Ongoing evaluation of these biomarkers suggests that specific insults may illicit different biomarker responses and that building biomarker profiles might be the ultimate tool for identifying injury. As a consequence, there is a specific need for additional biomarkers that enable the generation of such specific biomarker profiles. Ideally, the biomarkers should be easily accessible in a non-invasive way, and should be applicable in animal models, as well as in man. ����Omic���� technologies hold the promise to fulfil this need and enable identification of multiple biomarkers that reflect specific types of injury in the kidney. Several proteomics approaches have been described in this context. CE-MS methodology was validated as an analytical tool for the measurement of peptides in rat urine and subsequently used to profile the LEE011 CDK inhibitor urinary low-molecular proteome of the rat. In an earlier publication, CE-MS was used as a biomarker discovery tool for nephrotoxicity in rats treated with cis-platin. In the study reported here we aimed to identify common and disparate biomarkers of cis-platin- and gentamicin-induced nephrotoxicity by applying CE-MS proteomics in rat urine. The aim of the study was to detect multiple biomarkers that can be efficiently analysed in a non-invasive approach. Such biomarkers could form the basis for specific multi-marker models for displaying drug-induced kidney injury in pre-clinical and clinical application and may have substantial translational value. In this study, we use Drosophila as a model organism for the study of glycerol kinase deficiency. The metabolic role of glycerol kinase is to convert glycerol to glycerol 3-phosphate in an ATP-dependent reaction and is the rate-limiting step in glycerol utilization. Glycerol 3-phosphate can be directed towards gluconeogenesis or lipid metabolism and alteration of GK activity also has a substantial effect on metabolic flux through other metabolic pathways such as the pentose phosphate pathway. In humans, GKD patients can have severe metabolic and CNS abnormalities, while others possess hyperglycerolemia and glyceroluria with no other apparent phenotype. Extensive studies incorporating patient data, mutation analysis and protein tertiary structure reveal no obvious phenotype-genotype correlations. BAY 73-4506 VEGFR/PDGFR inhibitor Additionally, analysis of glycerol kinase activity in GKD patients shows a range of glycerol kinase activities that do not correspond to severity of the phenotype. The cause of the phenotypic variability in GKD is currently unknown. It has previously been hypothesized that glycerol kinase could possess alternative functions i.e. protein activities. This is supported by the identification of rat GK as an ATP stimulated glucocorticoid-receptor translocation promoter protein. Additionally, evidence for an apoptotic function of glycerol kinase has been identified by weighted gene co-expression network analysis of liver gene expression in glycerol kinase knockout mice liver gene expression.