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Journal ArticleDOI

Transcriptional regulation by the phosphorylation-dependent factor CREB

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TLDR
The transcription factor CREB functions in glucose homeostasis, growth-factor-dependent cell survival, and has been implicated in learning and memory, and how is specificity achieved in these signalling pathways?
Abstract
The transcription factor CREB -- for 'cyclic AMP response element-binding protein' -- functions in glucose homeostasis, growth-factor-dependent cell survival, and has been implicated in learning and memory. CREB is phosphorylated in response to various signals, but how is specificity achieved in these signalling pathways?

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Citations
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Journal ArticleDOI

β-Amyloid Disrupts Activity-Dependent Gene Transcription Required for Memory through the CREB Coactivator CRTC1

TL;DR: The findings suggest that CRTC1 plays a key role in coupling synaptic activity to gene transcription required for hippocampal-dependent memory, and that Aβ could disrupt cognition by affectingCRTC1 function.
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CREB-activity and nmnat2 transcription are down-regulated prior to neurodegeneration, while NMNAT2 over-expression is neuroprotective, in a mouse model of human tauopathy

TL;DR: It is found that over-expressing NMNAT2 or its homolog NMNAT1, but not NMNAT3, in rTg4510 hippocampi from 6 weeks of age using recombinant adeno-associated viral vectors significantly reduced neurodegeneration caused by tau(P301L) over-expression at 5 months of age.
Journal ArticleDOI

Axonal regeneration in adult CNS neurons--signaling molecules and pathways.

TL;DR: Modulations of the activity of another class of cellular signaling intermediate, the conventional protein kinase C (PKC), could result in a contrasting growth response by CNS neurons to myelin‐associated inhibitors.
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Insulin and IGF-1 improve mitochondrial function in a PI-3K/Akt-dependent manner and reduce mitochondrial generation of reactive oxygen species in Huntington's disease knock-in striatal cells.

TL;DR: Insulin and IGF-1 improve mitochondrial function and reduce mitochondrial ROS caused by mHtt by activating the PI-3K/Akt signaling pathway, in a process independent of Nrf2 transcriptional activity, but involving enhanced mitochondrial levels of Akt and mitochondrial-encoded complex IV subunit.
Journal ArticleDOI

Transcriptional Regulation of Murine IL-33 by TLR and Non-TLR Agonists

TL;DR: Treatment of primary murine macrophages with a panel of TLR agonists revealed a pattern of gene and protein expression consistent with a role for IFN regulatory factor-3 (IRF-3) in the expression of IL-33, which greatly extend what is currently known about the regulation ofIL-33 induction in macrophage stimulated by bacterial and viral agonists that engage distinct innate immune signaling pathways.
References
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Journal ArticleDOI

Cyclic AMP stimulates somatostatin gene transcription by phosphorylation of CREB at serine 133

TL;DR: Results suggest that phosphorylation of CREB may stimulate transcription by a mechanism other than by simply providing negative charge, as CREB mutants containing acidic residues in place of the Ser-133 phosphoacceptor were also transcriptionally inactive.
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Phosphorylated CREB binds specifically to the nuclear protein CBP

TL;DR: It is proposed that CBP may participate in cAMP-regulated gene expression by interacting with the activated phosphorylated form of CREB, which is activated as a result of phosphorylation by protein kinase A7.
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Cell survival promoted by the Ras-MAPK signaling pathway by transcription-dependent and -independent mechanisms.

TL;DR: The findings suggest that the MAPK signaling pathway promotes cell survival by a dual mechanism comprising the posttranslational modification and inactivation of a component of the cell death machinery and the increased transcription of pro-survival genes.
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Deficient long-term memory in mice with a targeted mutation of the cAMP-responsive element-binding protein

TL;DR: Consistent with models claiming a role for long-term potentiation (LTP) in memory, LTP in hippocampal slices from CREB mutants decayed to baseline 90 min after tetanic stimulation, however, paired-pulse facilitation and posttetanic potentiation are normal.
Journal ArticleDOI

Nuclear protein CBP is a coactivator for the transcription factor CREB

TL;DR: Fluorescence anisotropy measurements are used to define the equi-librium binding parameters of the phosphoCREB:CBP interaction and report here that CBP can activate transcription through a region in its carboxy terminus.
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