Relaxin-3 null mutation mice display a circadian hypoactivity phenotype

Grants

Funding Acknowledgements

This research was supported by grants from the National Health and Medical Research Council (NHMRC) of Australia (AJL, ALG), a collaborative research agreement between the Howard Florey Institute and Johnson & Johnson Pharmaceutical Research & Development, LLC (ALG), and the Victorian Government through the Operational Infrastructure Programme. During the course of these studies, CMS was the recipient of an NHMRC (Australia) Dora Lush Postgraduate Scholarship, and is currently a Florey Trust Fellow. AJL and ALG are NHMRC (Australia) Research Fellows. The authors wish to thank Simon Miller for his help in constructing the running wheels. We also thank the Pratt Foundation, the Besen Family Foundation, the Percy Baxter Charitable Trust and the ANZ Trustees Medical Research and Technology in Victoria for their support. Research in the laboratory of ALG was supported by a collaborative research agreement with Johnson & Johnson Pharmaceutical Research & Development, LLC (USA). SWS is a paid employee of Johnson & Johnson Pharmaceutical Research & Development, LLC (USA).