Project description:CaGAL102 is a sequence homolog of Rmlb. In Candida knock out of this gene causes abnormal hyphal morphogenesis and increased sensitivity to cell wall damaging agents. The knock out strain is also avirulent in mouse model of systemic infection. To get a larger insight into the function of the protein product of this gene we carried out global transcription analysis through micro array experiment. The gene is expressed under normal growth conditions and the knock out causes the cells to become hyphal under these conditions. Many of the cell wall proteins were upregulated recapitulating the cell morphology. Keywords: Candida albicans, Gene knockout, genome wide transcription profiling study
Project description:To understand the changes in gene expression at different stages of diet-induced atherosclerotic development, double knock out Apobtm2Sgy/Ldltm1Her mice were fed with either high-fat or normal chow diet. The microarray was performed using total RNA extracted from ascending aorta of the animals.
Project description:To understand the changes in microRNA expression regulating specific genes at different stages of diet-induced atherosclerotic development, double knock out Apobtm2Sgy/Ldltm1Her mice were fed with either high-fat or normal chow diet. The microarray was performed using total RNA extracted from ascending aorta of the animals.
Project description:To understand the changes in gene expression at different stages of diet-induced atherosclerotic development, double knock out Apobtm2Sgy/Ldltm1Her mice were fed with either high-fat or normal chow diet. The microarray was performed using total RNA extracted from ascending aorta of the animals. Double knockout mice fed with rich cholesterol diet and a normal diet were sacrificed after 0, 4, 8, 14 and 20 weeks and RNA was extracted for Microarray analysis
Project description:Klotho knock-out mice are an important model for CKD-induced calcification. In CKD, serum magnesium (Mg2+) inversely correlates with vascular calcification. This study aims to determine the effects of Mg2+ on aortic calcification in Klotho knock-out mice. Klotho knock-out mice were treated with either a minimal or a high Mg2+ diet from birth. After eight weeks, serum biochemistry was studied and organs were harvested. Protective effects of Mg2+ were characterized by RNA-sequencing of aortic tissue. Micro-CT analysis was performed to study bone integrity. High Mg2+ diet prevented vascular calcification and reduced aortic gene expression of Runx2 and matrix Gla protein, demonstrating the protective effect on pro-osteogenic signaling. Differential expression of inflammation and extracellular matrix remodeling genes accompany the beneficial effects of Mg2+ on calcification. High dietary Mg2+ did not affect serum parathyroid hormone, vitamin D3 and calcium. High Mg2+ intake prevented calcification despite increasing fibroblast growth factor-23 and phosphate concentration in knock-out mice. In addition, mice on the high Mg2+ diet had a 20% reduced femoral bone mineral density and increased osteoid formation indicating osteomalacia, while osteoclast activity was decreased in Klotho knock-out mice. In Saos-2 osteoblasts, Mg2+ supplementation reduced mineralization independent of osteoblastic matrix production, alkaline phosphatase activity and maturation markers alpha-1 type-I collagen and sclerostin. In conclusion, high dietary Mg2+ prevents calcification in Klotho knock-out mice. These effects are potentially mediated by reduction of inflammatory and extracellular matrix remodeling pathways in the aorta. Mg2+ treatment is promising to prevent vascular calcification, but the risk for osteomalacia should be considered.
Project description:Expression profiling of pancreatic islets in Tcf1 knock out mice. Experiment Overall Design: two biological replicates per condition; two conditions are WT and Tcf1 KO mice; platforms are Affy MG-U74A and B array