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Journal articles on the topic 'Zif268'

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Published: 4 June 2021
Last updated: 25 April 2022

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1

Penke, Zsuzsa, Elise Morice, Alexandra Veyrac, Alexandra Gros, Carine Chagneau, Pascale LeBlanc, Nathalie Samson, et al. "Zif268 / Egr1 gain of function facilitates hippocampal synaptic plasticity and long-term spatial recognition memory." Philosophical Transactions of the Royal Society B: Biological Sciences 369, no. 1633 (January 5, 2014): 20130159. http://dx.doi.org/10.1098/rstb.2013.0159.

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It is well established that Zif268/Egr1 , a member of the Egr family of transcription factors, is critical for the consolidation of several forms of memory; however, it is as yet uncertain whether increasing expression of Zif268 in neurons can facilitate memory formation. Here, we used an inducible transgenic mouse model to specifically induce Zif268 overexpression in forebrain neurons and examined the effect on recognition memory and hippocampal synaptic transmission and plasticity. We found that Zif268 overexpression during the establishment of memory for objects did not change the ability to form a long-term memory of objects, but enhanced the capacity to form a long-term memory of the spatial location of objects. This enhancement was paralleled by increased long-term potentiation in the dentate gyrus of the hippocampus and by increased activity-dependent expression of Zif268 and selected Zif268 target genes. These results provide novel evidence that transcriptional mechanisms engaging Zif268 contribute to determining the strength of newly encoded memories.
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2

Christy, B., and D. Nathans. "Functional serum response elements upstream of the growth factor-inducible gene zif268." Molecular and Cellular Biology 9, no. 11 (November 1989): 4889–95. http://dx.doi.org/10.1128/mcb.9.11.4889.

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The zif268 gene, which encodes a protein with three typical zinc finger sequences, is induced in mouse 3T3 cells by serum, phorbol 12-myristate 13-acetate platelet-derived growth factor, and fibroblast growth factor. The induction is coordinate with that of c-fos. The 5'-flanking region of zif268 contains sequences that resemble known regulatory elements, including four CC(A or T)6GG sequences similar to the core serum response elements (SREs) found upstream of c-fos and actin genes. To determine whether the zif268 SRE-like elements mediate induction, CAT (chloramphenicol acetyltransferase) plasmids with different lengths of zif268 upstream sequences were tested for inducibility in 3T3 cells by serum, platelet-derived growth factor, or phorbol 12-myristate 13-acetate. In addition, double-stranded oligonucleotides corresponding to each of the four zif268 putative SREs were tested individually for responsiveness when placed upstream of a thymidine kinase gene promoter. Each of the four SREs conferred inducibility by the agents tested, and multiple SREs resulted in greater inducibility than did a single element. Each of the zif268 SREs also competed with the c-fos SRE for binding by serum response factor present in HeLa cell nuclear extract. We conclude that the zif268 SRE-like sequences are functional and probably account for the coordinate induction of zif268 and c-fos.
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3

Christy, B., and D. Nathans. "Functional serum response elements upstream of the growth factor-inducible gene zif268." Molecular and Cellular Biology 9, no. 11 (November 1989): 4889–95. http://dx.doi.org/10.1128/mcb.9.11.4889-4895.1989.

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The zif268 gene, which encodes a protein with three typical zinc finger sequences, is induced in mouse 3T3 cells by serum, phorbol 12-myristate 13-acetate platelet-derived growth factor, and fibroblast growth factor. The induction is coordinate with that of c-fos. The 5'-flanking region of zif268 contains sequences that resemble known regulatory elements, including four CC(A or T)6GG sequences similar to the core serum response elements (SREs) found upstream of c-fos and actin genes. To determine whether the zif268 SRE-like elements mediate induction, CAT (chloramphenicol acetyltransferase) plasmids with different lengths of zif268 upstream sequences were tested for inducibility in 3T3 cells by serum, platelet-derived growth factor, or phorbol 12-myristate 13-acetate. In addition, double-stranded oligonucleotides corresponding to each of the four zif268 putative SREs were tested individually for responsiveness when placed upstream of a thymidine kinase gene promoter. Each of the four SREs conferred inducibility by the agents tested, and multiple SREs resulted in greater inducibility than did a single element. Each of the zif268 SREs also competed with the c-fos SRE for binding by serum response factor present in HeLa cell nuclear extract. We conclude that the zif268 SRE-like sequences are functional and probably account for the coordinate induction of zif268 and c-fos.
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4

McDade, Donna M., Ann-Marie Conway, Allan B. James, and Brian J. Morris. "Activity-dependent gene transcription as a long-term influence on receptor signalling." Biochemical Society Transactions 37, no. 6 (November 19, 2009): 1375–77. http://dx.doi.org/10.1042/bst0371375.

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The regulation of synaptic glutamate receptor and GABAAR (γ-aminobutyric acid subtype A receptor) levels is a key component of synaptic plasticity. Most forms of neuronal plasticity are associated with the induction of the transcription factor zif268 (egr1). Hence, it is predicted that zif268 may regulate transcription of genes associated with glutamate receptors and/or GABAARs. It turns out that receptor regulation by zif268 tends to be indirect. Induction of zif268 in neurons leads to altered expression of proteasome subunit and proteasome-regulatory genes, thereby changing the capacity of the neuron to degrade synaptic proteins, including receptors and receptor subunits. In addition, zif268 alters the transcription of genes associated with GABAAR expression and trafficking, such as ubiquilin and gephyrin. This indirect regulation of receptor turnover is likely to contribute to the delayed, but long-lasting, phases of synaptic plasticity and also to the synaptic dysfunction associated with diseases such as schizophrenia and Alzheimer's disease, where zif268 expression is reduced.
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5

Chaudhuri, Avi, Joanne A. Matsubara, and Max S. Cynader. "Neuronal activity in primate visual cortex assessed by immunostaining for the transcription factor Zif268." Visual Neuroscience 12, no. 1 (January 1995): 35–50. http://dx.doi.org/10.1017/s095252380000729x.

