Instead, genes are transcribed in large polycistronic units, with post-transcriptional regulation of mRNA processing and stability used to control mRNA abundance. In T. brucei the mRNAs from neighbouring genes will often display distinct developmentally regulated profiles. Additional processes such as regulated protein synthesis, modification and turnover will also contribute to regulated gene expression. The variation in mRNA abundance in T. brucei between lifecycle stages and during the differentiation process has recently been examined by three global transcriptomic studies using microarrays. Each found extensive regulation of mRNA abundance occurs between lifecycle stages and at different stages during the differentiation process. To date, there have been no genome-wide comparative proteomic studies between the lifecycle stages in T. brucei, and the correlation between mRNA and protein abundance is unclear. We have optimized a procedure for growing T. brucei procyclic form cells in conditions suitable for stable isotope labeling by amino acids in culture, and here we report a genome-wide comparative proteomic analysis of cultured procyclic form and bloodstream form T. brucei cells. Hirschsprung disease, a developmental disorder occurring in 1 of 5,000 live births, is characterized by the absence of ganglion cells along variable lengths of the distal gastrointestinal tract, which results in tonic contraction of the aganglionic gut segment and functional intestinal obstruction. Such aganglionosis is attributed to a failure of neural crest cells to migrate, proliferate, and/or differentiate during enteric nervous system development in the embryonic stage. The RET proto-oncogene is the major gene associated to HSCR with differential contributions of its rare and common, coding and noncoding mutations to the multifactorial nature of this pathology. In addition, numerous molecular genetic studies have identified rare coding mutations in many other genes related to HSCR. However, cumulatively, the conventional mutations related to HSCR reported so far explain less than 5% of cases, being the vast majority of them long segment HSCR/total colonic aganglionosis and syndromic forms of the disease. HSCR is regarded as a complex and multifactorial disorder, in which the contribution of AB1010 several different loci acting in an additive or multiplicative manner is usually required to cause the disease. Because of this evidence, many different techniques have emerged to identify new HSCR susceptibility loci, such as genome wide linkage and genome wide association studies. In this way, several HSCR associated regions, such as 16q23, 21q21, 9q31, 19q12, 3p21 or 4q31.3-q32.3 have been described, although the genes underlying such associations have not been identified yet in the majority of the cases. A recent GWAS has successfully identified NRG1 as a new candidate gene for HSCR. To refine the locus on 8p12 that had resulted to be linked, a total of 243 SNPs were genotyped in Chinese HSCR patients and controls. Genotype analysis narrowed down the HSCR-associated region to six of the most associated SNPs mapping to the NRG1 promoter. Moreover, significant differences in NRG1 expression levels between patients and controls bearing the same rs10088313 risk genotype were detected.