Abstract
•This study investigated how cereblon (CRBN), a substrate receptor of the E3 ubiquitin ligase complex that selectively degrades ion channels, targets cardiac transient receptor potential channel 1 (TRPC1).•Physiologically, CRBN ablation upregulated TRPC1 expression.•Mechanistically, the CRBN Lon domain directly interacts with the C- and N-terminals of TRPC1.•Increasing CRBN levels enhanced TRPC1 ubiquitination and proteasomal degradation.•TRPC1 overexpression in HEK293-CRBN KO cells enhanced TRPC1 current density and Ca2+ transients.•Pathologically, cardiac TRPC1 expression in CRBN-deficient mice was increased during ex vivo ischemic/reperfusion.•Targeting the CRBN-TRPC1 axis may serve as a novel therapeutic approach to address cardiac disease.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
