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The EMBO Journal|February 8, 2014
Arrestin makes T cells stop and become activeVsevolod V Gurevich, Eugenia V GurevichBritish Journal of Pharmacology|January 10, 2015
Beyond traditional pharmacology: new tools and approachesE V Gurevich, V V GurevichCurrent Protocols in Pharmacology|December 3, 2014
Overview of different mechanisms of arrestin-mediated signalingVsevolod V Gurevich, Eugenia V GurevichPharmacology & Therapeutics|March 24, 2020
Biased GPCR signaling: Possible mechanisms and inherent limitationsVsevolod V Gurevich, Eugenia V GurevichMolecular and Cellular Endocrinology|February 1, 2019
The structural basis of the arrestin binding to GPCRsVsevolod V Gurevich, Eugenia V GurevichProgress in Molecular Biology and Translational Science|February 4, 2019
Arrestin mutations: Some cause diseases, others promise cureVsevolod V Gurevich, Eugenia V GurevichCellular and Molecular Life Sciences : CMLS|August 19, 2019
Plethora of functions packed into 45 kDa arrestins: biological implications and possible therapeutic strategiesVsevolod V Gurevich, Eugenia V GurevichTrends in Neurosciences|January 18, 2008
GPCR monomers and oligomers: it takes all kindsVsevolod V Gurevich, Eugenia V GurevichCurrent Opinion in Cell Biology|April 1, 2014
Extensive shape shifting underlies functional versatility of arrestinsVsevolod V Gurevich, Eugenia V GurevichTrends in Pharmacological Sciences|April 4, 2008
How and why do GPCRs dimerize?Vsevolod V Gurevich, Eugenia V GurevichPageof 239