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)