Research Topics
| VSEVOLOD GUREVICHSummaryAffiliation: Vanderbilt University Country: USA Publications
Research Grants
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Detail Information
Publications
Synthetic biology with surgical precision: targeted reengineering of signaling proteinsVsevolod V Gurevich
Department of Pharmacology, Vanderbilt University, Nashville, TN 37232, USA
Cell Signal 24:1899-908. 2012..Engineered proteins with specific functional changes also have huge therapeutic potential in disorders associated with inherited or acquired signaling errors...- Arrestins: ubiquitous regulators of cellular signaling pathwaysEugenia V Gurevich
Department of Pharmacology, Vanderbilt University, 2200 Pierce Avenue, Preston Research Building, Nashville, TN 37232, USA
Genome Biol 7:236. 2006..Arrestins thus serve as ubiquitous signaling regulators in the cytoplasm and nucleus... - GPCR monomers and oligomers: it takes all kindsVsevolod V Gurevich
Department of Pharmacology, Vanderbilt University Medical Center, Nashville, TN 37232, USA
Trends Neurosci 31:74-81. 2008..Different GPCR subtypes, and even the same receptor at different stages of its life cycle, most likely exist in different oligomerization states, from monomers to dimers and possibly higher-order oligomers... - Custom-designed proteins as novel therapeutic tools? The case of arrestinsVsevolod V Gurevich
Vanderbilt University, Nashville, TN 37232, USA
Expert Rev Mol Med 12:e13. 2010..Although this approach is still in its infancy, targeted redesign of individual functions of many proteins offers a promise of a completely new therapeutic toolbox with huge potential... - The functional cycle of visual arrestins in photoreceptor cellsVsevolod V Gurevich
Department of Pharmacology, Vanderbilt University, 2200 Pierce Ave, PRB, Rm 417D, Nashville, TN 37232, USA
Prog Retin Eye Res 30:405-30. 2011.... - How and why do GPCRs dimerize?Vsevolod V Gurevich
Department of Pharmacology, Vanderbilt University Medical Center, Nashville, TN 37232, USA
Trends Pharmacol Sci 29:234-40. 2008..Thus, to figure out the biological role of receptor self-association we must focus on other functions of GPCRs at different stages of their functional cycle... - Rich tapestry of G protein-coupled receptor signaling and regulatory mechanismsVsevolod V Gurevich
Department of Pharmacology, Vanderbilt University, Nashville, TN 37232, USA
Mol Pharmacol 74:312-6. 2008..In this issue of Molecular Pharmacology, Luo et al. (p. 338) describe a complex pattern of the regulation of M3 muscarinic receptor signaling... - The structural basis of arrestin-mediated regulation of G-protein-coupled receptorsVsevolod V Gurevich
Department of Pharmacology, Vanderbilt University Medical Center, Nashville, TN 37232, USA
Pharmacol Ther 110:465-502. 2006.... - The differential engagement of arrestin surface charges by the various functional forms of the receptorSusan M Hanson
Department of Pharmacology, Vanderbilt University, Nashville, Tennessee 37232, USA
J Biol Chem 281:3458-62. 2006.... 