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AbstractIt is now well established that environmental signals mediated via neurotransmitters and hormones can induce responses in cells which involve a cascade of receptors, G proteins, and second messengers. These in turn can induce transcription factors which regulate long-term changes in gene expression. It has been proposed that the stimulus-transcription coupling properties of these DNA-binding proteins can be exploited to visualize activated neurons by way of immunostaining. We have used standard immunohistochemical techniques to detect the expression of one specific transcription factor, Zif268, in the visual cortex (area 17, V1) of vervet monkeys (Cercopithecus aethiops). Immunopositive neurons were present in large numbers throughout the visual cortex of the normal animal, being concentrated in layers 2/3 and 6 and at moderate levels in 4Cβ and 5. To determine if Zif268 expression was affected by visual stimulation in the monkey, we restricted light input to one eye with the aim of revealing ocular-dominance columns in striate cortex. We found that short-term monocular deprivation induced either by enucleation, intravitreal TTX injection, or eyelid suturing resulted in dramatic changes in Zif268 levels, revealing vertically oriented columns of reduced Zif268 staining interdigitated with columns of normal expression. Furthermore, these columns were discernible after just 2 h of monocular blockade. A comparison of the ocular-dominance pattern obtained with Zif268 immunostaining and cytochrome oxidase histochemistry in long-term monocularly deprived animals showed a coincident reduction of both markers along columns that were precisely aligned in adjacent sections, indicating that Zif268 expression is restricted to cortical regions of high metabolic activity. Simultaneous immunostaining for Zif268 and the calcium-binding proteins calbindin and parvalbumin showed a negative correlation, suggesting that the Zif268 protein may be expressed selectively within excitatory neurons. A similar approach with immunostaining for neurofilament and microtubule-associated proteins (SMI-32 and MAP2) revealed pyramidal neurons which were regularly found to contain a Zif268-positive nucleus. Furthermore, confocal images of lucifer yellow filled neurons possessing Zif268-positive nuclei all showed pyramidal morphology. Taken together, these results point to activity-dependent expression of Zif268 within a subset of excitatory neurons.
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6

Suva, L. J., M. Ernst, and G. A. Rodan. "Retinoic acid increases zif268 early gene expression in rat preosteoblastic cells." Molecular and Cellular Biology 11, no. 5 (May 1991): 2503–10. http://dx.doi.org/10.1128/mcb.11.5.2503.

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In this study we demonstrate that retinoic acid (RA) increases the expression of transcription factor zif268 mRNA in primary cultures of fetal rat calvarial cells and in simian virus 40-immortalized clonal rat calvarial preosteoblastic cells (RCT-1), which differentiate in response to RA, but not in the more differentiated RCT-3 and ROS 17/2.8 cells. The increased expression of zif268 mRNA is rapid (maximal within 1 h), transient (returns to basal levels by 3 h), detectable at RA doses of 10(-12)M, and independent of protein synthesis. The relative stimulation of zif268 mRNA by RA was much larger than that of other early genes, including c-fos, c-jun, and junB. The rate of transcription of RA-stimulated RCT-1 cells, estimated by nuclear run-on assays, was elevated, suggesting that RA regulation of zif268 gene transcription was at least in part transcriptional. Moreover, RA stimulated the transcriptional activity of a Zif268CAT (chloramphenicol acetyltransferase) plasmid containing 632 bp of zif268 5' regulatory sequences in RCT-1 cells but not in the more differentiated RCT-3 cells. These in vitro data support the in vivo observations which localize zif268 and RA receptor-gamma transcripts to bone and cartilage during development, suggesting that both RA and zif268 may play a role in osteoblast differentiation.
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7

Suva, L. J., M. Ernst, and G. A. Rodan. "Retinoic acid increases zif268 early gene expression in rat preosteoblastic cells." Molecular and Cellular Biology 11, no. 5 (May 1991): 2503–10. http://dx.doi.org/10.1128/mcb.11.5.2503-2510.1991.

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In this study we demonstrate that retinoic acid (RA) increases the expression of transcription factor zif268 mRNA in primary cultures of fetal rat calvarial cells and in simian virus 40-immortalized clonal rat calvarial preosteoblastic cells (RCT-1), which differentiate in response to RA, but not in the more differentiated RCT-3 and ROS 17/2.8 cells. The increased expression of zif268 mRNA is rapid (maximal within 1 h), transient (returns to basal levels by 3 h), detectable at RA doses of 10(-12)M, and independent of protein synthesis. The relative stimulation of zif268 mRNA by RA was much larger than that of other early genes, including c-fos, c-jun, and junB. The rate of transcription of RA-stimulated RCT-1 cells, estimated by nuclear run-on assays, was elevated, suggesting that RA regulation of zif268 gene transcription was at least in part transcriptional. Moreover, RA stimulated the transcriptional activity of a Zif268CAT (chloramphenicol acetyltransferase) plasmid containing 632 bp of zif268 5' regulatory sequences in RCT-1 cells but not in the more differentiated RCT-3 cells. These in vitro data support the in vivo observations which localize zif268 and RA receptor-gamma transcripts to bone and cartilage during development, suggesting that both RA and zif268 may play a role in osteoblast differentiation.
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8

Lonergan, Mary E., Georgette M. Gafford, Timothy J. Jarome, and Fred J. Helmstetter. "Time-Dependent Expression of Arc and Zif268 after Acquisition of Fear Conditioning." Neural Plasticity 2010 (2010): 1–12. http://dx.doi.org/10.1155/2010/139891.

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Memory consolidation requires transcription and translation of new protein. Arc, an effector immediate early gene, and zif268, a regulatory transcription factor, have been implicated in synaptic plasticity underlying learning and memory. This study explored the temporal expression profiles of these proteins in the rat hippocampus following fear conditioning. We observed a time-dependent increase of Arc protein in the dorsal hippocampus 30-to-90-minute post training, returning to basal levels at 4 h. Zif268 protein levels, however, gradually increased at 30-minute post training before peaking in expression at 60 minute. The timing of hippocampal Arc and zif268 expression coincides with the critical period for protein synthesis-dependent memory consolidation following fear conditioning. However, the expression of Arc protein appears to be driven by context exploration, whereas, zif268 expression may be more specifically related to associative learning. These findings suggest that altered Arc and zif268 expression are related to neural plasticity during the formation of fear memory.
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9

Waye, Shannon C., O. Chandani Dinesh, SM Nageeb Hasan, Joshua D. Conway, Roger Raymond, José N. Nobrega, Jacqueline Blundell, and Francis Rodriguez Bambico. "Antidepressant action of transcranial direct current stimulation in olfactory bulbectomised adolescent rats." Journal of Psychopharmacology 35, no. 8 (April 28, 2021): 1003–16. http://dx.doi.org/10.1177/02698811211000765.

