Macrophage Bmal1 controls the timing of the glycolytic to oxidative metabolism transition that dictates the extent of Hif-1a activation and the associated inflammatory response.

A protein within the nuclear membrane, MAN1, controls the expression of the circadian clock gene, BMAL1, in an example of cross-talk between two major gene regulatory pathways.

The myogenic lineage transcription factor, MYOD1, amplifies and works with the core clock factors to support a daily muscle gene expression program.

Conditional deletion of Bmal1 in the forebrain/SCN reveals an essential role of a functional master clock in maintaining synchronized and high amplitude rhythms of peripheral clocks.

Expression of transcription factor BMAL1 in skeletal muscle reduces the recovery response to sleep loss and is both necessary and sufficient to regulate total sleep amount.

Acetylation of the circadian transcription factor BMAL1 by the acetyltransferase TIP60 is crucial for recruitment of the pause release factors to clock gene promoters and productive elongation of these genes.

The BMAL1-REV-ERB axis controls expression of complement C4b expression and microglial synaptic phagoctyosis, providing a link between cellular circadian clock function and synaptic regulation.

Circadian neutrophil infiltration in the liver modulates liver clock-gene expression and daily hepatic metabolism through the secretion of elastase and activation of JNK-FGF21-Bmal1 axis in the hepatocyte.

Circadian clocks in murine myeloid cells are dispensable for circadian cytokine function, trafficking and endotoxic shock in response to LPS in vivo.

Dynamic interactions of core clock molecules are quantitively measured and mathematically modelled to reveal the hidden role of PER:CRY complexes in enhancing the mobility of CLOCK:BMAL1 to move to new DNA sites.