Home

SFS Des. GSK3 3d Rt 1 cropped_single EDL fiber_desmin_green_actin_red_actinin_white z- Transfected mouse muscle immunofluorescence of cytoskeleton Myofibrils cartoon EM of skeletal muscle cultured myotubes Imaris Snapshot beta-Dystroglycan-insulin receptor sited of association on skeletal muscle membrane Collage
SFS Des. GSK3 3d Rt 1
cropped_single EDL fiber_desmin_green_actin_red_actinin_white z-stack
<prop id="look-up-table-custom-values" type="int-arra
Imaris Snapshot
Imaris Snapshot

Skeletal muscle atrophy is an inevitable sequel of fasting, denervation, disuse and many human diseases including cancer, cachexia, diabetes, renal failure, cardiac failure, and neurodegenerative diseases. This debilitating process results primarily from the excessive destruction of the fundamental contractile machinery in muscle, the myofibrils, by the ubiquitin proteasome system. The major loss of muscle mass during atrophy leads to reduced contractile force, fatigue and weakness, and in many human diseases to reduced quality of life, increased morbidity and mortality.

The main focus of our lab is to understand how is the highly ordered complex structure of myofibrils disassemble during atrophy in order to identify rational therapies to combat various types of wasting.