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Background: Antidepressant drugs in adolescent depression are sometimes mired by efficacy issues and paradoxical effects. Transcranial direct current stimulation (tDCS) could represent an alternative. Aims/methods: We tested the antidepressant action of prefrontal tDCS and paroxetine (20 mg/kg, intraperitoneal) in olfactory bulbectomised (OBX) adolescent rats. Using enzyme-linked immunosorbent assays and in situ hybridisation, we examined treatment-induced changes in plasma brain-derived neurotrophic factor (BDNF) and brain serotonin transporter (SERT) and 5-HT-1A mRNA. Results: OBX-induced anhedonia-like reductions in sucrose preference (SP) correlated with open field (OF) hyperactivity. These were accompanied by decreased zif268 mRNA in the piriform/amygdalopiriform transition area, and increased zif268 mRNA in the hypothalamus. Acute paroxetine (2 days) led to a profound SP reduction, an effect blocked by combined tDCS–paroxetine administration. Chronic (14 days) tDCS attenuated hyperlocomotion and its combination with paroxetine blocked OBX-induced SP reduction. Correlations among BDNF, SP and hyperlocomotion scores were altered by OBX but were normalised by tDCS–paroxetine co-treatment. In the brain, paroxetine increased zif268 mRNA in the hippocampal CA1 subregion and decreased it in the claustrum. This effect was blocked by tDCS co-administration, which also increased zif268 in CA2. tDCS-paroxetine co-treatment had variable effects on 5-HT1A receptors and SERT mRNA. 5-HT1A receptor changes were found exclusively within depression-related parahippocampal/hippocampal subregions, and SERT changes within fear/defensive response-modulating brainstem circuits. Conclusion: These findings point towards potential synergistic efficacies of tDCS and paroxetine in the OBX model of adolescent depression via mechanisms associated with altered expression of BDNF, 5-HT1A, SERT and zif268 in discrete corticolimbic areas.
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10

Powell, Anna L., Emma Hindley, Andrew JD Nelson, Moira Davies, Eman Amin, John P. Aggleton, and Seralynne D. Vann. "Lesions of retrosplenial cortex spare immediate-early gene activity in related limbic regions in the rat." Brain and Neuroscience Advances 2 (January 2018): 239821281881123. http://dx.doi.org/10.1177/2398212818811235.

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The retrosplenial cortex forms part of a network of cortical and subcortical structures that have particular importance for spatial learning and navigation in rodents. This study examined how retrosplenial lesions affect activity in this network by visualising the expression of the immediate-early genes c- fos and zif268 after exposure to a novel location. Groups of rats with extensive cytotoxic lesions (areas 29 and 30) and rats with lesions largely confined to area 30 (dysgranular cortex) were compared with their respective control animals for levels of c- fos expression measured by immunohistochemistry. These cortical lesions had very limited effects on distal c- fos activity. Evidence of a restricted reduction in c-fos activity was seen in the septal dentate gyrus (superior blade) but not in other hippocampal and parahippocampal subareas, nor in the anterior cingulate and prelimbic cortices. Related studies examined zif268 activity in those cases with combined area 29 and 30 lesions. The only clear evidence for reduced zif268 activity following retrosplenial cell loss came from the septal CA3 area. The confined impact of retrosplenial tissue loss is notable as, by the same immediate-early gene measures, retrosplenial cortex is itself highly sensitive to damage in related limbic areas, showing a marked c- fos and zif268 hypoactivity across all of its subareas. This asymmetry in covert pathology may help to explain the apparent disparity between the severity of learning deficits after retrosplenial cortex lesions and after lesions in either the hippocampus or the anterior thalamic nuclei.
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11

HORTON, JONATHAN C., DAVINA R. HOCKING, and DANIEL L. ADAMS. "Rapid identification of ocular dominance columns in macaques using cytochrome oxidase, Zif268, and dark-field microscopy." Visual Neuroscience 17, no. 4 (July 2000): 495–508. http://dx.doi.org/10.1017/s0952523800174024.

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Strabismus induces an abnormal pattern of alternating light and dark columns of cytochrome oxidase (CO) activity in macaque striate cortex. This pattern may arise because visual perception is suppressed in one eye to avoid diplopia. To test whether CO activity is reduced in the ocular dominance columns of the suppressed eye, we performed monocular enucleation to co-label the ocular dominance columns with Zif268 immunohistochemistry in seven exotropic adult Macaca fascicularis. This approach was unsuccessful, for two reasons. First, Zif268 yielded inconsistent labelling, that was usually greater in the enucleated eye's ocular dominance columns, but was sometimes greater in the intact eye's columns. Therefore, Zif268 was not a reliable method for identifying the ocular dominance columns serving each eye. Second, in three control animals we found that a brief survival period following monocular enucleation (needed for Zif268 levels to change) was long enough to alter CO staining. For example, a survival time of only 3 h was sufficient to induce CO columns, indicating that the activity of this enzyme fluctuates more rapidly than realized previously. Independent of these findings, we have also discovered that acute monocular enucleation produces a vivid pattern of ocular dominance columns visible in unstained or CO-stained sections under dark-field illumination. The ocular dominance columns of the acutely enucleated eye appear dark. This was verified by labelling the ocular dominance columns with [3H]proline. Dark-field illumination of the cortex after acute monocular enucleation offers a new, easy method for identifying the ocular dominance columns in macaques.
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12

Elrod-Erickson, Monicia, and Carl O. Pabo. "Binding Studies with Mutants of Zif268." Journal of Biological Chemistry 274, no. 27 (July 2, 1999): 19281–85. http://dx.doi.org/10.1074/jbc.274.27.19281.

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13

Bhatt, Deepak K., Roshni Ramachandran, Sarah LT Christensen, Saurabh Gupta, Inger Jansen-Olesen, and Jes Olesen. "CGRP infusion in unanesthetized rats increases expression of c-Fos in the nucleus tractus solitarius and caudal ventrolateral medulla, but not in the trigeminal nucleus caudalis." Cephalalgia 35, no. 3 (June 3, 2014): 220–33. http://dx.doi.org/10.1177/0333102414535995.

