F
Fang-Tsyr Lin
Researcher at Howard Hughes Medical Institute
Publications - 14
Citations - 5498
Fang-Tsyr Lin is an academic researcher from Howard Hughes Medical Institute. The author has contributed to research in topics: G protein-coupled receptor & Beta-Arrestins. The author has an hindex of 12, co-authored 12 publications receiving 5219 citations.
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Journal ArticleDOI
Beta-arrestin-dependent formation of beta2 adrenergic receptor-Src protein kinase complexes.
Louis M. Luttrell,Stephen S. G. Ferguson,Yehia Daaka,William E. Miller,Stuart Maudsley,G. J. Della Rocca,Fang-Tsyr Lin,H. Kawakatsu,K. Owada,D. K. Luttrell,Marc G. Caron,Robert J. Lefkowitz +11 more
TL;DR: Data suggest that beta-arrestin binding, which terminates receptor-G protein coupling, also initiates a second wave of signal transduction in which the "desensitized" receptor functions as a critical structural component of a mitogenic signaling complex.
Journal ArticleDOI
Enhanced Morphine Analgesia in Mice Lacking β-Arrestin 2
Laura M. Bohn,Robert J. Lefkowitz,Raul R. Gainetdinov,Karsten Peppel,Marc G. Caron,Fang-Tsyr Lin +5 more
TL;DR: It is suggested that inhibition of beta-arrestin 2 function might lead to enhanced analgesic effectiveness of morphine and provide potential new avenues for the study and treatment of pain, narcotic tolerance, and dependence.
Journal ArticleDOI
β-Arrestin 2: A Receptor-Regulated MAPK Scaffold for the Activation of JNK3
Patricia McDonald,Chi-Wing Chow,William E. Miller,Stéphane A. Laporte,Michael Field,Fang-Tsyr Lin,Roger J. Davis,Robert J. Lefkowitz +7 more
TL;DR: In this article, c-Jun amino-terminal kinase 3 (JNK3) was identified as a binding partner of β-arrestin 2 using a yeast two-hybrid screen and by coimmunoprecipitation from mouse brain extracts or cotransfected COS-7 cells.
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Mu-opioid receptor desensitization by beta-arrestin-2 determines morphine tolerance but not dependence.
TL;DR: It is shown that in mice lacking β-arrestin-2, desensitization of the μ-opioid receptor does not occur after chronic morphine treatment, and that these animals fail to develop antinociceptive tolerance.
Journal ArticleDOI
beta-Arrestin 1 and 2 differentially regulate heptahelical receptor signaling and trafficking.
TL;DR: Results suggest that sequestration of various heptahelical receptors is regulated differently by the two beta-arrestins, whereas both isoforms are capable of supporting receptor desensitization and down-regulation.