Further, protective effects against lipotoxicity of free cholesterol and free saturated fatty acids, improvement of cell membrane fluidity and enhancement of cell function and integrity are assumed due to increased SCD1 abundance. Thus, the assumed increased sodium- and uric acidcotransport in proximal tubule might be caused not only to compensate volume depletion in UAKD but also might be in part caused by altered cell function of proximal tubule cells itself. In conclusion, transcriptome profiling analyses in whole kidneys of two Umod mutant mouse models for UAKD at two different stages of the disease resulted in the description of differentially regulated genes which were further classified according to disease and/or functions annotations. Localization and quantification analyses of ANGPTL7 and SCD1 gave novel hints for the function of these proteins in healthy and UAKD affected kidneys. A cross talk between two functionally distinct tubular segments, the TALH segment and the S3 segment of proximal tubule, was demonstrated, which might occur by direct contact or due to functional compensatory properties. Currently, there are a number of transgenic mouse lines that are used to study Parkinson’s disease, including those in which rodent or human tyrosine Carfilzomib hydroxylase, dopamine transporter or DA transcription factor promoters have been engineered to drive expression of EGFP reporter protein expression in midbrain dopamine neurons of the substantia nigra pars compacta and ventral tegmental area and in their respective terminals in the striatum and cortex. These mice have allowed researchers to study Pitx-3+ DA neural progenitors, immature TH+ and mature DAT+ DA neurons in vitro. In vivo, these models have enabled the study of PD, particularly when systemic MPTP is used to generate damage to DA neurons. However, the most well-established and commonly used animal model of PD remains the 6-hydroxydopamine lesioned rat, first described by Ungerstedt. Because of the larger size of the rat brain as compared to the mouse brain, this model allows local administration of toxin unilaterally into the SNpc, striatum or median forebrain bundle, resulting in ipsilateral motor deficits which can be assessed, quantified, and compared to the contralateral side over time and following various experimental treatments. Because of the ease and reliability of this behavioral model, it has been long-favored by researchers. However, until now, there has been no transgenic reporter rat line to facilitate these studies in vivo or in vitro. The Michael J. Fox Foundation has developed a strategy to directly sponsor the generation, phenotypic characterization and distribution of preclinical rodent models in order to aid and accelerate PD research. As part of this overall strategy, MJFF, partnered with Thomas Jefferson University and Taconic Inc. to generate new transgenic rat lines carrying 11 kb of the human TH gene promoter driving EGFP. With its high levels of GFP, hTH-GFP rat reporter line 12141 allows for anatomical visualization of the rat SNpc and/or VTA and detailed analysis of midbrain DA neurons and axonal projections after toxin treatment in vivo.