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Background and aims Calcitonin gene-related peptide (CGRP) and glyceryl trinitrate (GTN) infusion in migraineurs provokes headache resembling spontaneous migraine, and CGRP receptor antagonists are effective in the treatment of acute migraine. We hypothesized that CGRP infusion would increase molecular markers of neuronal activation in migraine-relevant tissues of the rat. Methods CGRP was infused intravenously (i.v.) in freely moving rats to circumvent factors like anesthesia, acute surgery and severe hypotension, the three confounding factors for c-Fos expression. The trigeminal nucleus caudalis (TNC) was isolated at different time points after CGRP infusion. The level of c-Fos mRNA and protein expression in TNC were analyzed by qPCR and immunohistochemistry. c-Fos-stained nuclei were also counted in the nucleus tractus solitarius (NTS) and caudal ventrolateral medulla (CVLM), integrative sites in the brain stem for processing cardiovascular signals. We also investigated Zif268 protein expression (another immediate early gene) in TNC. The protein expression of p-ERK, p-CREB and c-Fos was analyzed in dura mater, trigeminal ganglion (TG) and TNC samples using Western blot. Results CGRP infusion caused a significant dose-dependent fall in mean arterial blood pressure. No significant activation of c-Fos in the TNC at mRNA and protein levels was observed after CGRP infusion. A significant increase in c-Fos protein was observed in the NTS and CVLM in the brain stem. Zif268 expression in the TNC was also not changed after CGRP infusion. p-ERK was increased in the dura mater 30 minutes after CGRP infusion. Conclusion CGRP infusion increased the early expression of p-ERK in the dura mater but did not increase c-Fos and Zif268 expression in the TNC. The rats may, thus, differ from migraine patients, in whom infusion of CGRP caused headache and a delayed migraine attack. The rat CGRP infusion model with c-Fos or Zif268 as neuronal pain markers in TNC is unsuitable for antimigraine drug testing.
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14

GREEN, Andrew, and Bibudhendra SARKAR. "Alteration of zif268 zinc-finger motifs gives rise to non-native zinc-co-ordination sites but preserves wild-type DNA recognition." Biochemical Journal 333, no. 1 (July 1, 1998): 85–90. http://dx.doi.org/10.1042/bj3330085.

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Zinc fingers are among the major structural motifs found in proteins that are involved in eukaryotic gene regulation. Many of these zinc-finger domains are involved in DNA binding. This study investigated whether the zinc-co-ordinating (Cys)2(His)2 motif found in the three zinc fingers of zif268 could be replaced by a (Cys)4 motif while still preserving DNA recognition. (Cys)2(His)2-to-(Cys)4 mutations were generated in each of the three zinc fingers of zif268 individually, as well as in fingers 1 and 3, and fingers 2 and 3 together. Whereas finger 1 and finger 3 tolerate the switch, such an alteration in finger 2 renders the polypeptide incapable of DNA recognition. The protein–DNA interaction was examined in greater detail by using a methylation-interference assay. The mutant polypeptides containing the (Cys)4 motif in fingers 1 or 3 recognize DNA in a manner identical to the wild-type protein, suggesting that the (Cys)4 motif appears to give rise to a properly folded finger. Additional results indicate that a zif268 variant containing a (Cys)2(His)(Ala) arrangement in finger 1 is also capable of DNA recognition in a manner identical to the wild-type polypeptide. This appears to be the first time that such alterations, in the context of an intact DNA-binding domain, have still allowed for specific DNA recognition. Taken together, the work presented here enhances our understanding of the relationship between metal ligation and DNA-binding by zinc fingers.
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15

Ranieri, F., M. V. Podda, E. Riccardi, G. Frisullo, M. Dileone, P. Profice, F. Pilato, V. Di Lazzaro, and C. Grassi. "Modulation of LTP at rat hippocampal CA3-CA1 synapses by direct current stimulation." Journal of Neurophysiology 107, no. 7 (April 1, 2012): 1868–80. http://dx.doi.org/10.1152/jn.00319.2011.

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Transcranial direct current stimulation (tDCS) can produce a lasting polarity-specific modulation of cortical excitability in the brain, and it is increasingly used in experimental and clinical settings. Recent studies suggest that the after-effects of tDCS are related to molecular mechanisms of activity-dependent synaptic plasticity. Here we investigated the effect of DCS on the induction of one of the most studied N-methyl-d-aspartate receptor-dependent forms of long-term potentiation (LTP) of synaptic activity at CA3-CA1 synapses in the hippocampus. We show that DCS applied to rat brain slices determines a modulation of LTP that is increased by anodal and reduced by cathodal DCS. Immediate early genes, such as c-fos and zif268 ( egr1/NGFI-A/krox24), are rapidly induced following neuronal activation, and a specific role of zif268 in the induction and maintenance of LTP has been demonstrated. We found that both anodal and cathodal DCS produce a marked subregion-specific increase in the expression of zif268 protein in the cornus ammonis (CA) region, whereas the same protocols of stimulation produce a less pronounced increase in c-fos protein expression in the CA and in dentate gyrus regions of the hippocampus. Brain-derived neurotrophic factor expression was also investigated, and it was found to be reduced in cathodal-stimulated slices. The present data demonstrate that it is possible to modulate LTP by using DCS and provide the rationale for the use of DCS in neurological diseases to promote the adaptive and suppress the maladaptive forms of brain plasticity.
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Ishida, Yasushi, Hiroyuki Hashiguchi, Yuta Ishizuka, Kazunari Todaka, Itsumi Kuwahara, Yoshio Mitsuyama, and Toshikazu Nishimori. "Basal expression of c-Fos and Zif268 in the rat basal ganglia: immunohistochemical characterization of striatal Zif268-positive neurons." European Journal of Neuroscience 12, no. 2 (February 2000): 771–75. http://dx.doi.org/10.1046/j.1460-9568.2000.00968.x.

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Soulé, Jonathan, Zsuzsa Penke, Tambudzai Kanhema, Maria Nordheim Alme, Serge Laroche, and Clive R. Bramham. "Object-Place Recognition Learning Triggers Rapid Induction of Plasticity-Related Immediate Early Genes and Synaptic Proteins in the Rat Dentate Gyrus." Neural Plasticity 2008 (2008): 1–12. http://dx.doi.org/10.1155/2008/269097.

