L M Luttrell

Summary

Affiliation: Duke University Medical Center
Country: USA

Publications

  1. pmc Activation and targeting of extracellular signal-regulated kinases by beta-arrestin scaffolds
    L M Luttrell
    The Geriatrics Research, Education and Clinical Center, Durham Veterans Affairs Medical Center, Durham, NC 27705, USA
    Proc Natl Acad Sci U S A 98:2449-54. 2001
  2. ncbi request reprint Not so strange bedfellows: G-protein-coupled receptors and Src family kinases
    Deirdre K Luttrell
    Department of Medicine, Medical University of South Carolina, Charleston, SC, 29425, USA
    Oncogene 23:7969-78. 2004
  3. ncbi request reprint Signaling in time and space: G protein-coupled receptors and mitogen-activated protein kinases
    Deirdre K Luttrell
    Department of High Throughput Biology, GlaxoSmithKline, Research Triangle Park, North Carolina, USA
    Assay Drug Dev Technol 1:327-38. 2003
  4. ncbi request reprint 'Location, location, location': activation and targeting of MAP kinases by G protein-coupled receptors
    L M Luttrell
    Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Mol Endocrinol 30:117-26. 2003
  5. ncbi request reprint Transactivation of the EGF receptor mediates IGF-1-stimulated shc phosphorylation and ERK1/2 activation in COS-7 cells
    F L Roudabush
    Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Biol Chem 275:22583-9. 2000
  6. ncbi request reprint Activation and targeting of mitogen-activated protein kinases by G-protein-coupled receptors
    Louis M Luttrell
    Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA
    Can J Physiol Pharmacol 80:375-82. 2002
  7. ncbi request reprint Beta-arrestin-dependent formation of beta2 adrenergic receptor-Src protein kinase complexes
    L M Luttrell
    Howard Hughes Medical Institute and Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA
    Science 283:655-61. 1999
  8. ncbi request reprint beta-arrestin1 interacts with the catalytic domain of the tyrosine kinase c-SRC. Role of beta-arrestin1-dependent targeting of c-SRC in receptor endocytosis
    W E Miller
    Department of Medicine, Howard Hughes Medical Institute, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Biol Chem 275:11312-9. 2000
  9. ncbi request reprint The beta(2)-adrenergic receptor mediates extracellular signal-regulated kinase activation via assembly of a multi-receptor complex with the epidermal growth factor receptor
    S Maudsley
    Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Biol Chem 275:9572-80. 2000
  10. ncbi request reprint Direct binding of activated c-Src to the beta 3-adrenergic receptor is required for MAP kinase activation
    W Cao
    Departments of Psychiatry and Behavioral Sciences, Pharmacology, and Medicine and the Howard Hughes Medical Institute, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Biol Chem 275:38131-4. 2000

Collaborators

Detail Information

Publications52

  1. pmc Activation and targeting of extracellular signal-regulated kinases by beta-arrestin scaffolds
    L M Luttrell
    The Geriatrics Research, Education and Clinical Center, Durham Veterans Affairs Medical Center, Durham, NC 27705, USA
    Proc Natl Acad Sci U S A 98:2449-54. 2001
    ..These data suggest that beta-arrestins function both as scaffolds to enhance cRaf-1 and MEK-dependent activation of ERK2, and as targeting proteins that direct activated ERK to specific subcellular locations...
  2. ncbi request reprint Not so strange bedfellows: G-protein-coupled receptors and Src family kinases
    Deirdre K Luttrell
    Department of Medicine, Medical University of South Carolina, Charleston, SC, 29425, USA
    Oncogene 23:7969-78. 2004
    ..It is now clear that GPCRs and Src family kinases do not belong to separate, exclusive clubs. Rather, these strange bedfellows are intimately involved in multilayered forms of crosstalk that influence a host of cellular processes...
  3. ncbi request reprint Signaling in time and space: G protein-coupled receptors and mitogen-activated protein kinases
    Deirdre K Luttrell
    Department of High Throughput Biology, GlaxoSmithKline, Research Triangle Park, North Carolina, USA
    Assay Drug Dev Technol 1:327-38. 2003
    ....
