Inhibition of Constitutive Signaling of Kaposi's Sarcoma–associated Herpesvirus G Protein–Coupled Receptor by Protein Kinases in Mammalian Cells in Culture

التفاصيل البيبلوغرافية
العنوان: Inhibition of Constitutive Signaling of Kaposi's Sarcoma–associated Herpesvirus G Protein–Coupled Receptor by Protein Kinases in Mammalian Cells in Culture
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