MYC Disrupts the Circadian Clock and Metabolism in Cancer Cells.
Philadelphia, United States. In Cell Metab, Jan 2016
We report here that deregulated expression of MYC or N-MYC disrupts the molecular clock in vitro by directly inducing REV-ERBα to dampen expression and oscillation of BMAL1, and this could be rescued by knockdown of REV-ERB.
Circadian clock: Time for novel anticancer strategies?
Genova, Italy. In Pharmacol Res, Oct 2015
In this review, we focus on the functions of the druggable circadian nuclear receptors, REV-ERBα and REV-ERBβ, in cancer cell survival and describe the potential development of small molecule compounds that modulate REV-ERB activity as novel anticancer therapeutics.
Emerging models for the molecular basis of mammalian circadian timing.
Santa Cruz, United States. In Biochemistry, Feb 2015
At its core, the heterodimeric transcription factor CLOCK:BMAL1 activates expression of Period, Cryptochrome, and Rev-Erb genes, which feed back to repress transcription and create oscillations in gene expression that confer circadian timing cues to cellular processes.
Nuclear receptors in acute and chronic cholestasis.
Paris, France. In Dig Dis, 2014
Likewise, NRs from other physiological clusters with low hepatic expression, such as estrogen receptor α (ERα) or reverse-Erb α/β (REV-ERB α/β), may also control pathophysiological processes in cholestasis.
REV-ERB and ROR nuclear receptors as drug targets.
Jupiter, United States. In Nat Rev Drug Discov, 2014
The nuclear receptors REV-ERB (consisting of REV-ERBα and REV-ERBβ) and retinoic acid receptor-related orphan receptors (RORs; consisting of RORα, RORβ and RORγ) are involved in many physiological processes, including regulation of metabolism, development and immunity as well as the circadian rhythm.