  4. ncbi request reprint 'Location, location, location': activation and targeting of MAP kinases by G protein-coupled receptors
    L M Luttrell
    Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Mol Endocrinol 30:117-26. 2003
    ..Some signals lead to the targeting of activated MAP kinase to specific extranuclear locations, while others activate a MAP kinase pool that is free to translocate to the nucleus and contribute to a mitogenic response...
  5. ncbi request reprint Transactivation of the EGF receptor mediates IGF-1-stimulated shc phosphorylation and ERK1/2 activation in COS-7 cells
    F L Roudabush
    Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Biol Chem 275:22583-9. 2000
    ....
  6. ncbi request reprint Activation and targeting of mitogen-activated protein kinases by G-protein-coupled receptors
    Louis M Luttrell
    Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA
    Can J Physiol Pharmacol 80:375-82. 2002
    ..By controlling the spatial and temporal distribution of MAP kinase activity within the cell, the consequences of GPCR-stimulated MAP kinase activation may be determined by the mechanism by which they are activated...
  7. ncbi request reprint Beta-arrestin-dependent formation of beta2 adrenergic receptor-Src protein kinase complexes
    L M Luttrell
    Howard Hughes Medical Institute and Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA
    Science 283:655-61. 1999
    ....
  8. ncbi request reprint beta-arrestin1 interacts with the catalytic domain of the tyrosine kinase c-SRC. Role of beta-arrestin1-dependent targeting of c-SRC in receptor endocytosis
    W E Miller
    Department of Medicine, Howard Hughes Medical Institute, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Biol Chem 275:11312-9. 2000
    ....
  9. ncbi request reprint The beta(2)-adrenergic receptor mediates extracellular signal-regulated kinase activation via assembly of a multi-receptor complex with the epidermal growth factor receptor
    S Maudsley
    Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Biol Chem 275:9572-80. 2000
    ..Thus, RTK transactivation is revealed to be a process involving both association of receptors of distinct classes and the interaction of the transactivated RTK with the cells endocytic machinery...
  10. ncbi request reprint Direct binding of activated c-Src to the beta 3-adrenergic receptor is required for MAP kinase activation
    W Cao
    Departments of Psychiatry and Behavioral Sciences, Pharmacology, and Medicine and the Howard Hughes Medical Institute, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Biol Chem 275:38131-4. 2000
    ..Together, these data describe a novel mechanism of ERK activation by a G protein-coupled receptor in which the intracellular domains directly recruit c-Src...
  11. ncbi request reprint Epidermal growth factor (EGF) receptor-dependent ERK activation by G protein-coupled receptors: a co-culture system for identifying intermediates upstream and downstream of heparin-binding EGF shedding
    K L Pierce
    Howard Hughes Medical Institute and the Departments of Medicine and Biochemistry, Box 3821, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Biol Chem 276:23155-60. 2001
    ....
  12. ncbi request reprint Feedback regulation of beta-arrestin1 function by extracellular signal-regulated kinases
    F T Lin
    Howard Hughes Medical Institute, Departments of Medicine and Biochemistry, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Biol Chem 274:15971-4. 1999
    ..Our results suggest that dephosphorylated beta-arrestin1 mediates endocytosis-dependent ERK activation. Following activation, ERKs phosphorylate beta-arrestin1, thereby exerting an inhibitory feedback control of its function...
  13. ncbi request reprint Src-mediated tyrosine phosphorylation of dynamin is required for beta2-adrenergic receptor internalization and mitogen-activated protein kinase signaling
    S Ahn
    Howard Hughes Medical Institute, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Biol Chem 274:1185-8. 1999
    ..Thus, agonist-induced, c-Src-mediated tyrosine phosphorylation of dynamin is essential for its function in clathrin mediated G protein-coupled receptor endocytosis...
  14. ncbi request reprint New mechanisms in heptahelical receptor signaling to mitogen activated protein kinase cascades
    K L Pierce
    The Howard Hughes Medical Institute, Box 3821, Duke University Medical Center, Durham, North Carolina, NC 27710, USA
    Oncogene 20:1532-9. 2001
    ....
