GRK expression in GBM
نویسندگان
چکیده
Department of Pediatrics, Division of Biostatistics, Bright Institute, Department of Pathology and Immunology, Molecular Imaging Center, Mallinckrodt Institute of Radiology, Cell Biology and Physiology, Department of Anatomy and Neurobiology, Washington University School of Medicine, St Louis, MO, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, Department of Biochemistry and Molecular Biology, Thomas Jefferson University, Philadelphia, PA
منابع مشابه
Suppression of G-protein-coupled receptor kinase 3 expression is a feature of classical GBM that is required for maximal growth.
G-protein-coupled receptor kinases (GRK) regulate the function of G-protein-coupled receptors (GPCR). Previously, we found that GPCR (CXCR4)-mediated astrocytoma growth was dependent upon abnormally sustained CXCR4 signaling and was correlated with decreased GRK-mediated receptor phosphorylation. As CXCR4 has also been implicated in the stimulation of high-grade glioma growth, we sought to dete...
متن کاملSignaling and Regulation Suppression of G-protein–Coupled Receptor Kinase 3 Expression Is a Feature of Classical GBM That Is Required for Maximal Growth
G-protein–coupled receptor kinases (GRK) regulate the function of G-protein–coupled receptors (GPCR). Previously, we found that GPCR (CXCR4)-mediated astrocytoma growth was dependent upon abnormally sustained CXCR4 signaling and was correlated with decreased GRK-mediated receptor phosphorylation. As CXCR4 has also been implicated in the stimulation of high-grade glioma growth, we sought to dete...
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تاریخ انتشار 2011