## Abstract Diseases involving chronic inflammation can lead to prolonged exposure of skeletal muscle to inflammatory cytokines such as tumor necrosis factor α (TNFα), which may contribute to the skeletal muscle weakness seen in these conditions. In this study we examined the effect of a prolonged
Glutamine prevents myostatin hyperexpression and protein hypercatabolism induced in C2C12 myotubes by tumor necrosis factor-α
✍ Scribed by Andrea Bonetto; Fabio Penna; Valerio G. Minero; Patrizia Reffo; Domiziana Costamagna; Gabriella Bonelli; Francesco M. Baccino; Paola Costelli
- Publisher
- Springer
- Year
- 2010
- Tongue
- English
- Weight
- 551 KB
- Volume
- 40
- Category
- Article
- ISSN
- 0939-4451
No coin nor oath required. For personal study only.
📜 SIMILAR VOLUMES
## Abstract Amyloid precursor protein (APP) has been characterized as an adipocyte‐secreted protein that might contribute to obesity‐related insulin resistance, inflammation, and dementia. In the current study, regulation of APP by the proinflammatory and insulin resistance‐inducing cytokine tumor
## Abstract The proinflammatory cytokine tumor necrosis factor (TNF) α is mainly produced in cells from the monocyte/macrophage lineage. TNFα is also a key signaling molecule in the liver functioning as an important physiological and pathogenic mediator. In hepatocytes or human hepatoma cells TNFα
## Abstract ## Objective To examine the role of interferon regulatory factor 1 (IRF‐1) in tumor necrosis factor α (TNFα)–induced interleukin‐18 binding protein a (IL‐18BPa) expression in rheumatoid arthritis synovial fibroblasts (RASFs). ## Methods TNFα‐induced IRF‐1 expression was assessed by r