  15. pmc Platelet-derived growth factor receptor association with Na(+)/H(+) exchanger regulatory factor potentiates receptor activity
    S Maudsley
    Howard Hughes Medical Institute, Departments of Medicine and Biochemistry, Duke University Medical Center, Durham, NC 27710, USA
    Mol Cell Biol 20:8352-63. 2000
    ....
  16. ncbi request reprint Targeting the receptor-Gq interface to inhibit in vivo pressure overload myocardial hypertrophy
    S A Akhter
    Department of Surgery, Duke University Medical Center, Durham, NC 27710, USA
    Science 280:574-7. 1998
    ..The data demonstrate the role of myocardial Gq in the initiation of myocardial hypertrophy and indicate a possible strategy for preventing pathophysiological signaling by simultaneously blocking multiple receptors coupled to Gq...
  17. ncbi request reprint beta -Arrestin-mediated recruitment of the Src family kinase Yes mediates endothelin-1-stimulated glucose transport
    T Imamura
    Department of Medicine, Division of Endocrinology and Metabolism, University of California, San Diego, La Jolla, California 92093 0673, USA
    J Biol Chem 276:43663-7. 2001
    ....
  18. ncbi request reprint Gbetagamma subunits mediate Src-dependent phosphorylation of the epidermal growth factor receptor. A scaffold for G protein-coupled receptor-mediated Ras activation
    L M Luttrell
    Howard Hughes Medical Institute and the Departments of Medicine and Biochemistry, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Biol Chem 272:4637-44. 1997
    ....
  19. ncbi request reprint Cellular expression of the carboxyl terminus of a G protein-coupled receptor kinase attenuates G beta gamma-mediated signaling
    W J Koch
    Howard Hughes Medical Institute, Duke University Medical Center, Durham, North Carolina 27710
    J Biol Chem 269:6193-7. 1994
    ....
  20. ncbi request reprint Activation of extracellular signal-regulated kinase in human prostate cancer
    D T Price
    Department of Surgery, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Urol 162:1537-42. 1999
    ..To investigate the level of expression, activation state, and functional significance of extracellular signal regulated kinase (ERK) in prostate cancer...
  21. ncbi request reprint G protein-coupled receptors desensitize and down-regulate epidermal growth factor receptors in renal mesangial cells
    J S Grewal
    Nephrology Division, Department of Medicine, Medical University of South Carolina, Charleston, South Carolina 29425, USA
    J Biol Chem 276:27335-44. 2001
    ..Moreover, GPCRs induce profound desensitization of EGFRs by a process associated with the loss of cell-surface EGFRs through clathrin-mediated endocytosis...
  22. ncbi request reprint beta-Arrestin 2 expression determines the transcriptional response to lysophosphatidic acid stimulation in murine embryo fibroblasts
    Diane Gesty-Palmer
    Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Biol Chem 280:32157-67. 2005
    ..These data indicate that beta-arrestin 2 functions both to attenuate EGF receptor transactivation-dependent signaling and to promote a distinct subset of ERK1/2-mediated responses to LPA receptor activation...
  23. ncbi request reprint Arrestin-mediated ERK activation by gonadotropin-releasing hormone receptors: receptor-specific activation mechanisms and compartmentalization
    Christopher J Caunt
    Henry Wellcome Laboratories for Integrative Neuroscience and Endocrinology, University of Bristol, Whitson Street, Bristol BS1 3NY, United Kingdom
    J Biol Chem 281:2701-10. 2006
    ....
  24. ncbi request reprint Distinct beta-arrestin- and G protein-dependent pathways for parathyroid hormone receptor-stimulated ERK1/2 activation
    Diane Gesty-Palmer
    Department of Medicine, Howard Hughes Medical Institute, Duke University, Medical Center, Durham, North Carolina 27710, USA
    J Biol Chem 281:10856-64. 2006
    ..These findings imply the existence of distinct active conformations of the hPTH1R responsible for the two pathways, which can be stimulated by unique ligands. Such ligands may have distinct and valuable therapeutic properties...
