What turns CREB on?

Johannessen, Mona; Delghandi, Madjid; Moens, Ugo

doi:10.1016/j.cellsig.2004.05.001

Cited by 570 publications

(542 citation statements)

References 258 publications

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“…Analogous to these results, it has been reported that TGF-β1 signaling activates two independent A B pathways, the Smad-mediated and the TAK1-mediated pathways (Heldin et al, 1997;Moriguchi et al, 1996). In the TAK1 pathway, TGF-β1 activates TAK1-MKK6-p38MAPK (Hanafusa et al, 1999) and CREB, p38 MAPK downstream molecules (Chen and Xie, 2010;Johannessen et al, 2004). Between the two pathways, we do not distinguish at the moment which pathway is more relevant to TGFβ1-induced APRIL expression as often demonstrated by others (Hanafusa et al, 1999;Kamaraju and Roberts, 2005;Patel et al, 2010).…”

Section: Discussionsupporting

confidence: 65%

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TGF-β1 Stimulates Mouse Macrophages to Express APRIL through Smad and p38MAPK/CREB Pathways

Jang¹,

Kim²,

Seo³

et al. 2011

Molecules and Cells

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Section: Discussionsupporting

confidence: 65%

“…Further, p38MAPK is a downstream molecule of TGF-β-activated kinase 1 (TAK1) in TGF-β signaling (Hanafusa et al, 1999), and activates CREB in this pathway (Johannessen et al, 2004). Therefore, we tested these possibilities using appropriate inhibitors.…”

Section: Induction Of April Expression By Tgf-β1 Involves the P38mapkmentioning

confidence: 99%

TGF-β1 Stimulates Mouse Macrophages to Express APRIL through Smad and p38MAPK/CREB Pathways

Jang¹,

Kim²,

Seo³

et al. 2011

Molecules and Cells

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“…After activation of the cAMP signalling pathway through stimulation of adenylate cyclase, the former effect of lithium predominates, as lithium inhibits CRE/CREB-directed transcription induced by the adenylate cyclase activator forskolin (Boer et al, 2007b). This lithium action could explain the decrease in CREB phosphorylation and CREB activity observed in the present study in vivo, because PKA is well known to phosphorylate CREB at Ser-133 (Johannessen et al, 2004) and because, under the experimental conditions used, there was a slight lithium-induced decrease in brain cAMP concentrations, which approaches significance. Moreover, lithium may also inhibit PKA (Jensen and Mork, 1997;Mori et al, 1996).…”

Section: Discussionmentioning

confidence: 52%

“…There are three well-known targets of lithium in signalling pathways: inositol monophosphatase, adenylate cyclase, and GSK3, which all could be involved in the regulation of CREB activity (Johannessen et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

Chronic Lithium Salt Treatment Reduces CRE/CREB-Directed Gene Transcription and Reverses Its Upregulation by Chronic Psychosocial Stress in Transgenic Reporter Gene Mice

Böer

Cierny

Krause

et al. 2007

Neuropsychopharmacol

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The molecular mechanism of action of the mood stabilizer lithium is assumed to involve changes in gene expression leading to neuronal adaptation. The transcription factor CREB (cAMP-responsive element binding protein) regulates the expression of many genes and has been implicated in important brain functions and the action of psychogenic agents. We here investigated the effect of lithium on cAMPresponsive element (CRE)/CREB-mediated gene transcription in the brain, using transgenic reporter mice that express the luciferase reporter gene under the control of four copies of the rat somatostatin gene promoter CRE. Chronic (21 days) but not acute (24 h) treatment with lithium (7.5 mmol/kg) significantly decreased CRE/CREB-directed gene expression in hippocampus, cortex, hypothalamus, and striatum to 60-70%, and likewise reduced CREB phosphorylation. As bipolar disorder is also considered as a stress-related disorder, the effect of lithium was determined in mice submitted to a paradigm for chronic psychosocial stress. As shown before, stress for 25 days significantly increased CRE/CREB-directed gene expression in several brain regions by 100-150%. Treatment of stressed mice with lithium decreased stress-induced CRE/CREB-directed gene expression to control levels in nearly all brain regions and likewise reduced CREB phosphorylation. Chronic lithium treatment induced b-catenin accumulation and decreased cAMP levels, indicating an inhibitory effect of lithium on glycogen synthase kinase 3 and the adenylate cyclase/protein kinase A signalling cascade, which are known to modulate CREB activity. We here for the first time show that lithium regulates CRE/CREB-directed gene transcription in vivo and suggest CREB as a putative mediator of the neuronal adaptation after chronic lithium treatment.

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“…A number of studies in a wide range of animal species have shown that CREB plays a key role in the formation of long-term memory (LTM) (for review see [88]). CREB is a constitutively nuclear protein whose activity is regulated by phosphorylation of both subunits of the homodimer [38]. Phosphorylation promotes the interaction of CREB with the transcriptional co-activator CREB binding protein (CBP) or its homolog p300, which stimulates the transcriptional activity of CREB.…”

Section: Fisetin Can Enhance Cognitive Functionmentioning

confidence: 99%

Modulation of multiple pathways involved in the maintenance of neuronal function during aging by fisetin

Maher

2009

Genes Nutr

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Multiple factors have been implicated in the age-related declines in brain function. Thus, it is unlikely that modulating only a single factor will be effective at slowing this decline. A better approach is to identify small molecules that have multiple biological activities relevant to the maintenance of brain function. Over the last few years, we have identified an orally active, novel neuroprotective and cognition-enhancing molecule, the flavonoid fisetin. Fisetin not only has direct antioxidant activity but it can also increase the intracellular levels of glutathione, the major intracellular antioxidant. Fisetin can also maintain mitochondrial function in the presence of oxidative stress. In addition, it has anti-inflammatory activity against microglial cells and inhibits the activity of 5-lipoxygenase, thereby reducing the production of lipid peroxides and their pro-inflammatory by-products. This wide range of actions suggests that fisetin has the ability to reduce the age-related decline in brain function.

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What turns CREB on?

Cited by 570 publications

References 258 publications

TGF-β1 Stimulates Mouse Macrophages to Express APRIL through Smad and p38MAPK/CREB Pathways

TGF-β1 Stimulates Mouse Macrophages to Express APRIL through Smad and p38MAPK/CREB Pathways

Chronic Lithium Salt Treatment Reduces CRE/CREB-Directed Gene Transcription and Reverses Its Upregulation by Chronic Psychosocial Stress in Transgenic Reporter Gene Mice

Modulation of multiple pathways involved in the maintenance of neuronal function during aging by fisetin

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