Mass spectrometric studies on epigenetic interaction networks in cell differentiation.

摘要: Arrest of cell differentiation is one the leading causes leukemia and other cancers. Induction using pharmaceutical agents has been clinically attempted for treatment these Epigenetic regulation may be underlying molecular mechanisms controlling proliferation or differentiation. Here, we report on use proteomics-based differential protein expression analysis in conjunction with quantification histone modifications to decipher interconnections among epigenetic modifications, their modifying enzymes mediators, changes associated pathways/networks that occur during During phorbol-12-myristate 13-acetate-induced U937 cells, fatty acid synthesis its metabolic processing, clathrin-coated pit endocytosis pathway, ubiquitin/26 S proteasome degradation pathways were up-regulated. In addition, global H3/H4 acetylation H2B ubiquitination down-regulated concomitantly impaired chromatin remodeling machinery, RNA polymerase II complexes, DNA replication. Differential established networks linking hypoacetylation expression/activity p300 II-associated FACT-RTF1-PAF1 complex. Collectively, our approach provided an unprecedentedly systemic set insights into role