Specifically, coordinated up regu lation of genes related to SMAD binding, TGF beta sig naling and notch signaling may suggest a mechanism for a hampered hypertrophic LDP-341 effect of RE in females. These genes included SMAD family member 1, 3 and 7, transforming growth factor, beta receptor II, v fos FBJ murine osteosarcoma viral oncogene homolog, interleukin 6 receptor, hairy enhancer of split related with YRPW motif 1, 2 and motif like, hairy and enhancer of split 1 and 4, inhibitor of DNA binding 3. Smad 2 and Smad3 are the transcription factors downstream of myostatin TGF beta and are able to induce atrophy programming. Activation of Notch signaling Inhibitors,Modulators,Libraries was able to inhibit myogenesis via transcriptional repressors of HEY and HES family members.

This finding sug gests that, in response to RE, along with activation of hypertrophy signaling events, a concomitant activation of Inhibitors,Modulators,Libraries atrophic factors may work against a muscle hyper trophic effect in the female muscle. Furthermore, although muscle hypertrophy was found to be a significantly up regulated biological theme in both males and females, it is noteworthy that sex differ ences might exist in the fine regulatory system of gene transcription leading to muscle hypertrophy. Specifically, the expression patterns of the mammalian target of rapamycin signaling associated factors identi fied in male muscle indicate that there was a coordinated repression of negative regulators of mTOR signaling, which were not observed in females. The mTOR signaling pathway plays a crucial role in mediat ing muscle hypertrophy.

The regulatory mechan isms controlling the activation and inactivation of mTOR signaling in muscle contractile activity are just starting to be elucidated. Several negative regulators Brefeldin_A have been identified including DNA damage inducible transcript 4, DNA damage inducible transcript 4 like, AKT1 substrate 1, and tuberous sclerosis 1 and 2. In a previous study, Drummond et al. reported decreased mRNA expression of DDIT4, DDIT4L, TSC1, and TSC2 in skeletal muscle of young and or old men after an acute stimulation of pro tein synthesis via RE and essential amino acid ingestion. Consistent with their reports, our microarray data indi cated a significant down regulation of mTOR inhibitors in male muscle, DDIT4, DDIT4L, AKT1S1 were signifi cantly down regulated and TSC1 showed a trend towards a down regulation in male muscle.

However this coordinated negative regulation was not observed in female muscle. This finding may implicate a mechanism behind dispro portional Inhibitors,Modulators,Libraries muscle growth in males as compared with females working at the same relative intensity. Further Inhibitors,Modulators,Libraries research using larger sample Dasatinib side effects sizes and measurements of protein content along this pathway is needed to confirm these preliminary findings. Sex differences in these spe cific features have not been reported elsewhere.