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Science Signaling  17 Dec 2019:
Vol. 12, Issue 612, eaba2063
DOI: 10.1126/scisignal.aba2063

Post date 17 December 2019

In the Research Article “Metalloprotease cleavage of the N terminus of the orphan G protein–coupled receptor GPR37L1 reduces its constitutive activity” (1), the orphan receptor GPR37L1 was reported to signal through Gαs in the absence of ligand, and this signal was proposed to be reciprocally regulated by N-terminal cleavage. Support for the conclusion that GPR37L1 exhibited constitutive signaling came from transient transfection of HEK 293 cells with a construct expressing wild-type GPR37L1 and the observation that GPR37L1 expression caused an increase in CRE-luciferase (CRE-luc) reporter gene activity through Gαs, which was consistent with findings obtained using a yeast reporter system, FlpIN TREx cells, and mouse cerebellar slices. After publication of the work, we discovered a cloning error in the GPR37L1 construct used exclusively in the CRE-luc assays, and when experiments were repeated with the correct construct, they failed to confirm constitutive signaling by GPR37L1 in transfected HEK 293 cells, although N-terminal cleavage of the receptor was still apparent. In light of these findings, the authors have decided to retract the paper in full, and all authors agree with this decision. The authors very much regret this error and apologize to the scientific community for any inconvenience that this has caused.


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