Inhibition of Constitutive Signaling of Kaposi's Sarcoma–associated Herpesvirus G Protein–Coupled Receptor by Protein Kinases in Mammalian Cells in Culture
العنوان: | Inhibition of Constitutive Signaling of Kaposi's Sarcoma–associated Herpesvirus G Protein–Coupled Receptor by Protein Kinases in Mammalian Cells in Culture |
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المؤلفون: | Leandros Arvanitakis, Enrique A. Mesri, Carlos Bais, Marvin C. Gershengorn, Ethel Cesarman, Elizabeth Geras-Raaka |
المصدر: | The Journal of Experimental Medicine |
بيانات النشر: | Rockefeller University Press, 1998. |
سنة النشر: | 1998 |
مصطلحات موضوعية: | G-Protein-Coupled Receptor Kinase 5, Inositol Phosphates, viruses, Immunology, Receptor Protein-Tyrosine Kinases, Protein Serine-Threonine Kinases, Biology, Transfection, medicine.disease_cause, Mice, Viral Proteins, 03 medical and health sciences, 0302 clinical medicine, medicine, Animals, Immunology and Allergy, Kaposi's sarcoma-associated herpesvirus, Sarcoma, Kaposi, Cells, Cultured, Protein Kinase C, 030304 developmental biology, G protein-coupled receptor, 0303 health sciences, G protein-coupled receptor kinase, Phospholipase C, Kinase, Brief Definitive Report, virus diseases, 3T3 Cells, Cyclic AMP-Dependent Protein Kinases, 3. Good health, Cell biology, beta-Adrenergic Receptor Kinases, 030220 oncology & carcinogenesis, COS Cells, Herpesvirus 8, Human, Brief Definitive Reports, Receptors, Chemokine, Signal transduction, Cell Division, Signal Transduction |
الوصف: | Kaposi's sarcoma–associated herpesvirus (KSHV)/human herpesvirus 8, which is consistently present in tissues of patients with Kaposi's sarcoma and primary effusion lymphomas, contains a gene that encodes a G protein–coupled receptor (KSHV-GPCR). We recently showed that KSHV-GPCR exhibits constitutive signaling via activation of phosphoinositide-specific phospholipase C and stimulates cell proliferation and transformation. In this study, we determined whether normal cellular mechanisms could inhibit constitutive signaling by KSHV-GPCR and thereby KSHV-GPCR–stimulated proliferation. We show that coexpression of GPCR-specific kinases (GRKs) and activation of protein kinase C inhibit constitutive signaling by KSHV-GPCR in COS-1 monkey kidney cells and in mouse NIH 3T3 cells. Moreover, GRK-5 but not GRK-2 inhibits KSHV-GPCR–stimulated proliferation of rodent fibroblasts. These data provide evidence that cell regulatory pathways of receptor desensitization may be therapeutic targets in human diseases involving constitutively active receptors. |
تدمد: | 1540-9538 0022-1007 |
الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::f1ff3014d8f7b8b0ad3a21afe49e9b50Test https://doi.org/10.1084/jem.187.5.801Test |
حقوق: | OPEN |
رقم الانضمام: | edsair.doi.dedup.....f1ff3014d8f7b8b0ad3a21afe49e9b50 |
قاعدة البيانات: | OpenAIRE |
تدمد: | 15409538 00221007 |
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