The Regulation of Skeletal Muscle Protein Turnover during the Progression of Cancer Cachexia in the ApcMin/+ Mouse

@inproceedings{White2011TheRO,
  title={The Regulation of Skeletal Muscle Protein Turnover during the Progression of Cancer Cachexia in the ApcMin/+ Mouse},
  author={James A. White and John W. Baynes and Stephen Welle and Matthew C. Kostek and Lydia E. Matesic and Shuichi Sato and James A Carson},
  booktitle={PloS one},
  year={2011}
}
Muscle wasting that occurs with cancer cachexia is caused by an imbalance in the rates of muscle protein synthesis and degradation. The Apc(Min/+) mouse is a model of colorectal cancer that develops cachexia that is dependent on circulating IL-6. However, the IL-6 regulation of muscle protein turnover during the initiation and progression of cachexia in the Apc(Min/+) mouse is not known. Cachexia progression was studied in Apc(Min/+) mice that were either weight stable (WS) or had initial (≤5… CONTINUE READING

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References

Publications referenced by this paper.
Showing 1-10 of 79 references

PI3 kinase regulation of skeletal muscle hypertrophy and atrophy.

Current topics in microbiology and immunology • 2010
View 16 Excerpts
Highly Influenced

Muscle atrophy in experimental cancer cachexia: is the IGF-1 signaling pathway involved?

International journal of cancer • 2010
View 4 Excerpts
Highly Influenced

Muscle oxidative capacity during IL-6-dependent cancer cachexia.

American journal of physiology. Regulatory, integrative and comparative physiology • 2011
View 3 Excerpts

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