenger of betagamma-subunits released from activated G proteins, inhibited alpha1B-receptor but not alpha1A-receptor-stimulated PI 3-kinase activity. Stimulation of both alpha1A- and alpha1B-receptors activated p21ras and stimulated guanine nucleotide exchange on Ras protein. Overexpression of a dominant negative mutant of p21ras attenuated alpha1B-receptor but not alpha1A-receptor activation of PI 3-kinase. Overexpression of a dominant negative mutant of PI 3-kinase attenuated alpha1A- but not alpha1B-receptor-stimulated mitogen-activated protein kinase activity. These results demonstrate the capacity for heterologous signaling of the alpha1-adrenergic receptor subtypes in promoting cellular responses in NIH3T3 cells. |
| تدمد: | 1944-9917 0888-8809 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::b8ecffa667de67a9e0b91406b02283d7Test https://doi.org/10.1210/mend.13.1.0215Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....b8ecffa667de67a9e0b91406b02283d7 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 19449917 08888809 |
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