  25. ncbi request reprint Constitutive ERK1/2 activation by a chimeric neurokinin 1 receptor-beta-arrestin1 fusion protein. Probing the composition and function of the G protein-coupled receptor "signalsome"
    Farahdiba Jafri
    Department of Medicine, Medical University of South Carolina, Charleston, South Carolina 29425, USA
    J Biol Chem 281:19346-57. 2006
    ..These data suggest that beta-arrestin binding to GPCRs nucleates the formation of a stable "signalsome" that functions as a passive scaffold for the ERK1/2 cascade while confining ERK1/2 activity to an extranuclear compartment...
  26. ncbi request reprint Transmembrane signaling by G protein-coupled receptors
    Louis M Luttrell
    Department of Medicine and Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, USA
    Methods Mol Biol 332:3-49. 2006
    ..In some cases, these processes appear to generate signals in conjunction with, or even independent of, G protein activation...
  27. ncbi request reprint Insulin-like growth factors mediate heterotrimeric G protein-dependent ERK1/2 activation by transactivating sphingosine 1-phosphate receptors
    Hesham M El-Shewy
    Department of Medicine, Medical University of South Carolina, Charleston, South Carolina 29425, USA
    J Biol Chem 281:31399-407. 2006
    ..Given the ubiquity of SK and S1P receptor expression, S1P receptor transactivation may represent a general mechanism for G protein-dependent signaling by non-G protein-coupled receptors...
  28. pmc Beta-arrestins 1 and 2 differentially regulate LPS-induced signaling and pro-inflammatory gene expression
    Hongkuan Fan
    Department of Neurosciences, Medical University of South Carolina, Charleston, SC 29425, United States
    Mol Immunol 44:3092-9. 2007
    ..Understanding the role of beta-arrestins in regulation of TLR signaling pathways may provide novel insights into control mechanisms for inflammatory gene expression...
  29. ncbi request reprint The insulin-like growth factor type 1 and insulin-like growth factor type 2/mannose-6-phosphate receptors independently regulate ERK1/2 activity in HEK293 cells
    Hesham M El-Shewy
    Department of Medicine, Medical University of South Carolina, Charleston, South Carolina 29425, USA
    J Biol Chem 282:26150-7. 2007
    ..These data indicate that endogenous IGF-1 and IGF-2 receptors can independently initiate ERK1/2 signaling and point to a potential physiologic role for IGF-2 receptors in the cellular response to IGF-2...
  30. pmc Ubiquitination of beta-arrestin links seven-transmembrane receptor endocytosis and ERK activation
    Sudha K Shenoy
    Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Biol Chem 282:29549-62. 2007
    ....
  31. ncbi request reprint Role of beta-arrestin-mediated desensitization and signaling in the control of angiotensin AT1a receptor-stimulated transcription
    Mi Hye Lee
    Department of Medicine, Medical University of South Carolina, Charleston, South Carolina 29425, USA
    J Biol Chem 283:2088-97. 2008
    ....
  32. ncbi request reprint Heptahelical terpsichory. Who calls the tune?
    Diane Gesty-Palmer
    Department of Medicine Duke University Medical Center, Durham, North Carolina, USA
    J Recept Signal Transduct Res 28:39-58. 2008
    ....
  33. pmc The adiponectin receptors AdipoR1 and AdipoR2 activate ERK1/2 through a Src/Ras-dependent pathway and stimulate cell growth
    Mi Hye Lee
    Department of Medicine, Medical University of South Carolina, Charleston, South Carolina 29425, USA
    Biochemistry 47:11682-92. 2008
    ..These results suggest that adiponectin can exert proliferative effects by activating Ras signaling pathways...
  34. ncbi request reprint Composition and function of g protein-coupled receptor signalsomes controlling mitogen-activated protein kinase activity
    Louis M Luttrell
    Departments of Medicine and Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, SC 29425, USA
    J Mol Neurosci 26:253-64. 2005
    ..Together, these highly organized signaling complexes dictate the location, duration, and ultimate function of GPCR-stimulated MAP kinase activity...
  35. ncbi request reprint beta-Arrestin scaffolding of the ERK cascade enhances cytosolic ERK activity but inhibits ERK-mediated transcription following angiotensin AT1a receptor stimulation
    Akira Tohgo
    Howard Hughes Medical Institute and the Departments of Medicine and Biochemistry, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Biol Chem 277:9429-36. 2002
    ..These data demonstrate that beta-arrestins facilitate GPCR-mediated ERK activation but inhibit ERK-dependent transcription by binding to phospho-ERK1/2, leading to its retention in the cytosol...
