(C) 2009 Elsevier Ireland Ltd. All rights reserved.”
“The regulation of epithelial branching morphogenesis

by bone morphogenetic protein-7 depends, in part, on functionally defined cyclic adenosine monophosphate (cAMP)-dependent protein kinases. We previously identified protein kinase-X (PRKX), a cAMP-dependent kinase, as a regulator of epithelial morphogenesis during kidney development and found that it binds to and phosphorylates Polycystin-1. Overexpression of PRKX stimulates renal epithelial cell migration, tubulogenesis, ureteric bud branching, and glomerular induction in embryonic mouse kidney explants in organ cultures. Here we determined the physiological functions of endogenous PRKX. Knockdown by siRNA of PRKX gene expression in a human fetal collecting tubule (HFCT) cell line exceeded 70% and resulted in decreased cell

OTX015 migration and increased adhesion of the cells to a collagen I matrix. In embryonic mouse kidney explants, the Thiazovivin same degree of knockdown decreased ureteric bud branching and glomerular induction. Because PRKX BAG-3 PIN-1 and MAGI-1 are all expressed in ureteric bud derivatives, we tested for interactions among them and found that PRKX binds to all three proteins through its WW domain as determined by TransSignal domain arrays, and it coimmunoprecipitated with Pin-1 in HFCT cell lysates. These studies suggest that Polycystin-1 and Pin-1 may mediate the function of PRKX in kidney development. Kidney International (2009) 76, 54-62; doi: 10.1038/ki.2009.95; published online 15 April 2009″
“Grb10-Interacting GYF Protein-2 gene (GIGYF2) has been suggested as a candidate gene for PARK11 locus since seven different GIGYF2 missense mutations were identified in familial Parkinson’s disease (PD) patients of European descent. To evaluate the frequency and distribution of GIGYF2 Asn56Ser mutation in Chinese PD patients, we analyzed 469 patients with PD from

mainland China, including 36 cases with familial PD and 433 cases with sporadic PD. A total of 451 subjects without neurological disorders ACY-738 ic50 from the same region in China were set as a control group. The result showed that the GIGYF2 Asn56Ser mutation was not present in all subjects. Our finding suggests that the GIGYF2 Asn56Ser mutation is rare in Chinese PD patients. (C) 2009 Elsevier Ireland Ltd. All rights reserved.”
“Recent studies suggest that Stat3, a transcription factor that mediates cytokine signaling, plays a critical role in the pathogenesis of diabetic nephropathy. Complete Stat3 gene knockout is embryonic lethal; therefore, we crossed Stat3+/- mice with Stat3 mutant mice (SA/SA) that lack full Stat3 activity.