Markus Stratmann

TL;DR: It is shown that SIRT1, an NAD(+)-dependent protein deacetylase, is required for high-magnitude circadian transcription of several core clock genes, including Bmal1, Rorgamma, Per2, and Cry1.

TL;DR: Genetic loss-of-function studies have now established a role for mammalian circadian clock components in energy homeostasis and xenobiotic detoxification, and the latter manifests itself in the daytime-dependent modulation of drug efficacy and toxicity.

TL;DR: Simulation of body temperature cycles, but not peripheral oscillators, controlled the rhythmic expression of cold-inducible RNA-binding protein (CIRP) in cultured fibroblasts, and loss-of-function experiments indicated that CIRP was required for high-amplitude circadian gene expression, surmising that C IRP confers robustness to circadian oscillators through regulation of CLOCK expression.

TL;DR: Using precise temperature devices in conjunction with real-time monitoring of the bioluminescence produced by circadian luciferase reporter genes, it was shown that simulated body temperature cycles of mice and even humans, with daily temperature differences of only 3°C and 1°C, respectively, could gradually synchronize circadian gene expression in cultured fibroblasts.

TL;DR: BMAL1 and CLOCK may act as Kamikaze activators, in that they are rapidly degraded once bound to Dbp chromatin, as shown in cells harboring a single Dbp-luciferase reporter gene copy.