KLHL12-mediated ubiquitination of the dopamine D4 receptor does not target the receptor for degradation.
In previous studies, we identified KLHL12 as a novel interaction partner of the dopamine D4 receptor that functions as an adaptor in a Cullin3-based E3 ubiquitin ligase complex to target the receptor for ubiquitination. In this study, we show that KLHL12 promotes poly-ubiquitination of the receptor by performing ubiquitination assays ... in eukaryotic cells. Furthermore, we demonstrate that KLHL12 not only interacts with both immature, ER-associated and mature, plasma membrane-associated D4 receptors, but also promotes ubiquitination of both receptor subpools. Unexpectedly, however, KLHL12-mediated receptor ubiquitination does not promote proteasomal degradation of newly synthesized receptors through the ER-associated degradation pathway or lysosomal degradation of mature receptors. Moreover, our data reveal that D4 receptors do not undergo agonist-promoted ubiquitination or degradation, in contrast to many other G-protein-coupled receptors (GPCRs) indicating that ubiquitination of GPCRs does not defaultly lead to receptor degradation. Interestingly, KLHL12 does also interact with beta-arrestin2 but this has no effect on the ubiquitination or localization of beta-arrestin2 nor on the internalization of the D4 receptor.
Mesh Terms:
Adaptor Proteins, Signal Transducing, Animals, Arrestins, Cell Line, Cell Membrane, Cricetinae, Endoplasmic Reticulum, Humans, Receptors, Dopamine D4, Ubiquitination
Adaptor Proteins, Signal Transducing, Animals, Arrestins, Cell Line, Cell Membrane, Cricetinae, Endoplasmic Reticulum, Humans, Receptors, Dopamine D4, Ubiquitination
Cell. Signal.
Date: Jun. 01, 2010
PubMed ID: 20100572
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