VSEVOLOD GUREVICH

Summary

Affiliation: Vanderbilt University
Country: USA

Publications

  1. ncbi request reprint Role of matrix metalloproteinases 2 and 9 in determination of invasive potential of pancreatic tumors
    L E Gurevich
    M F Vladimirskii Moscow Regional Research and Clinical Institute, Moscow, Russia
    Bull Exp Biol Med 136:494-8. 2003
  2. pmc Synthetic biology with surgical precision: targeted reengineering of signaling proteins
    Vsevolod V Gurevich
    Department of Pharmacology, Vanderbilt University, Nashville, TN 37232, USA
    Cell Signal 24:1899-908. 2012
  3. pmc Arrestins: ubiquitous regulators of cellular signaling pathways
    Eugenia V Gurevich
    Department of Pharmacology, Vanderbilt University, 2200 Pierce Avenue, Preston Research Building, Nashville, TN 37232, USA
    Genome Biol 7:236. 2006
  4. pmc Custom-designed proteins as novel therapeutic tools? The case of arrestins
    Vsevolod V Gurevich
    Vanderbilt University, Nashville, TN 37232, USA
    Expert Rev Mol Med 12:e13. 2010
  5. pmc The structural basis of arrestin-mediated regulation of G-protein-coupled receptors
    Vsevolod V Gurevich
    Department of Pharmacology, Vanderbilt University Medical Center, Nashville, TN 37232, USA
    Pharmacol Ther 110:465-502. 2006
  6. pmc The functional cycle of visual arrestins in photoreceptor cells
    Vsevolod 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
  7. pmc Rich tapestry of G protein-coupled receptor signaling and regulatory mechanisms
    Vsevolod V Gurevich
    Department of Pharmacology, Vanderbilt University, Nashville, TN 37232, USA
    Mol Pharmacol 74:312-6. 2008
  8. pmc 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
  9. pmc GPCR monomers and oligomers: it takes all kinds
    Vsevolod V Gurevich
    Department of Pharmacology, Vanderbilt University Medical Center, Nashville, TN 37232, USA
    Trends Neurosci 31:74-81. 2008
  10. pmc The differential engagement of arrestin surface charges by the various functional forms of the receptor
    Susan M Hanson
    Department of Pharmacology, Vanderbilt University, Nashville, Tennessee 37232, USA
    J Biol Chem 281:3458-62. 2006

Research Grants

  1. Structure-function studies of visual arrestin
    VSEVOLOD GUREVICH; Fiscal Year: 2007
  2. Arrestin interactions with non-receptor binding partners
    VSEVOLOD GUREVICH; Fiscal Year: 2007
  3. Arrestin interactions with non-receptor binding partners
    VSEVOLOD GUREVICH; Fiscal Year: 2007
  4. Arrestin interactions with non-receptor binding partners
    Vsevolod V Gurevich; Fiscal Year: 2010
  5. Conformational regulation of arrestin-mediated signaling
    Vsevolod V Gurevich; Fiscal Year: 2010
  6. Structure-function studies of visual arrestin
    Vsevolod V Gurevich; Fiscal Year: 2010
  7. STRUCTURE/FUNCTION STUDIES OF VISUAL ARRESTIN
    VSEVOLOD GUREVICH; Fiscal Year: 2000
  8. Molecular mechanisms of arrestin function
    VSEVOLOD GUREVICH; Fiscal Year: 2004
  9. Structure-function studies of visual arrestin
    VSEVOLOD GUREVICH; Fiscal Year: 2004
  10. Conformational regulation of arrestin-mediated signaling
    VSEVOLOD GUREVICH; Fiscal Year: 2009

