Mutations in arrestin-3 differentially affect binding to neuropeptide Y receptor subtypes
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- 作者：Luis E. Gimeneza ; Stefanie Babilonb ; Lizzy Wankab ; Annette G. Beck-Sickingerb ; Vsevolod V. Gurevicha ; vsevolod.gurevich@vanderbilt.edu" class="auth_mail
- 关键词：GPCR ; G protein-coupled receptor ; arr ; arrestin ; NPY ; neuropeptide Y ; Y1R ; neuropeptide Y1 receptor ; Y2R ; neuropeptide Y2 receptor ; BRET ; bioluminescence resonance energy transfer ; ANOVA ; analysis of variance ; arr-3-K2A ; arrestin-3-Lys11 AlaLys12Ala ; arr-3-NCA ; arrestin-3 Leu49Ala ; Asp51Ala ; Arg52Ala ; Leu69Ala ; Tyr239Ala ; Asp241Ala ; Cys252Ala ; Pro253Ala ; Asp260Ala ; and Gln262Ala ; arr-3-KNC ; arrestin-3 Lys11Ala Lys12Ala ; Leu49Ala ; Asp51Ala ; Arg52Ala ; Leu69Ala ; Tyr239Ala ; Asp241Ala ; Cys252Ala ; Pro
- 刊名：Cellular Signalling
- 出版年：July 2014
- 年：2014
- 卷：26
- 期：7
- 页码：1523-1531
- 全文大小：1451 K
文摘
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Receptor specificity of arrestins can be enhanced by targeted mutagenesis.
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Arrestins selective for neuropeptide Y1 over Y2 receptor were developed.
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Mutations differentially affect agonist-dependent and -independent recruitment.
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Receptor-specific non-visual arrestins are novel tools for research and therapy.