CREB and the CRTC co-activators: sensors for hormonal and metabolic signals
By Judith Y. Altarejos, M. Montminy. Nature reviews. Molecular cell biology, 2011
1,009 citations recorded by the source corpus.
The cyclic AMP-responsive element-binding protein (CREB) is phosphorylated in response to a wide variety of signals, yet target gene transcription is only increased in a subset of cases. Recent studies indicate that CREB functions in concert with a family of latent cytoplasmic co-activators called cAMP-regulated transcriptional co-activators (CRTCs), which are activated through dephosphorylation. A dual requirement for CREB phosphorylation and CRTC dephosphorylation is likely to explain how these activator–co-activator cognates discriminate between different stimuli. Following their activation, CREB and CRTCs mediate the effects of fasting and feeding signals on the expression of metabolic programmes in insulin-sensitive tissues.
Subfields: Molecular Biology, Physiology, Surgery
View Paper: https://www.semanticscholar.org/paper/3504402352d12113e01be8baa79ec3f4bfe140c2
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Citations in the corpus
- Cyclic AMP Signaling in Mycobacteria (2014, background): “cAMP signaling in mammals controls biological processes ranging from metabolism to memory formation and innate immunity, although it was first discovered for its role in hormone signal transduction (1, 6, 7).”
- Hunger and memory; CRTC coordinates long-term memory with the physiological state, hunger (2013, positive): “CREB requires co-activators, CBP (CREB-binding protein) or CRTC (cAMP-regulated transcriptional coactivator) to activate transcription.(9) By knockdown experiments targeted to MBs, we found that spLTM is dependent on CBP, and fLTM is dependent on CRTC.”
- Time restricted feeding without reducing caloric intake prevents metabolic diseases in mice fed a high fat diet (2012, positive): “Temporal Feeding Pattern Shapes Rhythms in CREB, mTOR, and AMPK Activities and in the Circadian Oscillator A HFD fed under an ad lib regimen perturbs metabolic regulators, including CREB, mTOR, and AMPK, and contributes to metabolic diseases (Altarejos and Montminy, 2011; Inoki et al., 2011).”