Collaborators

Detail Information

Publications53

  1. ncbi request reprint Role of matrix metalloproteinases 2 and 9 in determination of invasive potential of pancreatic tumors
    L E Gurevich
    M F Vladimirskii Moscow Regional Research and Clinical Institute, Moscow, Russia
    Bull Exp Biol Med 136:494-8. 2003
    ..Co-expression of matrix metalloproteinases 2 and 9 is an unfavorable prognostic sign...
  2. pmc Synthetic biology with surgical precision: targeted reengineering of signaling proteins
    Vsevolod 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...
  3. pmc Arrestins: ubiquitous regulators of cellular signaling pathways
    Eugenia 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...
  4. pmc Custom-designed proteins as novel therapeutic tools? The case of arrestins
    Vsevolod 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...
  5. pmc The structural basis of arrestin-mediated regulation of G-protein-coupled receptors
    Vsevolod V Gurevich
    Department of Pharmacology, Vanderbilt University Medical Center, Nashville, TN 37232, USA
    Pharmacol Ther 110:465-502. 2006
    ....
  6. pmc The functional cycle of visual arrestins in photoreceptor cells
    Vsevolod 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
    ....
  7. pmc Rich tapestry of G protein-coupled receptor signaling and regulatory mechanisms
    Vsevolod 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...
  8. pmc 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...
  9. pmc GPCR monomers and oligomers: it takes all kinds
    Vsevolod 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...
  10. pmc The differential engagement of arrestin surface charges by the various functional forms of the receptor
    Susan M Hanson
    Department of Pharmacology, Vanderbilt University, Nashville, Tennessee 37232, USA
    J Biol Chem 281:3458-62. 2006
    ....
  11. ncbi request reprint Mapping the arrestin-receptor interface. Structural elements responsible for receptor specificity of arrestin proteins
    Sergey A Vishnivetskiy
    Department of Pharmacology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA
    J Biol Chem 279:1262-8. 2004
    ....
  12. ncbi request reprint mu-Opioid receptors desensitize less rapidly than delta-opioid receptors due to less efficient activation of arrestin
    Janet 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...
  13. ncbi request reprint Transition of arrestin into the active receptor-binding state requires an extended interdomain hinge
    Sergey A Vishnivetskiy
    Department of Pharmacology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA
    J Biol Chem 277:43961-7. 2002
    ....
  14. pmc Arrestin mobilizes signaling proteins to the cytoskeleton and redirects their activity
    Susan 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...
  15. pmc Each rhodopsin molecule binds its own arrestin
    Susan 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...
  16. pmc Visual arrestin binding to microtubules involves a distinct conformational change
    Susan 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...
  17. ncbi request reprint Arrestin2 expression selectively increases during neural differentiation
    Eugenia 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...
  18. ncbi request reprint The molecular acrobatics of arrestin activation
    Vsevolod 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...
  19. ncbi request reprint The new face of active receptor bound arrestin attracts new partners
    Vsevolod 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...
  20. pmc Cone arrestin binding to JNK3 and Mdm2: conformational preference and localization of interaction sites
    Xiufeng 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...
  21. pmc Enhanced arrestin facilitates recovery and protects rods lacking rhodopsin phosphorylation
    Xiufeng 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...
  22. pmc Structure and function of the visual arrestin oligomer
    Susan 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...
  23. pmc The role of arrestin alpha-helix I in receptor binding
    Sergey A Vishnivetskiy
    Department of Pharmacology, Vanderbilt University, Nashville, TN 37232, USA
    J Mol Biol 395:42-54. 2010
    ....
  24. pmc Differential interaction of spin-labeled arrestin with inactive and active phosphorhodopsin
    Susan 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...
  25. pmc Opposing effects of inositol hexakisphosphate on rod arrestin and arrestin2 self-association
    Susan 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...
  26. pmc Regulation of arrestin binding by rhodopsin phosphorylation level
    Sergey 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...
  27. pmc 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...
  28. ncbi request reprint Conservation of the phosphate-sensitive elements in the arrestin family of proteins
    Jeremy Celver
    Department of Pharmacology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA
    J Biol Chem 277:9043-8. 2002
    ....
  29. ncbi request reprint The nature of the arrestin x receptor complex determines the ultimate fate of the internalized receptor
    Ling 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...
  30. pmc A model for the solution structure of the rod arrestin tetramer
    Susan 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...
  31. pmc Haloperidol and clozapine differentially affect the expression of arrestins, receptor kinases, and extracellular signal-regulated kinase activation
    Mohamed 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...
  32. pmc Lentiviral overexpression of GRK6 alleviates L-dopa-induced dyskinesia in experimental Parkinson's disease
    Mohamed R Ahmed
