Authors
BA Hain, H Xu, AM VanCleave, et al
Lab
Department of Cellular and Molecular Physiology, The Penn State College of Medicine, Hershey, Pennsylvania
Journal
Journal of Applied Physiology
Abstract
Cancer cachexia is a debilitating and lethal consequence of many advanced cancers. REDD1, a negative regulator of mTORC1 activity, is an emerging target in cachexia. Our data show that skeletal muscle REDD1 expression is increased in LLC-induced cancer cachexia. Mice lacking REDD1 have attenuated skeletal muscle atrophy that is likely due to maintaining both protein synthesis and inhibiting protein degradation.
BIOSEB Instruments Used
Grip strength test (BIO-GS3)