mu-Opioid receptors desensitize less rapidly than delta-opioid receptors due to less efficient activation of arrestinJanet D Lowe
Department of Pharmacology, University of Washington, Seattle, Washington 98195-7280, USA
J Biol Chem 277:15729-35. 2002..These results suggest that DOR desensitization involves phosphorylation of both the carboxyl-terminal tail and the second intracellular loop that together leads to a more efficient activation of arrestin and thus faster desensitization...- Mapping the arrestin-receptor interface. Structural elements responsible for receptor specificity of arrestin proteinsSergey A Vishnivetskiy
Department of Pharmacology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA
J Biol Chem 279:1262-8. 2004.... - Arrestin mobilizes signaling proteins to the cytoskeleton and redirects their activitySusan M Hanson
Department of Pharmacology, Vanderbilt University School of Medicine, Nashville, TN 37232, USA
J Mol Biol 368:375-87. 2007..The mobilization of signaling molecules to MTs is a novel biological function of arrestin proteins... - Transition of arrestin into the active receptor-binding state requires an extended interdomain hingeSergey A Vishnivetskiy
Department of Pharmacology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA
J Biol Chem 277:43961-7. 2002.... - Each rhodopsin molecule binds its own arrestinSusan M Hanson
Department of Pharmacology, Vanderbilt University, 2200 Pierce Avenue, PRB, Room 418, Nashville, TN 37232, USA
Proc Natl Acad Sci U S A 104:3125-8. 2007..Thus, a single Rh molecule is necessary and sufficient to bind Arr. Remarkable structural conservation among receptors and Arrs strongly suggests that all Arr subtypes bind individual molecules of their cognate receptors... - Visual arrestin binding to microtubules involves a distinct conformational changeSusan M Hanson
Department of Pharmacology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232
J Biol Chem 281:9765-72. 2006..Thus, microtubule and rhodopsin binding induce different conformational changes in arrestin, suggesting that arrestin assumes three distinct conformations in the cell, likely with different functional properties... - Cone arrestin binding to JNK3 and Mdm2: conformational preference and localization of interaction sitesXiufeng Song
Department of Pharmacology, Vanderbilt University, Nashville, Tennessee 37232, USA
J Neurochem 103:1053-62. 2007..N-domain of rod arrestin binds Mdm2, which localizes its main interaction site to this region. Comparable binding of JNK3 and Mdm2 to four arrestin subtypes allowed us to identify conserved residues likely involved in these interactions... - The molecular acrobatics of arrestin activationVsevolod V Gurevich
Department of Pharmacology, Vanderbilt University Medical Center, Nashville, TN 37232, USA
Trends Pharmacol Sci 25:105-11. 2004..In this article, we discuss the molecular mechanisms that underlie the sequential multi-site binding that ensures arrestin selectivity for the active phosphoreceptor and high fidelity of signal regulation by arrestin proteins... - Arrestin2 expression selectively increases during neural differentiationEugenia V Gurevich
Department of Pharmacology, Vanderbilt University Medical Center, Nashville, Tennessee 37232, USA
J Neurochem 91:1404-16. 2004..The data demonstrate selective increases in the expression of arrestin2 associated with neural development and suggest specific yet unappreciated roles for arrestin2 in neural differentiation... - The new face of active receptor bound arrestin attracts new partnersVsevolod V Gurevich
Department of Pharmacology, Vanderbilt University Medical Center, Nashville, TN 37232, USA
Structure 11:1037-42. 2003..Conformational change in arrestin induced by receptor binding promotes its interaction with the majority of recently identified nonreceptor binding partners... - The role of arrestin alpha-helix I in receptor bindingSergey A Vishnivetskiy
Department of Pharmacology, Vanderbilt University, Nashville, TN 37232, USA
J Mol Biol 395:42-54. 2010.... - Structure and function of the visual arrestin oligomerSusan M Hanson
Department of Pharmacology, Vanderbilt University, Nashville, TN 37232, USA
EMBO J 26:1726-36. 2007..Thus, the tetramer likely serves as a 'storage' form of arrestin, increasing the arrestin-binding capacity of microtubules while readily dissociating to supply active monomer when it is needed to quench rhodopsin signaling... - Regulation of arrestin binding by rhodopsin phosphorylation levelSergey A Vishnivetskiy
Department of Pharmacology, Vanderbilt University, Nashville, Tennessee 37232, USA
J Biol Chem 282:32075-83. 2007..The complex of arrestin with heavily phosphorylated rhodopsin, which appears to form in certain disease states, has distinct characteristics that may contribute to the phenotype of these visual disorders... - Differential interaction of spin-labeled arrestin with inactive and active phosphorhodopsinSusan M Hanson
