Prohormone convertase 2 (PC2) is a member of a family of mammalian subtilisin-like endoproteases that are involved in the processing of prohormones, neuropeptides and many other precursor derived proteins. The expression of PC2 is restricted to neuroendocrine tissues such as pancreatic islets, the pituitary and the brain. To understand the regulation of the PC2 gene, we cloned and characterized the promoter region of the mouse PC2 gene. The transcriptional start site of the mouse PC2 gene is identical to that of the human. There is 79% identity in the sequences of the promoter regions between the mouse and human PC2 genes. The mouse PC2 gene, like the human, does not have a TATA-like motif in the region just upstream of the start of the transcription. Studies with promoter-reporter gene, chloramphenicol acetyltransferase (CAT), constructs showed that the region from -400 to -170 bp was necessary for high level expression of the mouse PC2 gene in the betaTC-3 insulinoma cells.
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http://dx.doi.org/10.1507/endocrj.45.569 | DOI Listing |
Am J Physiol Cell Physiol
December 2024
Department of Biological Sciences, University of Pittsburgh, Pittsburgh, PA, USA.
Autosomal dominant polycystic kidney disease (ADPKD) is a common genetic disorder leading to end-stage renal disease. ADPKD arises from mutations in the and genes, which encode polycystin 1 (PC1) and polycystin 2 (PC2), respectively. PC2 is a non-selective cation channel, and disease-linked mutations disrupt normal cellular processes, including signaling and fluid secretion.
View Article and Find Full Text PDFFASEB J
November 2024
Department of Medicine IV - Nephrology and Primary Care, Faculty of Medicine and Medical Center, University of Freiburg, Freiburg, Germany.
Autosomal dominant polycystic kidney disease (ADPKD) is caused by mutations in PKD1 and PKD2, encoding polycystin-1 (PC1) and polycystin-2 (PC2), which are required for the regulation of the renal tubular diameter. Loss of polycystin function results in cyst formation. Atypical forms of ADPKD are caused by mutations in genes encoding endoplasmic reticulum (ER)-resident proteins through mechanisms that are not well understood.
View Article and Find Full Text PDFJ Cereb Blood Flow Metab
October 2024
Department of Microbiology and Molecular Cell Biology, Eastern Virginia Medical School, Norfolk, Virginia, USA.
While the concept of pericyte heterogeneity in the brain microvasculature is becoming more widely accepted, little is known about how they arise, or their functional contributions to the blood-brain barrier (BBB). We therefore set out to examine the distribution of subtypes of pericytes at the BBB and sought to elucidate some of their functional characteristics by examining their unique mRNA expression patterns. We demonstrate that type-1 pericytes (PC1) that are associated with young healthy brains and BBB homeostasis, can transition into type-2 pericytes (PC2) that are associated with disease and BBB breakdown, both in vitro and in vivo, in the presence of both endogenous and disease associated ligands.
View Article and Find Full Text PDFPlant Cell Rep
October 2024
Stockbridge School of Agriculture, University of Massachusetts, Amherst, MA, 01003, USA.
Am J Orthod Dentofacial Orthop
December 2024
Adelaide Dental School, The University of Adelaide, Adelaide, South Australia, Australia.
Introduction: The objective of this study was to assess the relative contribution of genes to shape variation in the permanent dental arches in individuals of Western European descent.
Methods: The dental casts from 64 monozygotic and 38 dizygotic twins, housed in the Adelaide Dental School's twin record collection, Australia, were assessed. The subjects were of Western European descent, with a mean age of 19.
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