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albuquerque2009 v1.0.0

This file encodes the article Mammalian Nicotinic Acetylcholine Receptors: From Structure to Function by Albuquerque et al, 2009

Tau Modifications v1.9.5

Tau Modifications Sections of NESTOR

In-Edges 6

a(CHEBI:"calcium(2+)", loc(GO:intracellular)) increases act(p(FPLX:CREB), ma(tscript)) View Subject | View Object

For example, during a low degree of activation of alpha7 and alpha3beta4 nAChRs, Ca2+ can enter the cells through nAChRs or NMDA receptors and favor activation (i.e., phosphorylation) of the transcription factor CREB, which in turn modifies gene expression (82). PubMed:19126755

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act(a(CHEBI:nicotine)) increases act(p(FPLX:CREB)) View Subject | View Object

Downstream from the nicotine-stimulated kinases, a number of transcription factors have been shown to be activated. Among these factors are the cAMP response element binding protein (CREB) and the activating transcription factor 2 (ATF-2) in PC12 cells (211, 337, 460), the Ets-like transcription factor Elk-1 in the rat hippocampus (349), and the signal transducer and activator of transcription (STAT3) in macrophages and skin cells (114, 354). PubMed:19126755

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PC12 Cells
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bp(MESH:"Neuronal Plasticity") association act(p(FPLX:CREB)) View Subject | View Object

Recent studies have supported a role for ERK and CREB activity in neural plasticity associated with nicotine addiction (71, 381, 484). It has also been proposed that the ERK and JAK-2/STAT-3 signaling pathways contribute to the toxic effects of nicotine in skin cells (42), and other pathways contribute to the effects of nicotine and other nicotinic ligands on inflammatory responses as described below. PubMed:19126755

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act(complex(GO:"voltage-gated calcium channel complex")) decreases act(p(FPLX:CREB), ma(tscript)) View Subject | View Object

If there is intense stimulation of all three nAChRs, the resulting depolarization can trigger activation of voltage- gated Ca2+ channels (VGCC), which in turn would activate the calcineurin pathway and prevent CREB activation. PubMed:19126755

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path(MESH:"Tobacco Use Disorder") association act(p(FPLX:CREB)) View Subject | View Object

Recent studies have supported a role for ERK and CREB activity in neural plasticity associated with nicotine addiction (71, 381, 484). It has also been proposed that the ERK and JAK-2/STAT-3 signaling pathways contribute to the toxic effects of nicotine in skin cells (42), and other pathways contribute to the effects of nicotine and other nicotinic ligands on inflammatory responses as described below. PubMed:19126755

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act(p(HGNC:PDE5A)) negativeCorrelation act(p(FPLX:CREB)) View Subject | View Object

Here we report the discovery of a new first-in-class small-molecule (CM-414) that acts as a dual inhibitor of PDE5 and HDACs. We have used this compound as a chemical probe to validate this systems therapeutics strategy, where an increase in the activation of cAMP/cGMP-responsive element-binding protein (CREB) induced by PDE5 inhibition, combined with moderate HDAC class I inhibition, leads to efficient histone acetylation. This molecule rescued the impaired long-term potentiation evident in hippocampal slices from APP/PS1 mice. Chronic treatment of Tg2576 mice with CM-414 diminished brain Aβ and tau phosphorylation (pTau) levels, increased the inactive form of GSK3β, reverted the decrease in dendritic spine density on hippocampal neurons, and reversed their cognitive deficits, at least in part by inducing the expression of genes related to synaptic transmission. PubMed:27550730

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Out-Edges 5

act(p(FPLX:CREB), ma(tscript)) regulates bp(GO:"gene expression") View Subject | View Object

For example, during a low degree of activation of alpha7 and alpha3beta4 nAChRs, Ca2+ can enter the cells through nAChRs or NMDA receptors and favor activation (i.e., phosphorylation) of the transcription factor CREB, which in turn modifies gene expression (82). PubMed:19126755

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Text Location
Review

act(p(FPLX:CREB)) association bp(MESH:"Neuronal Plasticity") View Subject | View Object

Recent studies have supported a role for ERK and CREB activity in neural plasticity associated with nicotine addiction (71, 381, 484). It has also been proposed that the ERK and JAK-2/STAT-3 signaling pathways contribute to the toxic effects of nicotine in skin cells (42), and other pathways contribute to the effects of nicotine and other nicotinic ligands on inflammatory responses as described below. PubMed:19126755

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Text Location
Review

act(p(FPLX:CREB)) association path(MESH:"Tobacco Use Disorder") View Subject | View Object

Recent studies have supported a role for ERK and CREB activity in neural plasticity associated with nicotine addiction (71, 381, 484). It has also been proposed that the ERK and JAK-2/STAT-3 signaling pathways contribute to the toxic effects of nicotine in skin cells (42), and other pathways contribute to the effects of nicotine and other nicotinic ligands on inflammatory responses as described below. PubMed:19126755

Appears in Networks:
Annotations
Text Location
Review

act(p(FPLX:CREB)) negativeCorrelation act(p(HGNC:PDE5A)) View Subject | View Object

Here we report the discovery of a new first-in-class small-molecule (CM-414) that acts as a dual inhibitor of PDE5 and HDACs. We have used this compound as a chemical probe to validate this systems therapeutics strategy, where an increase in the activation of cAMP/cGMP-responsive element-binding protein (CREB) induced by PDE5 inhibition, combined with moderate HDAC class I inhibition, leads to efficient histone acetylation. This molecule rescued the impaired long-term potentiation evident in hippocampal slices from APP/PS1 mice. Chronic treatment of Tg2576 mice with CM-414 diminished brain Aβ and tau phosphorylation (pTau) levels, increased the inactive form of GSK3β, reverted the decrease in dendritic spine density on hippocampal neurons, and reversed their cognitive deficits, at least in part by inducing the expression of genes related to synaptic transmission. PubMed:27550730

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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.