Department of Pharmacology, Vanderbilt University School of Medicine, Nashville, TN 37232, USA
Proc Natl Acad Sci U S A 103:4900-5. 2006..This result identifies this loop as a key recognition site in the arrestin-P-Rh* complex and supports the view that flexible sequences are key elements in protein-protein interactions... - Enhanced arrestin facilitates recovery and protects rods lacking rhodopsin phosphorylationXiufeng Song
Department of Pharmacology, Vanderbilt University Medical Center, Nashville, TN 37232, USA
Curr Biol 19:700-5. 2009..Successful modification of protein-protein interactions by appropriate mutations paves the way to targeted redesign of signaling pathways to achieve desired functional outcomes... - Opposing effects of inositol hexakisphosphate on rod arrestin and arrestin2 self-associationSusan M Hanson
Department of Pharmacology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA
Biochemistry 47:1070-5. 2008..In contrast to arrestin2, IP6 inhibits self-association of rod arrestin, indicating that the structure of these two tetramers in solution is likely different... - The nature of the arrestin x receptor complex determines the ultimate fate of the internalized receptorLing Pan
Department of Pharmacology, Vanderbilt University Medical Center, Nashville, Tennessee 37232, USA
J Biol Chem 278:11623-32. 2003..Thus, targeted manipulation of the characteristics of an arrestin protein that binds to a G protein-coupled receptors can dramatically change receptor trafficking and its ultimate fate in a cell... - Conservation of the phosphate-sensitive elements in the arrestin family of proteinsJeremy Celver
Department of Pharmacology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA
J Biol Chem 277:9043-8. 2002.... - How does arrestin assemble MAPKs into a signaling complex?Xiufeng Song
Department of Pharmacology, Vanderbilt University, Nashville, Tennessee 37232, USA
J Biol Chem 284:685-95. 2009..We found that both arrestin domains interact with all six kinases. These findings shed new light on the mechanism of arrestin-mediated MAPK activation and the spatial arrangement of the three kinases on arrestin molecule... - A model for the solution structure of the rod arrestin tetramerSusan M Hanson
Department of Pharmacology, Vanderbilt University, Nashville, TN 37232, USA
Structure 16:924-34. 2008..The structure of the solution tetramer explains its inability to bind rhodopsin and paves the way for experimental studies of the physiological role of rod arrestin self-association... - Haloperidol and clozapine differentially affect the expression of arrestins, receptor kinases, and extracellular signal-regulated kinase activationMohamed Rafiuddin Ahmed
Department of Pharmacology, Vanderbilt University Medical Center, Preston Research Building, Room 422, Nashville, TN 37232, USA
J Pharmacol Exp Ther 325:276-83. 2008..The data demonstrate that haloperidol and clozapine differentially affect the expression of arrestins and GRKs and ERK activity, which may play a role in determining their clinical profile... - Visual and both non-visual arrestins in their "inactive" conformation bind JNK3 and Mdm2 and relocalize them from the nucleus to the cytoplasmXiufeng Song
Department of Pharmacology, Vanderbilt University, Nashville, Tennessee 37232, USA
J Biol Chem 281:21491-9. 2006.... - Altered expression and subcellular distribution of GRK subtypes in the dopamine-depleted rat basal ganglia is not normalized by l-DOPA treatmentM Rafiuddin Ahmed
Department of Pharmacology, Vanderbilt University Medical Center, Nashville, Tennessee 37232, USA
J Neurochem 104:1622-36. 2008..The data suggest that alterations in the expression and subcellular distribution of arrestins and GRKs contribute to pathophysiology of Parkinson's disease. Thus, these proteins may be targets for antiparkinsonian therapy... - Calmodulin kinase II inhibition protects against structural heart diseaseRong Zhang
Department of Medicine, Vanderbilt University School of Medicine, 2220 Pierce Avenue, Nashville, Tennessee 37232 6300, USA
Nat Med 11:409-17. 2005..These findings mark CaMKII as a determinant of clinically important heart disease phenotypes, and suggest CaMKII inhibition can be a highly selective approach for targeting adverse myocardial remodeling linked to betaAR signaling... - Lentiviral overexpression of GRK6 alleviates L-dopa-induced dyskinesia in experimental Parkinson's diseaseMohamed R Ahmed
Department of Pharmacology, Vanderbilt University, 2200 Pierce Avenue, PRB422, Nashville, TN 37232, USA
Sci Transl Med 2:28ra28. 2010.... - Conformational differences between arrestin2 and pre-activated mutants as revealed by hydrogen exchange mass spectrometryJennifer M Carter
Department of Chemistry, University of New Mexico, Albuquerque, NM 87131, USA