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Long-term recognition memory requires protein synthesis, but little is known about the coordinate regulation of specific genes. Here, we examined expression of the plasticity-associated immediate early genes (Arc, Zif268, and Narp) in the dentate gyrus following long-term object-place recognition learning in rats. RT-PCR analysis from dentate gyrus tissue collected shortly after training did not reveal learning-specific changes in Arc mRNA expression. In situ hybridization and immunohistochemistry were therefore used to assess possible sparse effects on gene expression. Learning about objects increased the density of granule cells expressing Arc, and to a lesser extent Narp, specifically in the dorsal blade of the dentate gyrus, while Zif268 expression was elevated across both blades. Thus, object-place recognition triggers rapid, blade-specific upregulation of plasticity-associated immediate early genes. Furthermore, Western blot analysis of dentate gyrus homogenates demonstrated concomitant upregulation of three postsynaptic density proteins (Arc, PSD-95, andα-CaMKII) with key roles in long-term synaptic plasticity and long-term memory.
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James, A. B. "Regulation of the Neuronal Proteasome by Zif268 (Egr1)." Journal of Neuroscience 26, no. 5 (February 1, 2006): 1624–34. http://dx.doi.org/10.1523/jneurosci.4199-05.2006.

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Palanivel, Umadevi, and Senthilkumar Lakshmipathi. "Hydrogen bonds in Zif268 proteins – a theoretical perspective." Journal of Biomolecular Structure and Dynamics 34, no. 8 (October 20, 2015): 1607–24. http://dx.doi.org/10.1080/07391102.2015.1085903.

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20

Trask, Sydney, Brooke N. Dulka, and Fred J. Helmstetter. "Age-Related Memory Impairment Is Associated with Increased zif268 Protein Accumulation and Decreased Rpt6 Phosphorylation." International Journal of Molecular Sciences 21, no. 15 (July 28, 2020): 5352. http://dx.doi.org/10.3390/ijms21155352.

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Aging is associated with cognitive decline, including impairments in the ability to accurately form and recall memories. Some behavioral and brain changes associated with aging are evident as early as middle age, making the understanding of associated neurobiological mechanisms essential to aid in efforts aimed at slowing cognitive decline throughout the lifespan. Here, we found that both 15-month-old and 22-month-old rats showed impaired memory recall following trace fear conditioning. This behavioral deficit was accompanied by increased zif268 protein accumulation relative to 3-month-old animals in the medial prefrontal cortex, the dorsal and ventral hippocampi, the anterior and posterior retrosplenial cortices, the lateral amygdala, and the ventrolateral periaqueductal gray. Elevated zif268 protein levels corresponded with decreases in phosphorylation of the Rpt6 proteasome regulatory subunit, which is indicative of decreased engagement of activity-driven protein degradation. Together, these results identify several brain regions differentially impacted by aging and suggest that the accumulation of proteins associated with memory retrieval, through reduced proteolytic activity, is associated with age-related impairments in memory retention.
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Han, Jeongsoo, Minjee Kwon, Myeounghoon Cha, Motomasa Tanioka, Seong-Karp Hong, Sun Joon Bai, and Bae Hwan Lee. "Plasticity-Related PKMζSignaling in the Insular Cortex Is Involved in the Modulation of Neuropathic Pain after Nerve Injury." Neural Plasticity 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/601767.

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The insular cortex (IC) is associated with important functions linked with pain and emotions. According to recent reports, neural plasticity in the brain including the IC can be induced by nerve injury and may contribute to chronic pain. Continuous active kinase, protein kinase Mζ(PKMζ), has been known to maintain the long-term potentiation. This study was conducted to determine the role of PKMζin the IC, which may be involved in the modulation of neuropathic pain. Mechanical allodynia test and immunohistochemistry (IHC) of zif268, an activity-dependent transcription factor required for neuronal plasticity, were performed after nerve injury. Afterζ-pseudosubstrate inhibitory peptide (ZIP, a selective inhibitor of PKMζ) injection, mechanical allodynia test and immunoblotting of PKMζ, phospho-PKMζ(p-PKMζ), and GluR1 and GluR2 were observed. IHC demonstrated that zif268 expression significantly increased in the IC after nerve injury. Mechanical allodynia was significantly decreased by ZIP microinjection into the IC. The analgesic effect lasted for 12 hours. Moreover, the levels of GluR1, GluR2, and p-PKMζwere decreased after ZIP microinjection. These results suggest that peripheral nerve injury induces neural plasticity related to PKMζand that ZIP has potential applications for relieving chronic pain.
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Wang, Xinkang, Tian-Li Yue, Peter R. Young, Frank C. Barone, and Giora Z. Feuerstein. "Expression of Interleukin-6, c-Fos, and zif268 mRNAs in Rat Ischemic Cortex." Journal of Cerebral Blood Flow & Metabolism 15, no. 1 (January 1995): 166–71. http://dx.doi.org/10.1038/jcbfm.1995.18.

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The expression of interleukin-6 (IL-6) mRNA in the focal ischemic rat cortex was studied by means of Northern hybridization. IL-6 mRNA was induced after permanent occlusion of the middle cerebral artery, reached a significant level at 3 h, and peaked at 12 h, i.e., ∼ 10-fold increase in the ischemic zone compared with the nonischemic cortex or sham-operated controls. The increased IL-6 mRNA was elevated for at least 24 h. Low levels of IL-6 mRNA were detected in sham-operated rats or in the contralateral nonischemic cortex. The expression of c- fos and zif268 mRNAs, two early response genes, was rapid (increased by 1 h postischemia) and transient (returned to basal levels by 24 and 12 h, respectively), clearly having different kinetic patterns from that of IL-6 mRNA. The early response kinetic pattern of c- fos and zif268 mRNAs in focal ischemia suggests their transcriptional regulatory roles in response to ischemic insult, while the delayed induction pattern of IL-6 mRNA suggests a role for this pleiotropic cytokine in the inflammatory response to the focal ischemic damage of the brain.
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Gao, X. M., L. W. Chen, and C. A. Tamminga. "Blockade of phencyclidine- and MK801-induced regional zif268 mRNA expression." Schizophrenia Research 24, no. 1-2 (January 1997): 76. http://dx.doi.org/10.1016/s0920-9964(97)82206-2.

