Expression data from P4H-TM knockout mouse cortexes

Genetic deletion of transmembrane prolyl-4-hydroxylase (P4H-TM) in mice leads to changes in calcium signaling accompiened by attenuation of calcium agonist-induced gliotransmission and redistribution of mitochondria in primary astrocytes Cortexes from wild-type (WT) and P4H-TM knockout (KO) mice were collected for further mRNA extraction and microarray analysis. mRNA from 4 individual mice were pooled per experimental condition. Comparison was done between two experimental conditions: WT and KO.