More alkaline conditions, considering that acidosis is one of the crucial hallmark of ischemic injury, which further triggers other neuroprotective pathways. We do not know precisely time profile of evidently common pathways, so it is hard to presume time and place of activation or which pathway dominates and leads to activation of enzymes involved in antioxidant defense. We need additional biochemical and molecular investigations bearing in mind all possible interactions of all elements of central nervous system. The nuclear factor c-Myc is a basic helix-loop-helix leucine zipper transcription factor that binds the consensus DNA sequence known as the E-Box when dimerized with Max. This dimer regulates the transcriptional activation of target genes. Myc is a master regulatory transcription factor that has been estimated to bind to over 15% of all promoters in different cell types, modulating the expression of a large number of its target genes. Myc is considered a global gene regulator that acts by recruiting enzymes to the chromatin that induce covalent modifications in histone tails. In response to environmental stimuli, Myc modulates a large number of cellular processes, such as proliferation, growth, differentiation, metabolism, and even apoptosis. Myc also plays a role in ES cell pluripotency. Chromatin immunoprecipitation coupled with massive parallel sequencing is a powerful method for the identification of binding sites of chromatin-associated proteins, and several experiments have been performed to identify Myc binding sites. However, ChIP experiments are limited by the specificity of the antibody used and the degree of enrichment achieved in the immunoprecipitation step. The list of identified genes to which Myc binds is largely incomplete, mainly because genome-wide analyses of Myc binding sites are hampered by the quality of the available antibodies. One way to circumvent this problem is the expression of epitope-tagged proteins. To generate a more comprehensive map of Myc binding within the genome in mouse embryonic stem cells, we compared the chromatin immunoprecipitation efficiency of four affinity tags. We generated ESC clones expressing Myc tagged at its N-terminus with either a Biotag, a FLAG-HA, or a V5 epitope and compared the efficiency and selectivity of each in ChIP experiments under different conditions. A genome-wide analysis was performed to compare the results of Bio-Myc ChIP-Seq with previously published ChIP-Seq data obtained with an antibody recognizing endogenous Myc. We identified a large number of Myc binding sites that were previously undetected. Because Myc must form a dimer with Max to bind to an E-Box element, we also performed ChIP-Seq with Max and found that Myc with Max share over 85% of their genomic binding sites. The validation of a group of newly identified genes showed that these genes are actually bound and NVP-BEZ235 clinical trial regulated by Myc in ESCs.