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Toscano, Christopher D., Jennifer L. McGlothan, and Tomás R. Guilarte. "Experience-dependent regulation of zif268 gene expression and spatial learning." Experimental Neurology 200, no. 1 (July 2006): 209–15. http://dx.doi.org/10.1016/j.expneurol.2006.02.006.

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Christy, B., and D. Nathans. "DNA binding site of the growth factor-inducible protein Zif268." Proceedings of the National Academy of Sciences 86, no. 22 (November 1, 1989): 8737–41. http://dx.doi.org/10.1073/pnas.86.22.8737.

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Herms, Jochen, Uwe Zurmöhle, Reimar Schlingensiepen, Wolfgang Brysch, and Karl-Hermann Schlingensiepen. "Developmental expression of the transcription factor zif268 in rat brain." Neuroscience Letters 165, no. 1-2 (January 1994): 171–74. http://dx.doi.org/10.1016/0304-3940(94)90737-4.

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Yamagata, K., W. E. Kaufmann, A. Lanahan, M. Papapavlou, C. A. Barnes, K. I. Andreasson, and P. F. Worley. "Egr3/Pilot, a zinc finger transcription factor, is rapidly regulated by activity in brain neurons and colocalizes with Egr1/zif268." Learning & Memory 1, no. 2 (1994): 140–52. http://dx.doi.org/10.1101/lm.1.2.140.

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Programs of gene activation may underlie long-term adaptive cellular responses to extracellular ligands. We have used a differential cDNA cloning strategy to identify genes that are strongly induced by excitatory stimuli in the adult rat hippocampus. Here, we report the rat cDNA sequence of a zinc-finger transcription factor, Egr3/Pilot, and characterize its regulated mRNA expression in brain. Egr3 mRNA is rapidly and transiently induced in neurons of the hippocampus and cortex by electroconvulsive seizure. mRNA levels peak 2 hr after the seizure and remain elevated for as long as 8 hr. Egr3 mRNA is also rapidly induced in granule cells of the dentate gyrus by synaptic NMDA receptor activation elicited by patterned stimulation of the perforant pathway and by drugs that alter dopamine neurotransmission in the striatum. Basal levels of Egr3 mRNA in the cortex appear to be driven by natural synaptic activity because monocular deprivation rapidly decreases Egr3 mRNA in the deafferented visual cortex. Aspects of the protein structure, sequence-specific DNA binding, transcriptional activity, and regulation of Egr3 are highly similar to another zinc-finger transcription factor, Egr1/zif268. Moreover, we demonstrate colocalization of Egr3 and zif268 mRNAs in neurons of normal and stimulated cortex. Our studies suggest that interactions between these coregulated transcription factors may be important in defining long-term, neuroplastic responses.
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28

Munoz, Francisco Ventura. "Mind-body medicine epigenetic technique (MET) and EGR1 (zif268) gene expression." Journal of Clinical Oncology 33, no. 29_suppl (October 10, 2015): 4. http://dx.doi.org/10.1200/jco.2015.33.29_suppl.4.

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4 Background: This is a pilot study update on the potential of MET to up-regulate EGR1 gene expression in patients diagnosed with breast cancer. EGR1 gene expression is associated with learning and memory. Methods: The selection process for the study participants was nonrandom. The following was the eligibility criteria. 1. Inclusion Criteria: Breast Cancer, Stages II, III 2. Exclusion Criteria: Cognitively impaired, weak or ill. The study utilized two groups. Each group was assigned two research participants. Group One received one session of MET. Group Two received two sessions of MET. Each MET session was approximately 25-35 minutes in duration. Blood samples were taken at baseline and post-MET sessions to provide evidence in gene expression changes. For Group Two, the post-MET session blood draw was done 7 days after baseline. 1. Primary Endpoint: To determine whether MET can up-regulate EGR1 gene expression. 2. Secondary Endpoint: To determine whether there is a correlation between up-regulated EGR1 gene expression with up-regulated TP53 and TP53AIP1 gene expression. The blood samples were sent to genomics labs at the Childrens Hospital of Los Angeles and the University of Nevada Las Vegas for mRNA extraction and microarray analysis. The gene expression was measured by DNA microarray results using the “PrimeView gene chip” and “Partek Genomics Suite” statistical software. Results: For two participants in Group 1 and one participant in Group 2, there was biologically significant up-regulation in EGR1 gene expression. However, only one participant from Group 1 evidenced a biologically significant up-regulation of EGR1 gene expression along with a biologically significant up-regulation of TP53 and TP53AIP1 gene expression. One major limitation of these findings is the statistical insignificance of the results due to the small number of participants. Conclusions: This pilot study evidenced the up-regulation of EGR1 gene expression potentially due to MET and provided evidence for potential correlation between EGR1, TP53 and TP53AIP1 gene expression. TP53 and TP53AIP1 gene expression are known to induce apoptosis. This study also provided a foundation for a larger study with more participants.
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Worley, P. F., B. A. Christy, Y. Nakabeppu, R. V. Bhat, A. J. Cole, and J. M. Baraban. "Constitutive expression of zif268 in neocortex is regulated by synaptic activity." Proceedings of the National Academy of Sciences 88, no. 12 (June 15, 1991): 5106–10. http://dx.doi.org/10.1073/pnas.88.12.5106.

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Fehr, Friederike, André Nadler, Florian Brodhun, Ivo Feussner, and Ulf Diederichsen. "Semi-Synthesis and Analysis of Chemically Modified Zif268 Zinc-Finger Domains." ChemistryOpen 1, no. 1 (January 2, 2012): 26–32. http://dx.doi.org/10.1002/open.201100002.

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Baumgärtel, Karsten, David Genoux, Hans Welzl, Ry Y. Tweedie-Cullen, Kyoko Koshibu, Magdalena Livingstone-Zatchej, Céline Mamie, and Isabelle M. Mansuy. "Control of the establishment of aversive memory by calcineurin and Zif268." Nature Neuroscience 11, no. 5 (April 20, 2008): 572–78. http://dx.doi.org/10.1038/nn.2113.