    Department of Pharmacology, Vanderbilt University, 2200 Pierce Avenue, PRB422, Nashville, TN 37232, USA
    Sci Transl Med 2:28ra28. 2010
    ....
  33. pmc Altered expression and subcellular distribution of GRK subtypes in the dopamine-depleted rat basal ganglia is not normalized by l-DOPA treatment
    M 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...
  34. pmc Visual and both non-visual arrestins in their "inactive" conformation bind JNK3 and Mdm2 and relocalize them from the nucleus to the cytoplasm
    Xiufeng Song
    Department of Pharmacology, Vanderbilt University, Nashville, Tennessee 37232, USA
    J Biol Chem 281:21491-9. 2006
    ....
  35. ncbi request reprint Calmodulin kinase II inhibition protects against structural heart disease
    Rong 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...
  36. ncbi request reprint Soluble mimics of the cytoplasmic face of the human V1-vascular vasopressin receptor bind arrestin2 and calmodulin
    Nan 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...
  37. ncbi request reprint Dopamine D1 receptor interaction with arrestin3 in neostriatal neurons
    Tara 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...
  38. ncbi request reprint The third intracellular loop of alpha 2-adrenergic receptors determines subtype specificity of arrestin interaction
    Jessica 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...
  39. ncbi request reprint ARF6: a newly appreciated player in G protein-coupled receptor desensitization
    Mary 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...
  40. pmc Light-dependent redistribution of arrestin in vertebrate rods is an energy-independent process governed by protein-protein interactions
    K 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...
  41. ncbi request reprint Aspartic acid 564 in the third cytoplasmic loop of the luteinizing hormone/choriogonadotropin receptor is crucial for phosphorylation-independent interaction with arrestin2
    Sutapa 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...
  42. ncbi request reprint Conformational differences between arrestin2 and pre-activated mutants as revealed by hydrogen exchange mass spectrometry
    Jennifer M Carter
    Department of Chemistry, University of New Mexico, Albuquerque, NM 87131, USA
    J Mol Biol 351:865-78. 2005
    ....
  43. ncbi request reprint Crystal structure of cone arrestin at 2.3A: evolution of receptor specificity
    R 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...
  44. ncbi request reprint The interaction with the cytoplasmic loops of rhodopsin plays a crucial role in arrestin activation and binding
    Dayanidhi 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...
  45. ncbi request reprint Preferential Interaction between the dopamine D2 receptor and Arrestin2 in neostriatal neurons
    Tara 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...
  46. ncbi request reprint The interaction of a constitutively active arrestin with the arrestin-insensitive 5-HT(2A) receptor induces agonist-independent internalization
    John 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...
  47. pmc Arrestin binding to calmodulin: a direct interaction between two ubiquitous signaling proteins
    Nan 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...
  48. ncbi request reprint Direct binding of visual arrestin to microtubules determines the differential subcellular localization of its splice variants in rod photoreceptors
    K 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
    ....
  49. pmc Functional comparisons of visual arrestins in rod photoreceptors of transgenic mice
    Sanny 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...
  50. ncbi request reprint Arrestin variants display differential binding characteristics for the phosphorylated N-formyl peptide receptor carboxyl terminus
    Ross 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...
  51. ncbi request reprint Functional capabilities of an N-formyl peptide receptor-G(alpha)(i)(2) fusion protein: assemblies with G proteins and arrestins
    Mei 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...
  52. ncbi request reprint N-formyl peptide receptor phosphorylation domains differentially regulate arrestin and agonist affinity
    T 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...
  53. ncbi request reprint Inhibition of chemoattractant N-formyl peptide receptor trafficking by active arrestins
    T Alexander Key
    Department of Cell Biology and Physiology, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA
    Traffic 6:87-99. 2005
    ....

Research Grants30

  1. Structure-function studies of visual arrestin
    VSEVOLOD GUREVICH; Fiscal Year: 2007
    ..abstract_text> ..
  2. Arrestin interactions with non-receptor binding partners
    VSEVOLOD 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. ..
  3. Arrestin interactions with non-receptor binding partners
    VSEVOLOD 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. ..
  4. Arrestin interactions with non-receptor binding partners
    Vsevolod 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. ..
  5. Conformational regulation of arrestin-mediated signaling
    Vsevolod 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. ..
  6. Structure-function studies of visual arrestin
    Vsevolod V Gurevich; Fiscal Year: 2010
    ....
  7. STRUCTURE/FUNCTION STUDIES OF VISUAL ARRESTIN
    VSEVOLOD 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. ..
  8. Molecular mechanisms of arrestin function
    VSEVOLOD 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. ..
  9. Structure-function studies of visual arrestin
    VSEVOLOD GUREVICH; Fiscal Year: 2004
    ....
  10. Conformational regulation of arrestin-mediated signaling
    VSEVOLOD 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. ..