  36. ncbi request reprint The role of beta-arrestins in the termination and transduction of G-protein-coupled receptor signals
    Louis M Luttrell
    The Howard Hughes Medical Institute, Duke University Medical Center, Durham, NC 27710, USA
    J Cell Sci 115:455-65. 2002
    ..Thus, their binding to GPCRs might initiate a second wave of signaling and represent a novel mechanism of GPCR signal transduction...
  37. ncbi request reprint Src-dependent tyrosine phosphorylation regulates dynamin self-assembly and ligand-induced endocytosis of the epidermal growth factor receptor
    Seungkirl Ahn
    Howard Hughes Medical Institute, Department of Pharmacology, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Biol Chem 277:26642-51. 2002
    ..Thus, c-Src-mediated tyrosine phosphorylation is required for the function of dynamin in ligand-induced signaling receptor internalization...
  38. ncbi request reprint Protein kinase A-mediated phosphorylation of the beta 2-adrenergic receptor regulates its coupling to Gs and Gi. Demonstration in a reconstituted system
    A Musa Zamah
    Howard Hughes Medical Institute, Duke University Medical Center, Durham, NC 27710, USA
    J Biol Chem 277:31249-56. 2002
    ..These results provide strong experimental support for the idea that PKA-mediated phosphorylation of the beta(2)-adrenergic receptor switches its predominant coupling from G(s) to G(i)...
  39. ncbi request reprint Dancing with different partners: protein kinase a phosphorylation of seven membrane-spanning receptors regulates their G protein-coupling specificity
    Robert J Lefkowitz
    Department of Medicine, Howard Hughes Medical Institute, Duke University Medical Center, Durham, North Carolina 27710, USA
    Mol Pharmacol 62:971-4. 2002
  40. ncbi request reprint The stability of the G protein-coupled receptor-beta-arrestin interaction determines the mechanism and functional consequence of ERK activation
    Akira Tohgo
    Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Biol Chem 278:6258-67. 2003
    ....
  41. ncbi request reprint Selective inhibition of heterotrimeric Gs signaling. Targeting the receptor-G protein interface using a peptide minigene encoding the Galpha(s) carboxyl terminus
    David S Feldman
    Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Biol Chem 277:28631-40. 2002
    ..ERK activation by the G(q/11)-coupled alpha(1B)AR was unaffected by GsCT. These findings suggest that peptide G protein inhibitors can provide insights into the complex interplay between G protein pools in cellular regulation...
  42. ncbi request reprint Transactivation of the epidermal growth factor receptor mediates parathyroid hormone and prostaglandin F2 alpha-stimulated mitogen-activated protein kinase activation in cultured transgenic murine osteoblasts
    Intekhab Ahmed
    Department of Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA
    Mol Endocrinol 17:1607-21. 2003
    ..These data suggest that autocrine/paracrine cross-talk between EGF receptors and Gi- or Gq/11-coupled GPCRs represents the predominant mechanism of GPCR-mediated activation of ERK1/2 in cultured TMOb osteoblasts...
  43. ncbi request reprint Protein kinase A and G protein-coupled receptor kinase phosphorylation mediates beta-1 adrenergic receptor endocytosis through different pathways
    Antonio Rapacciuolo
    Department of Medicine and Cell Biology, Medical Center, Duke University, Durham, North Carolina 27710, USA
    J Biol Chem 278:35403-11. 2003
    ..e. PKA-mediated phosphorylation directs internalization via a caveolae pathway, whereas GRK-mediated phosphorylation directs it through clathrin-coated pits...
  44. pmc Independent beta-arrestin 2 and G protein-mediated pathways for angiotensin II activation of extracellular signal-regulated kinases 1 and 2
    Huijun Wei
    Howard Hughes Medical Institute and Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA
    Proc Natl Acad Sci U S A 100:10782-7. 2003
    ..These findings imply the existence of independent G protein- and beta-arrestin 2-mediated pathways leading to ERK1/2 activation and the existence of distinct "active" conformations of a seven-membrane-spanning receptor coupled to each...
