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In humans, body temperature increases during wakefulness and decreases during sleep ( Duffy et al. The body temperature rhythm (BTR) is one of the most conspicuous outputs of the circadian clock ( Aschoff 1983 Krauchi 2002 Weinert 2010) and is crucial for maintaining homeostasis in metabolism and sleep as well as entraining the peripheral clock in mammals ( Refinetti and Menaker 1992 Gilbert et al. Our results represent the first molecular evidence that BTR is regulated distinctly from locomotor activity rhythms and show that DH31R/Calcr is an ancient specific mediator of BTR during the active phase in organisms ranging from ectotherms to endotherms. Importantly, DH31R and Calcr are not required for coordinating locomotor activity rhythms. Surprisingly, the mouse homolog of DH31R, calcitonin receptor (Calcr), is expressed in the suprachiasmatic nucleus (SCN) and mediates body temperature fluctuations during the active phase in mice. DH31R is expressed in clock cells, and its ligand, DH31, acts on clock cells to regulate TPR during the active phase. Here, we demonstrate that the diuretic hormone 31 receptor (DH31R) mediates TPR during the active phase in Drosophila. While mammals internally regulate BTR, ectotherms, including Drosophila, exhibit temperature preference rhythm (TPR) behavior to regulate BTR. BTR is regulated separately from locomotor activity rhythms, but its molecular basis is largely unknown. (PMID: 20379614) Rose JE … Uhl GR (Molecular medicine (Cambridge, Mass.Daily body temperature rhythm (BTR) is essential for maintaining homeostasis.

Molecular cloning and sequence analysis of human placental ferredoxin.(PMID: 12699818) Johnson D … Martin LL (Bioelectrochemistry (Amsterdam, Netherlands) 2003) 3 4 21 Electrochemical behaviour of human adrenodoxin on a pyrolytic graphite electrode.(PMID: 20547883) Sheftel AD … Lill R (Proceedings of the National Academy of Sciences of the United States of America 2010) 2 3 4

Humans possess two mitochondrial ferredoxins, Fdx1 and Fdx2, with distinct roles in steroidogenesis, heme, and Fe/S cluster biosynthesis.Corticosterone Methyl Oxidase Type Ii Deficiency.

Corticosterone Methyl Oxidase Type I Deficiency.Aldosterone Deficiency Due To Defect In 18-Hydroxylase.Corticosterone Methyloxidase 1 Deficiency.Aldosterone Deficiency Due To Defect In 18 Hydroxylase.Hyperreninemic Hypoaldosteronism, Familial, 1.Corticosterone Methyloxidase Type 1 Deficiency.Corticosterone Methyloxidase Deficiency 1.Hypoaldosteronism, Congenital, Due To Cmo I Deficiency.