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Altemus, M., R. Paletzki, C. R. Gerfen, and D. L. Murphy. "Differential activation of ZIF268 in the amygdala in response to mCPP." Biological Psychiatry 39, no. 7 (April 1996): 583. http://dx.doi.org/10.1016/0006-3223(96)84230-2.

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Clements, K. M., and P. E. Wainwright. "Swim stress increases hippocampal Zif268 expression in the spontaneously hypertensive rat." Brain Research Bulletin 82, no. 5-6 (July 2010): 259–63. http://dx.doi.org/10.1016/j.brainresbull.2010.05.002.

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34

Williams, G. T., and L. F. Lau. "Activation of the inducible orphan receptor gene nur77 by serum growth factors: dissociation of immediate-early and delayed-early responses." Molecular and Cellular Biology 13, no. 10 (October 1993): 6124–36. http://dx.doi.org/10.1128/mcb.13.10.6124.

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We have characterized the genetic elements that mediate the transcriptional activation of nur77, a growth factor-inducible gene encoding a member of the steroid/thyroid hormone receptor superfamily. Although initially identified as a serum-inducible immediate-early gene with expression kinetics similar to those of c-fos, we found that transcriptional activation of nur77 by serum growth factors in fibroblasts is in fact composed of two components: an immediate-early component, which can occur in the absence of de novo protein synthesis, and a delayed-early component, which is dependent on de novo protein synthesis. The expression of nur77 following serum stimulation reflects the superimposition of immediate-early and delayed-early expression. Immediate-early and delayed-early expression can be dissociated from one another by deletion or base substitution mutations of the nur77 promoter. Immediate-early expression of nur77 is mediated primarily by sequences located between nucleotides -86 and -126 upstream of the transcription start site. This region includes a sequence that resembles but differs from the CArG element found in other serum-inducible promoters. Upstream of the CArG-like element is a potential binding site for a transcription factor of the Ets family; the presence of this site is required for significant transcriptional induction. Delayed-early expression of nur77 is mediated by multiple AP-1-like and GC-rich elements, which can interact with products of immediate-early genes such as Fos/Jun and Zif268, respectively. Furthermore, we show that Zif268 can activate transcription of the nur77 promoter, suggesting that it may play a role in the delayed-early expression of nur77.
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35

Williams, G. T., and L. F. Lau. "Activation of the inducible orphan receptor gene nur77 by serum growth factors: dissociation of immediate-early and delayed-early responses." Molecular and Cellular Biology 13, no. 10 (October 1993): 6124–36. http://dx.doi.org/10.1128/mcb.13.10.6124-6136.1993.

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We have characterized the genetic elements that mediate the transcriptional activation of nur77, a growth factor-inducible gene encoding a member of the steroid/thyroid hormone receptor superfamily. Although initially identified as a serum-inducible immediate-early gene with expression kinetics similar to those of c-fos, we found that transcriptional activation of nur77 by serum growth factors in fibroblasts is in fact composed of two components: an immediate-early component, which can occur in the absence of de novo protein synthesis, and a delayed-early component, which is dependent on de novo protein synthesis. The expression of nur77 following serum stimulation reflects the superimposition of immediate-early and delayed-early expression. Immediate-early and delayed-early expression can be dissociated from one another by deletion or base substitution mutations of the nur77 promoter. Immediate-early expression of nur77 is mediated primarily by sequences located between nucleotides -86 and -126 upstream of the transcription start site. This region includes a sequence that resembles but differs from the CArG element found in other serum-inducible promoters. Upstream of the CArG-like element is a potential binding site for a transcription factor of the Ets family; the presence of this site is required for significant transcriptional induction. Delayed-early expression of nur77 is mediated by multiple AP-1-like and GC-rich elements, which can interact with products of immediate-early genes such as Fos/Jun and Zif268, respectively. Furthermore, we show that Zif268 can activate transcription of the nur77 promoter, suggesting that it may play a role in the delayed-early expression of nur77.
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36

Bozon, Bruno, Áine Kelly, Sheena A. Josselyn, Alcino J. Silva, Sabrina Davis, and Serge Laroche. "MAPK, CREB and zif268 are all required for the consolidation of recognition memory." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 358, no. 1432 (April 29, 2003): 805–14. http://dx.doi.org/10.1098/rstb.2002.1224.

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There has been nearly a century of interest in the idea that encoding and storage of information in the brain requires changes in the efficacy of synaptic connections between neurons that are activated during learning. Recent research into the molecular mechanisms of long-term potentiation (LTP) has brought about new knowledge that has provided valuable insights into the neural mechanisms of memory storage. The evidence indicates that rapid activation of the genetic machinery can be a key mechanism underlying the enduring modification of neural networks required for the stability of memories. In recent years, a wealth of experimental data has highlighted the importance of mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) signalling in the regulation of gene transcription in neurons. Here, we briefly review experiments that have shown MAPK/ERK, cAMP response element-binding protein (CREB) and the immediate early gene (IEG) zif268 are essential components of a signalling cascade required for the expression of late phase LTP and of certain forms of long-term memory. We also present experiments in which we have assessed the role of these three molecules in recognition memory. We show that pharmacological blockade of MAPK/ERK phosphorylation, functional inactivation of CREB in an inducible transgenic mouse and inactivation of zif268 in a mutant mouse result in a similar deficit in long-term recognition memory. In the continuing debate about the role of LTP mechanisms in memory, these findings provide an important complement to the suggestion that synaptic changes brought about by LTP and memory consolidation and storage share, at least in part, common underlying molecular mechanisms.
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Nobuhara, K., T. Matsuura, I. Urabe, and T. Yomo. "3P078 Function of DNA binding protein Zif268 is tolerant to domain substitution." Seibutsu Butsuri 45, supplement (2005): S223. http://dx.doi.org/10.2142/biophys.45.s223_2.

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38

Essali, Norah, and Jeff Sanders. "Interdependent adrenergic receptor regulation of Arc and Zif268 mRNA in cerebral cortex." Neuroscience Letters 612 (January 2016): 38–42. http://dx.doi.org/10.1016/j.neulet.2015.12.002.

