in a higher resting rate of O2 consumption. Substantial variability in absolute OCRs was observed due to 16352702 differences in plating, viability, and cell distribution, making it difficult to accurately compare absolute basal and glutamate-stimulated rates among groups in individual experiments. However, we were able to detect statistical differences by MedChemExpress c-Met inhibitor 2 analyzing a large number of experiments. Type I neurons had a significantly higher resting OCR compared to Type II neurons, consistent with a greater energy demand at rest. MgSO4 significantly lowered the basal OCR of both Type I and Type II neurons; however the magnitude of the decrease was greater for Type I neurons. For Type I neurons, absolute OCR measured after glutamate treatment was significantly higher in the presence of MgSO4 compared to in its absence. In contrast, MgSO4 did not significantly affect the absolute OCR after 16707462 glutamate treatment in Type II neurons. OCR measured after glutamate receptor stimulation was significantly higher in Type II neurons compared to Type I neurons either in the absence or presence of MgSO4. This finding is indicative of an impaired bioenergetic response to glutamate in Type I neurons that was partially but not completely alleviated by MgSO4 pretreatment. 3 Magnesium Preserves Neuronal Metabolism cell line. Each of the four probes formed a similar pair of nucleoprotein complexes. Formation of the paired complexes was inhibited in the presence of a 100-fold molar excess of unlabeled cognate probe, as well as two known Sp1-binding sequences from the OX40 promoter . These results show that each of the four predicted Sp1/3 sites in Mina P1 can form complexes with EL4 nuclear factors. Binding of Sp1/3 to the Mina P1 Promoter in EL4 Cells Next, we investigated whether Sp1 and/or Sp3 occurred within nucleoprotein complexes 1 and 2. Using gel shift assays with Mina P1 probes and EL4 nuclear extract we found that antibodies against YY1, Runx3 and Mina failed to perturb either complex. By contrast, an Sp1-specific antibody caused a supershift of the upper band of the complex 1 doublet, while an Sp3specific antibody abolished the lower band of the complex 1 doublet and the upper of band of the complex 2 doublet. Combining antibodies against Sp1 and Sp3 led to a summation of their individual effects on complexes 1 and 2. Together, these data indicate that probes p1p4 each form 3 distinct nucleoprotein complexes, one containing Sp1 and two containing Sp3. Binding of Sp1/3 to the H3K4me3-enriched Mina P1 Promoter in Primary T Cells We chose to explore Sp1/3 binding to the endogenous Mina promoter in primary naive CD4 T lymphocytes as they are known to express Mina at high level. We assessed the enrichment of Mina P1 promoterproximal and distal intron 2 sequences in chromatin immunoprecipitated with control IgG and antibodies against Sp1 and Sp3. As was the case with EL4 cells we found that in Mina Activation by Sp1/Sp3 primary naive CD4 T cells both Sp1 and Sp3 bound to the Mina P1 promoter but not to distal intron2. Histone modifications are implicated in regulating gene expression by modulating chromatin structure, DNA accessibility and recruitment of transcription regulatory machinery. Tri-methylation of histone 3 at lysine 4 marks the promoters of actively transcribed genes, whereas tri-methylation of 
histone 3 at lysine 27 is associated with gene repression and silenced chromatin. To determine whether the epigenetic landscape of the Mina locus correlated with i