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EXERCISE AND POLYPOSIS IN THE APCMIN/+ MOUSE

EXERCISE AND POLYPOSIS IN THE APCMIN/+ MOUSE
APCMIN/小鼠的运动和息肉病
批准号：
7610470
负责人：
James A Carson
金额：
$12.09万
依托单位：
UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA
依托单位国家：
美国
项目类别：
财政年份：
2007
资助国家：
美国
项目状态：
已结题
起止时间：
2007-08-01 至 2008-05-31
来源：
https://reporter.nih.gov/project-details/7610470
关键词：
AgingCachexiaComputer Retrieval of Information on Scientific Projects DatabaseExerciseFatty acid glycerol estersFundingGrantInflammatoryInstitutionInterleukin-6Malignant NeoplasmsMediator of activation proteinMolecularMusMusclePolypsProcessResearchResearch PersonnelResourcesSignaling MoleculeSourceUnited States National Institutes of Healthcytokinepolyposis

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中文摘要
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英文摘要
This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Dr. Carson's project examines the mechanisms by which exercise reduces polyp formation in the cancer-predisposed ApcMin/+ mouse. Mechanisms of the effects are assessed. In addition, the project examines the cachexic process, i.e., muscle and fat loss, in aging ApcMin/+ mice. Cellular and molecular factors promoting cachexia, such as inflammatory cytokines (interleukin-6) and signaling molecules, are being examined as mediators of cachexia.
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Muscle GPRC6A regulation of protein turnover with overload and disuse recovery
Muscle GPRC6A regulation of protein turnover with overload and disuse recovery
(PQ 12) The Regulation of Physical Function and Skeletal Muscle Metabolic Signaling After Cessation of 5-Fluorouracil Treatment
Cachexia in ApcMin/+ mice: The role of IL-6
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