J Mol Biol 351:865-78. 2005.... - The interaction with the cytoplasmic loops of rhodopsin plays a crucial role in arrestin activation and bindingDayanidhi Raman
Department of Cell and Developmental Biology, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7090, USA
J Neurochem 84:1040-50. 2003..These results suggest that arrestin bound to rhodopsin is in a distinct conformation that is co-ordinately regulated by association with the cytoplasmic loops and the C-terminus of rhodopsin... - Arrestin binding to calmodulin: a direct interaction between two ubiquitous signaling proteinsNan Wu
Department of Biochemistry, Case Western Reserve University, Cleveland, OH 44106, USA
J Mol Biol 364:955-63. 2006..The arrestin-calmodulin interaction likely regulates the localization of both proteins and their availability for other interaction partners... - Preferential Interaction between the dopamine D2 receptor and Arrestin2 in neostriatal neuronsTara A Macey
Department of Behavioral Neuroscience, Oregon Health and Science University and Veterans Affairs Medical Center, Portland, Oregon 97239 2999, USA
Mol Pharmacol 66:1635-42. 2004..All three measures of receptor/arrestin interaction (colocalization, translocation, and coprecipitation) demonstrated selective agonist-induced interaction between the D2 receptor and arrestin2 in neurons... - Crystal structure of cone arrestin at 2.3A: evolution of receptor specificityR Bryan Sutton
Department of Neuroscience and Cell Biology, University of Texas Medical Branch, and Sealy Center for Molecular Science and Structural Biology, Galveston, TX 77555, USA
J Mol Biol 354:1069-80. 2005..Transient arrestin binding to the photopigment in cones may be responsible for the extremely rapid regeneration and reuse of the photopigment that is essential for cone function at high levels of illumination... - Soluble mimics of the cytoplasmic face of the human V1-vascular vasopressin receptor bind arrestin2 and calmodulinNan Wu
Department of Biochemistry, Case Western Reserve University, 10900 Euclid Ave, Cleveland, OH 44106-4935, USA
Mol Pharmacol 70:249-58. 2006..These findings set the stage for the detailed structural analysis of these protein-protein interactions that are important for understanding the mechanism of signaling... - Aspartic acid 564 in the third cytoplasmic loop of the luteinizing hormone/choriogonadotropin receptor is crucial for phosphorylation-independent interaction with arrestin2Sutapa Mukherjee
Department of Cell and Molecular Biology, Northwestern University Medical School, Chicago, Illinois 60611, USA
J Biol Chem 277:17916-27. 2002..Unlike other GPCRs that additionally require receptor phosphorylation, LH/CG R activation is sufficient to expose a conformation in which Asp-564 in the 3i loop confers high affinity binding selectively to arrestin2... - ARF6: a newly appreciated player in G protein-coupled receptor desensitizationMary Hunzicker-Dunn
Department of Cell and Molecular Biology, Northwestern University Medical School, 303 East Chicago Avenue, Chicago, IL 60611, USA
FEBS Lett 521:3-8. 2002..We hypothesize that ARF6 might also serve GPCRs other than the LH/CG R to regulate the availability of arrestin 2 for receptor desensitization... - The interaction of a constitutively active arrestin with the arrestin-insensitive 5-HT(2A) receptor induces agonist-independent internalizationJohn A Gray
Department of Biochemistry, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106 4935, USA
Mol Pharmacol 63:961-72. 2003..This is the first demonstration that a constitutively active arrestin mutant can both induce agonist-independent internalization and stabilize the agonist-high affinity state of an arrestin-insensitive G protein coupled receptor... - Direct binding of visual arrestin to microtubules determines the differential subcellular localization of its splice variants in rod photoreceptorsK Saidas Nair
Department of Molecular and Cellular Pharmacology and Neuroscience Program, University of Miami, Miami, Florida 33136, USA
J Biol Chem 279:41240-8. 2004.... - Dopamine D1 receptor interaction with arrestin3 in neostriatal neuronsTara A Macey
Department of Behavioral Neuroscience, Oregon Health and Science University and Veterans Affairs Medical Center, Portland, Oregon 97239-2999, USA
J Neurochem 93:128-34. 2005..These data indicate that the D1 receptor preferentially interacts with arrestin3 in neostriatal neurons... - Light-dependent redistribution of arrestin in vertebrate rods is an energy-independent process governed by protein-protein interactionsK Saidas Nair
Department of Molecular and Cellular Pharmacology and Neuroscience Program, University of Miami, Miami, Florida 33136, USA
Neuron 46:555-67. 2005..These results indicate that the distribution of arrestin in rods is controlled by its dynamic interactions with rhodopsin in the OS and microtubules in the IS and that its movement occurs by simple diffusion... - The third intracellular loop of alpha 2-adrenergic receptors determines subtype specificity of arrestin interactionJessica L DeGraff
