• Publications
  • Influence
Bowman-Birk inhibitor concentrate prevents atrophy, weakness, and oxidative stress in soleus muscle of hindlimb-unloaded mice.
Antigravity muscles atrophy and weaken during prolonged mechanical unloading caused by bed rest or spaceflight. Unloading also induces oxidative stress in muscle, a putative cause of weakness. WeExpand
  • 81
  • 10
  • PDF
Doxorubicin acts via mitochondrial ROS to stimulate catabolism in C2C12 myotubes.
Doxorubicin, a commonly prescribed chemotherapeutic agent, causes skeletal muscle wasting in cancer patients undergoing treatment and increases mitochondrial reactive oxygen species (ROS) production.Expand
  • 96
  • 7
Stretch‐stimulated glucose uptake in skeletal muscle is mediated by reactive oxygen species and p38 MAP‐kinase
Alternatives to the canonical insulin‐stimulated pathway for glucose uptake are exercise‐ and exogenous reactive oxygen species (ROS)‐stimulated glucose uptake. We proposed a model wherein mechanicalExpand
  • 114
  • 7
TNF-alpha acts via TNFR1 and muscle-derived oxidants to depress myofibrillar force in murine skeletal muscle.
Tumor necrosis factor-alpha (TNF) diminishes specific force of skeletal muscle. To address the mechanism of this response, we tested the hypothesis that TNF acts via the type 1 (TNFR1) receptorExpand
  • 118
  • 6
TNF induction of atrogin-1/MAFbx mRNA depends on Foxo4 expression but not AKT-Foxo1/3 signaling.
Murine models of starvation-induced muscle atrophy demonstrate that reduced protein kinase B (AKT) function upregulates the atrophy-related gene atrogin-1/MAFbx (atrogin). The mechanism involvesExpand
  • 100
  • 6
  • PDF
Interleukin-1 stimulates catabolism in C2C12 myotubes.
Interleukin-1 (IL-1) is an inflammatory cytokine that has been linked to muscle catabolism, a process regulated by muscle-specific E3 proteins of the ubiquitin-proteasome pathway. To address cellularExpand
  • 98
  • 5
  • PDF
Sphingomyelinase stimulates oxidant signaling to weaken skeletal muscle and promote fatigue.
Sphingomyelinase (SMase) hydrolyzes membrane sphingomyelin into ceramide, which increases oxidants in nonmuscle cells. Serum SMase activity is elevated in sepsis and heart failure, conditions whereExpand
  • 41
  • 4
  • PDF
Intrinsic muscle clock is necessary for musculoskeletal health
The endogenous molecular clock in skeletal muscle is necessary for maintenance of phenotype and function. Loss of Bmal1 solely from adult skeletal muscle (iMSBmal1−/−) results in reductions inExpand
  • 58
  • 3
  • PDF
Sphingomyelinase depresses force and calcium sensitivity of the contractile apparatus in mouse diaphragm muscle fibers.
Diseases that result in muscle weakness, e.g., heart failure, are characterized by elevated sphingomyelinase (SMase) activity. In intact muscle, SMase increases oxidants that contribute to diminishedExpand
  • 25
  • 2
  • PDF
Neurite elongation on chondroitin sulfate proteoglycans is characterized by axonal fasciculation
In the developing or regenerating nervous system, migrating growth cones are exposed to regulatory molecules that positively and/or negatively affect guidance. Chondroitin sulfate proteoglycansExpand
  • 56
  • 1