Genome-Wide Analysis of CREB Target Genes Reveals A Core Promoter Requirement for cAMP Responsiveness

Conkright, Michael D.; Guzmán, Ernesto; Flechner, Lawrence; Su, Andrew I.; Hogenesch, John B.; Montminy, Marc

doi:10.1016/s1097-2765(03)00199-0

Cited by 68 publications

(92 citation statements)

References 2 publications

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“…cFos was significantly increased in the DH after fear conditioning (one-way ANOVA, F (2,26) = 23.3, po0.001), with significantly higher expression at 30 min (Sidak post hoc, po0.001) and 60 min (po0.001) relative to homecage controls ( Figure 1b). We also measured Nr4a2, which is both CREB-dependent (Conkright et al, 2003;McNulty et al, 2012;Vecsey et al, 2007) and regulated by HDAC3 . Nr4a2 was significantly increased after acquisition (F (2,26) = 7.8, po0.01), with significantly higher expression 30 min after conditioning (po0.01) and 60 min after learning (Figure 1c; po0.01).…”

Section: Fear Conditioning Drives Hdac3-mediated Gene Expression In Tmentioning

confidence: 99%

Context and Auditory Fear are Differentially Regulated by HDAC3 Activity in the Lateral and Basal Subnuclei of the Amygdala

Kwapis

Alaghband

López

et al. 2016

Neuropsychopharmacol

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Histone acetylation is a fundamental epigenetic mechanism that is dynamically regulated during memory formation. Histone acetyltransferases (HATs) and histone deacetylases (HDACs) compete to modulate histone acetylation, allowing for rapid changes in acetylation in response to a learning event. HDACs are known to be powerful negative regulators of memory formation, but it is not clear whether this function depends on HDAC enzymatic activity per se. Here, we tested whether the enzymatic activity of an individual Class I HDAC, HDAC3, has a role in fear memory formation in subregions of the hippocampus and amygdala. We found that fear conditioning drove expression of the immediate early genes cFos and Nr4a2 in the hippocampus, which coincided with reduced HDAC3 occupancy at these promoters. Using a dominant-negative, deacetylase-dead point mutant virus (AAV-HDAC3(Y298H)-v5), we found that selectively blocking HDAC3 deacetylase activity in either the dorsal hippocampus or basal nucleus of the amygdala enhanced context fear without affecting tone fear. Blocking HDAC3 activity in the lateral nucleus of the amygdala, on the other hand, enhanced tone, but not context fear memory. These results show for the first time that the enzymatic activity of HDAC3 functions to negatively regulate fear memory formation. Further, HDAC3 activity regulates different aspects of fear memory in the basal and lateral subregions of the amygdala. Thus, the deacetylase activity of HDAC3 is a powerful negative regulator of fear memory formation in multiple subregions of the fear circuit.

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Section: Fear Conditioning Drives Hdac3-mediated Gene Expression In Tmentioning

confidence: 99%

Context and Auditory Fear are Differentially Regulated by HDAC3 Activity in the Lateral and Basal Subnuclei of the Amygdala

Kwapis

Alaghband

López

et al. 2016

Neuropsychopharmacol

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“…10A), which is the functional half-site of the CREBtargeting palindrome (5Ј-TGACGTCA-3Ј) (47), suggesting that MBZ1 is also the CREB site or half-site activator. Heterologous expression of MBZ1 in Escherichia coli failed to obtain soluble protein for the electrophoretic mobility shift assay.…”

Section: Journal Of Biological Chemistrymentioning

confidence: 99%

Basic Leucine Zipper (bZIP) Domain Transcription Factor MBZ1 Regulates Cell Wall Integrity, Spore Adherence, and Virulence in Metarhizium robertsii

Huang

Shang

Chen

et al. 2015

Journal of Biological Chemistry

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Background:The bZIP-type transcription factors are widely distributed in eukaryotes to control an array of biological activities. Results: MBZ1 from Metarhizium robertsii regulates fungal growth, cell wall integrity, spore adherence, and virulence against insects. Conclusion: MBZ1 is required for development and virulence of insect pathogenic fungi. Significance: The orthologs of bZIP-type transcription factors are functionally divergent in different organisms.

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“…CREB activation downstream of ERK appears critical in the induction of long-lasting changes in synaptic plasticity and memory (148)(149)(150) and disruption of CREB activity specifically blocks the formation of long-term memory (151) , whereas agents that increase the amount or activity of CREB accelerate the process (152) . CREB is known to be a critical transcription factor linking the actions of neurotrophins such as BDNF to neuronal survival, differentiation and synaptic function (153)(154)(155) . Consequently, the central role of CREB in these processes has led to considerable interest in identifying safe effective agents that may enhance the activity of CREB in specific regions of the brain, as these agents may lead to an improvement in memory (152) .…”

Section: Modulation Of Synaptic Plasticity and Neuro-cognitive Performentioning

confidence: 99%

Beyond antioxidants: the cellular and molecular interactions of flavonoids and how these underpin their actions on the brain

Spencer

2010

Proc. Nutr. Soc.

142

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The consumption of flavonoid-rich foods and beverages has been suggested to limit the neurodegeneration associated with a variety of neurological disorders and to prevent or reverse normal or abnormal deteriorations in cognitive performance. Flavonoids mediate these effects via a number of routes, including a potential to protect neurons against injury induced by neurotoxins, an ability to suppress neuroinflammation and a potential to promote memory, learning and cognitive function. Originally, it was thought that such actions were mediated by the antioxidant capacity of flavonoids. However, their limited absorption and their low bioavailability in the brain suggest that this explanation is unlikely. Instead, this multiplicity of effects appears to be underpinned by three separate processes: first, through their interactions with important neuronal and glial signalling cascades in the brain, most notably the phosphatidylinositol 3-kinase/Akt and mitogen-activated protein kinase pathways that regulate prosurvival transcription factors and gene expression; second, through an ability to improve peripheral and cerebral blood flow and to trigger angiogenesis and neurogenesis in the hippocampus; third, by their capacity to directly react with and scavenge neurotoxic species and pro-inflammatory agents produced in the brain as a result of both normal and abnormal brain ageing. The present review explores the potential inhibitory or stimulatory actions of flavonoids within these three systems and describes how such interactions are likely to underlie neurological effects.

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Genome-Wide Analysis of CREB Target Genes Reveals A Core Promoter Requirement for cAMP Responsiveness

Abstract: stimulate cooperative interactions with TFIID that facilitate recruitment of RNA polymerase II complexes (Horikoshi et al., 1988). In this regard, CREB has been found to interact with the hTAF II 130 component of TFIID via a glutamine-rich Q2 trans-activation domain; and this

Cited by 68 publications

References 2 publications

Context and Auditory Fear are Differentially Regulated by HDAC3 Activity in the Lateral and Basal Subnuclei of the Amygdala

Context and Auditory Fear are Differentially Regulated by HDAC3 Activity in the Lateral and Basal Subnuclei of the Amygdala

Basic Leucine Zipper (bZIP) Domain Transcription Factor MBZ1 Regulates Cell Wall Integrity, Spore Adherence, and Virulence in Metarhizium robertsii

Beyond antioxidants: the cellular and molecular interactions of flavonoids and how these underpin their actions on the brain

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