Department of Microbiology and Immunology, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA
J Biol Chem 277:43247-52. 2002..These results demonstrate that arrestin-3 binds to two discrete regions within the alpha(2b)AR third intracellular loop and that disruption of arrestin binding selectively abrogates agonist-promoted receptor internalization... - N-formyl peptide receptor phosphorylation domains differentially regulate arrestin and agonist affinityT Alexander Key
Department of Cell Biology and Physiology, University of New Mexico Health Sciences Center, Albuquerque 87131, USA
J Biol Chem 278:4041-7. 2003..Furthermore, this is the first demonstration that agonist affinity of a GPCR and the affinity of arrestin binding to the phosphorylated receptor are regulated by distinct receptor phosphodomains... - Inhibition of chemoattractant N-formyl peptide receptor trafficking by active arrestinsT Alexander Key
Department of Cell Biology and Physiology, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA
Traffic 6:87-99. 2005.... - Functional capabilities of an N-formyl peptide receptor-G(alpha)(i)(2) fusion protein: assemblies with G proteins and arrestinsMei Shi
Department of Pathology, University of New Mexico Health Sciences Center, Albuquerque, New Mexico 87131, USA
Biochemistry 42:7283-93. 2003..Together, these results indicate that complex interactions exist between GPCRs, in their unphosphorylated and phosphorylated states, G proteins, and arrestins, which result in the highly regulated control of GPCR function... - Arrestin variants display differential binding characteristics for the phosphorylated N-formyl peptide receptor carboxyl terminusRoss M Potter
Department of Cell Biology, University of New Mexico Health Sciences Center, Albuquerque, New Mexico 87131, USA
J Biol Chem 277:8970-8. 2002..The results suggest that the carboxyl terminus of arrestin is a critical determinant in regulating the binding affinity of arrestin for the phosphorylated domains of GPCRs... - Functional comparisons of visual arrestins in rod photoreceptors of transgenic miceSanny Chan
Department of Cell and Neurobiology, Zilkha Neurogenetic Institute of the Keck School of Medicine, University of Southern California, Los Angeles, California, USA
Invest Ophthalmol Vis Sci 48:1968-75. 2007..To examine the biochemical characteristics of rod and cone arrestin with respect to their ability to quench the activity of light-activated rhodopsin in transgenic mice...
Research Grants
- Structure-function studies of visual arrestinVSEVOLOD GUREVICH; Fiscal Year: 2007..abstract_text> ..
- Arrestin interactions with non-receptor binding partnersVSEVOLOD GUREVICH; Fiscal Year: 2007..This information will set the stage for designing peptide and small molecule mimics of the interaction surfaces that can be used as experimental and therapeutic tools. ..
- Arrestin interactions with non-receptor binding partnersVSEVOLOD GUREVICH; Fiscal Year: 2007..This information will set the stage for designing peptide and small molecule mimics of the interaction surfaces that can be used as experimental and therapeutic tools. ..
- Arrestin interactions with non-receptor binding partnersVsevolod V Gurevich; Fiscal Year: 2010..This information will set the stage for designing peptide and small molecule mimics of the interaction surfaces that can be used as experimental and therapeutic tools. ..
- Conformational regulation of arrestin-mediated signalingVsevolod V Gurevich; Fiscal Year: 2010..This information will set the stage for designing arrestin-based molecular tools for targeted manipulation of cellular signaling that can be used for experimental and therapeutic purposes. ..
- Structure-function studies of visual arrestinVsevolod V Gurevich; Fiscal Year: 2010....
- STRUCTURE/FUNCTION STUDIES OF VISUAL ARRESTINVSEVOLOD GUREVICH; Fiscal Year: 2000..The characterization of the functional consequences of expressing mutant arrestins in vivo is expected to pave the way for future use of such mutants for gene therapy of congenital retinal disorders. ..
- Molecular mechanisms of arrestin functionVSEVOLOD GUREVICH; Fiscal Year: 2004..Arrestin mutants with enhanced specificity for these receptors and enhanced capability to attenuate such faulty signaling promise to become useful tools for gene therapy of these disorders. ..
- Structure-function studies of visual arrestinVSEVOLOD GUREVICH; Fiscal Year: 2004....
- Conformational regulation of arrestin-mediated signalingVSEVOLOD GUREVICH; Fiscal Year: 2009..This information will set the stage for designing arrestin-based molecular tools for targeted manipulation of cellular signaling that can be used for experimental and therapeutic purposes. ..