Nuclear Calcium Signaling Controls Methyl-CpG-binding Protein 2 (MeCP2) Phosphorylation on Serine 421 following Synaptic Activity

Buchthal, Bettina; Lau, David Tai-Wai; Weiß, Ursula; Weislogel, Jan-Marek; Bading, Hilmar

doi:10.1074/jbc.m112.382507

Cited by 44 publications

(44 citation statements)

References 48 publications

(66 reference statements)

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“…Pharmacological studies using hippocampal neurons also indicate an involvement of CaMKs in regulating the subcellular localization of HDAC5 and, although to a lesser extent, of HDAC4 (33). This suggests that CaMKII and CaM-KIV, which are present in the cell nucleus of hippocampal neuron (19,78), are key signaling intermediates in the nuclear calcium-dependent export of HDAC4 and HDAC5 from the nucleus. Given the presence of CaMKII in the cytosol, CaMKII may also be part of the nuclear calcium-independent HDAC nucleo-cytoplasmic shuttling.…”

Section: Discussionmentioning

confidence: 93%

Nuclear Calcium Signaling Regulates Nuclear Export of a Subset of Class IIa Histone Deacetylases following Synaptic Activity

Schlumm¹,

Mauceri²,

Freitag

et al. 2013

Journal of Biological Chemistry

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Background: Class IIa HDACs shuttle in a signal-regulated manner between the nucleus and cytosol. Results: Nuclear calcium signaling is required for the nuclear export of a subset of class IIa HDAC. Conclusion: Transcriptional regulation by nuclear calcium signaling involves changes in the subcellular localization of specific HDACs. Significance: Through regulating HDAC nucleo-cytoplasmic shuttling nuclear calcium signaling may cause genome-wide alterations in chromatin structure in response to synaptic activity.

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Section: Discussionmentioning

confidence: 93%

Nuclear Calcium Signaling Regulates Nuclear Export of a Subset of Class IIa Histone Deacetylases following Synaptic Activity

Schlumm¹,

Mauceri²,

Freitag

et al. 2013

Journal of Biological Chemistry

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“…In the present study, we thoroughly examined DOR’s effect on total and phosphorylated CREB proteins in all three major regions, i.e., the cortex, striatum and hippocampus, with and without ischemic condition. We used specific and well-documented CREB antibodies (Millpore, 06-519) [53,54]) that recognize both p43 phosphorylated CREB and phosphorylated ATF-1, another CRE-binding protein that has a similar sequence structure as CREB, especially in the phosphorylation domain. The total CREB was dramatically reduced in the ischemic striatum, while DOR inhibition with Naltrindole significantly reduced the expression of total CREB and phosphorylated CREB protein, implying that DOR may play a role in CREB signaling in this particular region.…”

Section: Discussionmentioning

confidence: 99%

δ-Opioid Receptor Activation Rescues the Functional TrkB Receptor and Protects the Brain from Ischemia-Reperfusion Injury in the Rat

et al. 2013

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Objectivesδ-opioid receptor (DOR) activation reduced brain ischemic infarction and attenuated neurological deficits, while DOR inhibition aggravated the ischemic damage. The underlying mechanisms are, however, not well understood yet. In this work, we asked if DOR activation protects the brain against ischemic injury through a brain-derived neurotrophic factor (BDNF) -TrkB pathway.MethodsWe exposed adult male Sprague-Dawley rats to focal cerebral ischemia, which was induced by middle cerebral artery occlusion (MCAO). DOR agonist TAN-67 (60 nmol), antagonist Naltrindole (100 nmol) or artificial cerebral spinal fluid was injected into the lateral cerebroventricle 30 min before MCAO. Besides the detection of ischemic injury, the expression of BDNF, full-length and truncated TrkB, total CREB, p-CREB, p-ATF and CD11b was detected by Western blot and fluorescence immunostaining.ResultsDOR activation with TAN-67 significantly reduced the ischemic volume and largely reversed the decrease in full-length TrkB protein expression in the ischemic cortex and striatum without any appreciable change in cerebral blood flow, while the DOR antagonist Naltrindole aggregated the ischemic injury. However, the level of BDNF remained unchanged in the cortex, striatum and hippocampus at 24 hours after MCAO and did not change in response to DOR activation or inhibition. MCAO decreased both total CREB and pCREB in the striatum, but not in the cortex, while DOR inhibition promoted a further decrease in total and phosphorylated CREB in the striatum and decreased pATF-1 expression in the cortex. In addition, MCAO increased C11b expression in the cortex, striatum and hippocampus, and DOR activation specifically attenuated the ischemic increase in the cortex but not in the striatum and hippocampus.ConclusionsDOR activation rescues TrkB signaling by reversing ischemia/reperfusion induced decrease in the full-length TrkB receptor and reduces brain injury in ischemia/reperfusion

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“…Important mediators of nuclear calcium-regulated genomic responses include the nuclear calcium/calmodulin-dependent enzymes calcium/calmodulin-dependent kinase II (CaMKII) and calcium/calmodulin-dependent kinase IV (CaMKIV), which control the activity of several transcriptional regulators, including CREB, CREB-binding protein, and MeCP2 (7,40,41). Our experiments uncovered that the levels of calcium buffering in the nucleus, which have a direct influence on the amplitude and kinetics of neuronal activity-induced nuclear calcium rises, can also influence the kinetics of CREB activation following synaptic activity so that high levels of nuclear calcium buffering eliminate the fast component (Fig.…”

Section: Discussionmentioning

confidence: 99%

Nuclear Calcium Buffering Capacity Shapes Neuronal Architecture

Mauceri

Hagenston

Schramm

et al. 2015

Journal of Biological Chemistry

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Background: Calcium-binding proteins regulate calcium dynamics and downstream signaling events. Results: Increasing the calcium buffering capacity of the nucleus alters the expression of genes that regulate neuronal architecture. Conclusion: The nuclear calcium buffering capacity is an important determinant of neuronal morphology. Significance: Nuclear calcium buffers represent a new target for modulating gene expression and neuronal structure.

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Nuclear Calcium Signaling Controls Methyl-CpG-binding Protein 2 (MeCP2) Phosphorylation on Serine 421 following Synaptic Activity

Cited by 44 publications

References 48 publications

Nuclear Calcium Signaling Regulates Nuclear Export of a Subset of Class IIa Histone Deacetylases following Synaptic Activity

Nuclear Calcium Signaling Regulates Nuclear Export of a Subset of Class IIa Histone Deacetylases following Synaptic Activity

δ-Opioid Receptor Activation Rescues the Functional TrkB Receptor and Protects the Brain from Ischemia-Reperfusion Injury in the Rat

Nuclear Calcium Buffering Capacity Shapes Neuronal Architecture

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