  45. ncbi request reprint Dual inhibition of beta-adrenergic and angiotensin II receptors by a single antagonist: a functional role for receptor-receptor interaction in vivo
    Liza Barki-Harrington
    Department of Medicine, Duke University Medical Center, Durham, NC, 27710, USA
    Circulation 108:1611-8. 2003
    ..Although the renin-angiotensin and the beta-adrenergic systems are interrelated, a direct interaction between beta-adrenergic receptors (betaARs) and angiotensin II type 1 receptors (AT1Rs) has not been identified...
  46. ncbi request reprint Ectodomain shedding-dependent transactivation of epidermal growth factor receptors in response to insulin-like growth factor type I
    Hesham M El-Shewy
    Department of Medicine, Medical University of South Carolina, 96 Jonathan Lucas Street, 816 Clinical Sciences Building, P O Box 250624, Charleston, South Carolina 29425, USA
    Mol Endocrinol 18:2727-39. 2004
    ..In contrast, the contribution of transactivated EGF receptors to IGF-I-stimulated downstream events, such as ERK1/2 activation, varies in a cell type-dependent manner...
  47. ncbi request reprint 5-HT2A receptor induces ERK phosphorylation and proliferation through ADAM-17 tumor necrosis factor-alpha-converting enzyme (TACE) activation and heparin-bound epidermal growth factor-like growth factor (HB-EGF) shedding in mesangial cells
    Monika Gooz
    Nephrology, Rheumatology and Endocrinology Divisions, Department of Medicine of the Medical University of South Carolina, Charleston, 29425, USA
    J Biol Chem 281:21004-12. 2006
    ..To our knowledge, this is the first time that TACE has been implicated in 5-HT-induced EGFR transactivation or in proliferation induced by a G protein-coupled receptor in native cells in culture...
  48. pmc The origins of diversity and specificity in g protein-coupled receptor signaling
    Stuart Maudsley
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Gerontology Research Center, 5600 Nathan Shock Drive, Johns Hopkins Medical Center, Baltimore, MD, USA
    J Pharmacol Exp Ther 314:485-94. 2005
    ..As a more comprehensive understanding of the complexity of GPCR signaling is developed, the rational design of ligands possessing increased specific efficacy and attenuated side effects may become the standard mode of drug development...
  49. ncbi request reprint Reviews in molecular biology and biotechnology: transmembrane signaling by G protein-coupled receptors
    Louis M Luttrell
    Division of Endocrinology, Diabetes and Medical Genetics, Department of Medicine, Medical University of South Carolina, 96 Jonathan Lucas Street, 816 CSB, P O Box 250624, Charleston, SC 29425, USA
    Mol Biotechnol 39:239-64. 2008
    ..While the physiologic relevance of many of these novel mechanisms of GPCR signaling remains to be established, their existence suggests that the mechanisms of GPCR signaling are even more diverse than previously imagined...
  50. ncbi request reprint Big G, little G: G proteins and actin cytoskeletal reorganization
    Louis M Luttrell
    The Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA
    Mol Cell 9:1152-4. 2002
    ..A recent report in Developmental Cell demonstrates that the activation of a tyrosine kinase, C-terminal Src kinase, by heterotrimeric G protein subunits provides the trigger for Rho-dependent actin stress fiber formation...
  51. ncbi request reprint G protein-coupled receptor signaling complexity in neuronal tissue: implications for novel therapeutics
    Stuart Maudsley
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Gerontology Research Center, Johns Hopkins Medical Center, Baltimore, MD 21224, USA
    Curr Alzheimer Res 4:3-19. 2007
    ..As a more comprehensive understanding of the complexity of GPCR signaling is developed, the rational design of ligands possessing increased specific efficacy and attenuated side effects may become the standard mode of drug development...
  52. ncbi request reprint Beta-arrestin- and G protein receptor kinase-mediated calcium-sensing receptor desensitization
    Min Pi
    Department of Internal Medicine, University of Kansas Medical Center, Kansas City, Kansas 66160, USA
    Mol Endocrinol 19:1078-87. 2005
    ..We conclude that GRKs and beta-arrestins play key roles in regulating CASR responsiveness in parathyroid glands...