Project description:We generated skeletal muscle-specific knockout mice lacking the transcription factor Yin Yang 1 (YY1) and analyzed expression patterns in the skeletal muscle these mice. We used microarrays to detail the global programme of gene expression regulated by YY1.
Project description:Expression profiles of mouse skeletal muscle tissues, mouse skeletal muscle from Aged animals with high fat diet and chemical treatment
Project description:Evidence suggests that diabetes mellitus is a promoting factor of sarcopenia; mechanism of how diabetes mellitus accelerates the development of sarcopenia is not known. We have recently established a model of diabetes-induced skeletal muscle mass loss in mice by using streptozotocin. We used microarrays to detail the global programme of gene expression underlying skeletal muscle atrophy in STZ treated mice and identified up-regulated or down-regulated genes during this process.
Project description:We generated skeletal muscle-specific knockout mice lacking the transcription factor Yin Yang 1 (YY1) and analyzed expression patterns in the skeletal muscle these mice. We used microarrays to detail the global programme of gene expression regulated by YY1. Wild type or knockout mice at 6 months were sacrificed and the soleus was isolated for RNA extraction.
Project description:Metabolic responses begin promptly upon the initiation of infection, and progress as a series of coordinated events. Mitochondria may play a key role in the development of insulin resistance. Reduced energy production and mitochondrial dysfunctional may further favor infection, and be an important step in the establishment of chronic and persistent infections. We have used mouse skeletal muscle transcriptome data which have led to the hypothesis that 2-AA causes harm to the host by triggering mitochondrial dysfunction in skeletal muscle.
Project description:Metabolic responses begin promptly upon the initiation of infection, and progress as a series of coordinated events. Mitochondria may play a key role in the development of insulin resistance. Reduced energy production and mitochondrial dysfunctional may further favor infection, and be an important step in the establishment of chronic and persistent infections. We have used mouse skeletal muscle transcriptome data which have led to the hypothesis that 2-AA causes harm to the host by triggering mitochondrial dysfunction in skeletal muscle. The gastrocnemius muscles were isolated from control and 4days 2-AA treated mouse for RNA extraction and hybridization on Affymetrix microarrays.