Cohen Shenhav, Assistant Professor

Phone:  Lab: (972)-4-829-3423, Office: (972)-4-829-4214
Fax:  (972)-4-829-3423

Building/Auditory:  Biology 214

Research interests

We are interested in the molecular mechanisms of muscle atrophy and the specific role that the ubiquitin proteasome system plays in this process. Using a sophisticated in-vivo gene transfection approach we can study gene effects in normal or atrophying muscle of adult wild type mouse, while avoiding developmental defects often seen in transgenic or knockout animals.

Atrophy of skeletal muscle is an inevitable sequela of lack of use (e.g., bed-ridden patients, spinal cord injuries), fasting or many diseases (e.g., cancer cachexia, diabetes, renal failure, cardiac failure, sepsis and neuromuscular diseases (ALS)). The major loss of mass during atrophy results largely from the accelerated destruction of the muscle’s contractile unit, the myofibrils, which contain the motor proteins actin and myosin. Their loss leads to reduced contractile force, fatigue and weakness, and in many human diseases to reduced quality of life, morbidity and mortality.

We focus on the mechanisms promoting myofibril disassembly and degradation by probing the functions of certain atrophy-related ubiquitin ligases. Our goal is to identify key players in order to develop countermeasures to block or attenuate this debilitating process.