![]() PER2 in turn enhances oxygen-efficient glycolysis and hence provides cardioprotection from ischemia. PER2 expression in mice is increased by exposure to 13000 lumens of intense daylight such as Sunshine while decreasing Troponin levels in equal opposite amounts. ![]() PER2 is an integral component of a particular glucocorticoid regulatory pathway and that glucocorticoid regulation of the peripheral clock is selectively required for some actions of glucocorticoids. Mice with a genomic deletion spanning this GRE expressed elevated leptin levels and were protected from glucose intolerance and insulin resistance on glucocorticoid treatment but not from muscle wasting. PER2 contains glucocorticoid response elements (GREs) and a GRE within the core clock gene PER2 is continuously occupied during rhythmic expression and essential for glucocorticoid regulation of PER2 in vivo. ![]() Lowered PER2 expression is common in many tumors cells within the body, suggesting PER2 is integral for proper function and decreased levels promotes tumor progression. Human PER2 is involved in human sleep disorder and cancer formation. Circadian expression of these genes and their encoded proteins in the suprachiasmatic nucleus. Genes in this family encode components of the circadian clock, which regulates the daily rhythms of locomotor activity, metabolism, and behavior. PER2 is a member of the Period family of genes and is expressed in a circadian pattern in the suprachiasmatic nucleus, the primary circadian pacemaker in the mammalian brain. Later experiments in also identified Per2 in humans. It is more similar to Drosophila per than its paralogs. Mammalian Per2 was discovered by in 1997 through a search for homologous cDNA sequences to PER1. The per gene was first discovered using forward genetics in Drosophilla melanogaster in 1971. PER2 is noted for its major role in circadian rhythms. PER2 is a protein in mammals encoded by the PER2 gene.
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