Phosphorylation by p44 MAP Kinase/ERK1 Stimulates CBP Histone Acetyl Transferase Activity in Vitro

Ait‐Si‐Ali, Slimane; Carlisi, Didier; Ramírez, Sandra; Upegui-Gonzalez, Lia-Cristina; Duquet, Arnaud; Robin, Philippe; Rudkin, Brian B.; Harel‐Bellan, Annick; Trouche, Didier

doi:10.1006/bbrc.1999.1132

Cited by 114 publications

(29 citation statements)

References 28 publications

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“…Furthermore, Erk has well established roles in the late-phase LTP, a more persistent, transcription- and translation-dependent form of synaptic plasticity (Impey et al, 1998; Kelleher et al, 2004). Reminiscent of late LTP, TSA treatment in the aged slices enabled induction of a LTP component sensitive to the transcription inhibitor Act-D. Erk is known to phosphorylate CBP and enhance its HAT activity (Ait-Si-Ali et al, 1999). Activation of Erk during learning tasks increases H3 acetylation in the hippocampus (Levenson et al, 2004) and insular cortex (Swank and Sweatt, 2001).…”

Section: Discussionmentioning

confidence: 99%

Epigenetic Enhancement of BDNF Signaling Rescues Synaptic Plasticity in Aging

et al. 2011

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Aging-related cognitive declines are well documented in humans and animal models. Yet the synaptic and molecular mechanisms responsible for cognitive aging are not well understood. Here we demonstrated age-dependent deficits in long-term synaptic plasticity and loss of dendritic spines in the hippocampus of aged Fisher 344 rats, which were closely associated with reduced histone acetylation, upregulation of histone deacetylase 2 (HDAC2), and decreased expression of a histone acetyltransferase. Further analysis showed that one of the key genes affected by such changes was the brain-derived neurotrophic factor (Bdnf) gene. Age-dependent reductions in H3 and H4 acetylation were detected within multiple promoter regions of the Bdnf gene, leading to a significant decrease in BDNF expression and impairment of downstream signaling in the aged hippocampus. These synaptic and signaling deficits could be rescued by enhancing BDNF and trkB expression via HDAC inhibition or by directly activating trkB receptors with 7, 8-dihydroxyflavone, a newly identified, selective agonist for trkB. Taken together, our findings suggest that age-dependent declines in chromatin histone acetylation and the resulting changes in BDNF expression and signaling are key mechanisms underlying the deterioration of synaptic function and structure in the aging brain. Furthermore, epigenetic or pharmacological enhancement of BDNF-trkB signaling could be a promising strategy for reversing cognitive aging.

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Section: Discussionmentioning

confidence: 99%

Epigenetic Enhancement of BDNF Signaling Rescues Synaptic Plasticity in Aging

et al. 2011

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“…The histone acetyltransferase activity of CBP/p300 can be regulated upstream by Erk1/2 and its downstream regulator, Elk-1 [38,58]. Erk1/2-dependent phosphorylation of Elk-1 results in interaction with p300 and increased histone acetyltransferase activity [38].…”

Section: Discussionmentioning

confidence: 99%

Zyflamend, a polyherbal mixture, down regulates class I and class II histone deacetylases and increases p21 levels in castrate-resistant prostate cancer cells

Huang

Zhao

Chen

et al. 2014

BMC Complement Altern Med

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BackgroundZyflamend, a mixture containing extracts of ten herbs, has shown promise in a variety of preclinical cancer models, including prostate cancer. The current experiments were designed to investigate the effects of Zyflamend on the expression of class I and II histone deacetylases, a family of enzymes known to be over expressed in a variety of cancers.MethodsCWR22Rv1 cells, a castrate-resistant prostate cancer cell line, were treated with Zyflamend and the expression of class I and II histone deacetylases, along with their downstream target the tumor suppressor gene p21, was investigated. Involvement of p21 was confirmed with siRNA knockdown and over expression experiments.ResultsZyflamend down-regulated the expression of all class I and II histone deacetylases where Chinese goldthread and baikal skullcap (two of its components) appear to be primarily responsible for these results. In addition, Zyflamend up regulated the histone acetyl transferase complex CBP/p300, potentially contributing to the increase in histone 3 acetylation. Expression of the tumor suppressor gene p21, a known downstream target of histone deacetylases and CBP/p300, was increased by Zyflamend treatment and the effect on p21 was, in part, mediated through Erk1/2. Knockdown of p21 with siRNA technology attenuated Zyflamend-induced growth inhibition. Over expression of p21 inhibited cell growth and concomitant treatment with Zyflamend enhanced this effect.ConclusionsOur results suggest that the extracts of this polyherbal combination increase histone 3 acetylation, inhibit the expression of class I and class II histone deacetylases, increase the activation of CBP/p300 and inhibit cell proliferation, in part, by up regulating p21 expression.

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“…Another protein upstream of CREB is mitogen-activated protein kinase (MAPK) [61, 62], which is differentially activated after spaced and massed training in a number of systems [63, 64]. In cultured hippocampal neurons, four spaced 3 min depolarizations with 10 min rest periods evoke persistent activation of MAPK, whereas massing the depolarizations into one 12 min pulse failed to persistently activate MAPK [64].…”

Section: Proteins Acting Upstream Of Creb To Regulate the Spacing mentioning

confidence: 99%

Molecular Determinants of the Spacing Effect

2012

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Long-term memory formation is sensitive to the pattern of training sessions. Training distributed over time (spaced training) is superior at generating long-term memories than training presented with little or no rest interval (massed training). This spacing effect was observed in a range of organisms from invertebrates to humans. In the present paper, we discuss the evidence supporting cyclic-AMP response element-binding protein 2 (CREB), a transcription factor, as being an important molecule mediating long-term memory formation after spaced training. We also review the main upstream proteins that regulate CREB in different model organisms. Those include the eukaryotic translation initiation factor (eIF2α), protein phosphatase I (PP1), mitogen-activated protein kinase (MAPK), and the protein tyrosine phosphatase corkscrew. Finally, we discuss PKC activation and protein synthesis and degradation as mechanisms by which neurons decode the spacing intervals.

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Phosphorylation by p44 MAP Kinase/ERK1 Stimulates CBP Histone Acetyl Transferase Activity in Vitro

Cited by 114 publications

References 28 publications

Epigenetic Enhancement of BDNF Signaling Rescues Synaptic Plasticity in Aging

Epigenetic Enhancement of BDNF Signaling Rescues Synaptic Plasticity in Aging

Zyflamend, a polyherbal mixture, down regulates class I and class II histone deacetylases and increases p21 levels in castrate-resistant prostate cancer cells

Molecular Determinants of the Spacing Effect

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