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39

Moratalla, R., HA Robertson, and AM Graybiel. "Dynamic regulation of NGFI-A (zif268, egr1) gene expression in the striatum." Journal of Neuroscience 12, no. 7 (July 1, 1992): 2609–22. http://dx.doi.org/10.1523/jneurosci.12-07-02609.1992.

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40

Beligere, Gangamani S., and Philip E. Dawson. "Synthesis of a three zinc finger protein, Zif268, by native chemical ligation." Biopolymers 51, no. 5 (1999): 363–69. http://dx.doi.org/10.1002/(sici)1097-0282(1999)51:5<363::aid-bip6>3.0.co;2-o.

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41

Zheng, Jing, Fang Yin, Guoqin Jin, Xueli Zhang, Lina Zhang, Zhangbin Gong, Xiangping Kang, and Haiyan Hu. "In Vitro Neuroprotection of Rat Hippocampal Neurons by Manninotriose and Astragaloside IV Against Corticosterone-Induced Toxicity." Molecules 23, no. 12 (December 17, 2018): 3339. http://dx.doi.org/10.3390/molecules23123339.

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A chronically elevated glucocorticoid level impairs memory and cognition. Manninotriose is the main oligosaccharide of Prepared Radix Rehmanniae, and Astragaloside IV (AS-IV) is the primary ingredient of Astragali Radix; they have been reported to possess neuroprotective effects. The aim of the present study was to investigate the protective effects of Manninotriose and AS-IV on corticosterone (CORT) induced neurotoxicity and the underlying mechanisms. Primary cultured hippocampal neurons from newborn Sprague Dawley rats were treated with CORT in the absence or presence of Manninotriose and AS-IV. Cell Counting Kit-8 experiments and fluorescein diacetate (FDA)/propidium iodide (PI) double staining were conducted to assess the activity and survival rate of neurons. Quantitative Real-time PCR (qRT-PCR) and western blot analysis were performed to detect the expression of glucocorticoid receptor (GR), zinc finger protein (Zif268) and synapsin 1 (SYN1). DNA methylation of the gene promoter was assessed by bisulfite sequencing (BSP) analysis. The results demonstrated that pre-treatment with Manninotriose and AS-IV significantly improved cell viability and survival rate, and ameliorated the downregulation of GR, Zif268 and SYN1 genes in CORT injured neurons. BSP analysis revealed that CORT was able to improve the CpG island methylation rate of SYN1. AS-IV was observed to decrease the hypermethylation of the SYN1 gene induced by CORT. The results of the present study indicated that Manninotriose and AS-IV may have a protective effect against CORT-induced damage and the downregulation of learning and memory associated genes in hippocampal neurons. Regulation of DNA methylation may be important in the pharmaceutical activities of AS-IV. Thus, Manninotriose and AS-IV may be effective agents against learning and memory impairment.
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42

Alter, David, Joel A. Beverley, Ronak Patel, Carlos A. Bolaños-Guzmán, and Heinz Steiner. "The 5-HT1B serotonin receptor regulates methylphenidate-induced gene expression in the striatum: Differential effects on immediate-early genes." Journal of Psychopharmacology 31, no. 8 (July 18, 2017): 1078–87. http://dx.doi.org/10.1177/0269881117715598.

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Drug combinations that include a psychostimulant such as methylphenidate (Ritalin) and a selective serotonin reuptake inhibitor such as fluoxetine are indicated in several medical conditions. Co-exposure to these drugs also occurs with “cognitive enhancer” use by individuals treated with selective serotonin reuptake inhibitors. Methylphenidate, a dopamine reuptake inhibitor, by itself produces some addiction-related gene regulation in the striatum. We have demonstrated that co-administration of selective serotonin reuptake inhibitors potentiates these methylphenidate-induced molecular effects, thus producing a more “cocaine-like” profile. There is evidence that the 5-HT1B serotonin receptor subtype mediates some of the cocaine-induced gene regulation. We thus investigated whether the 5-HT1B receptor also modifies methylphenidate-induced gene regulation, by assessing effects of a selective 5-HT1B receptor agonist (CP94253) on immediate-early gene markers ( Zif268, c- Fos, Homer1a) in adolescent male rats. Gene expression was measured by in situ hybridization histochemistry. Our results show that CP94253 (3, 10 mg/kg) produced a dose-dependent potentiation of methylphenidate (5 mg/kg)-induced expression of Zif268 and c- Fos. This potentiation was widespread in the striatum and was maximal in lateral (sensorimotor) sectors, thus mimicking the effects seen after cocaine alone, or co-administration of fluoxetine. However, in contrast to fluoxetine, this 5-HT1B agonist did not influence methylphenidate-induced expression of Homer1a. CP94253 also potentiated methylphenidate-induced locomotor activity. These findings indicate that stimulation of the 5-HT1B receptor can enhance methylphenidate (dopamine)-induced gene regulation. This receptor may thus participate in the potentiation induced by fluoxetine (serotonin) and may serve as a pharmacological target to attenuate methylphenidate + selective serotonin reuptake inhibitor-induced “cocaine-like” effects.
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43

Zandarashvili, Levani, Alexandre Esadze, Dana Vuzman, Catherine A. Kemme, Yaakov Levy, and Junji Iwahara. "Balancing between affinity and speed in target DNA search by zinc-finger proteins via modulation of dynamic conformational ensemble." Proceedings of the National Academy of Sciences 112, no. 37 (August 31, 2015): E5142—E5149. http://dx.doi.org/10.1073/pnas.1507726112.

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Although engineering of transcription factors and DNA-modifying enzymes has drawn substantial attention for artificial gene regulation and genome editing, most efforts focus on affinity and specificity of the DNA-binding proteins, typically overlooking the kinetic properties of these proteins. However, a simplistic pursuit of high affinity can lead to kinetically deficient proteins that spend too much time at nonspecific sites before reaching their targets on DNA. We demonstrate that structural dynamic knowledge of the DNA-scanning process allows for kinetically and thermodynamically balanced engineering of DNA-binding proteins. Our current study of the zinc-finger protein Egr-1 (also known as Zif268) and its nuclease derivatives reveals kinetic and thermodynamic roles of the dynamic conformational equilibrium between two modes during the DNA-scanning process: one mode suitable for search and the other for recognition. By mutagenesis, we were able to shift this equilibrium, as confirmed by NMR spectroscopy. Using fluorescence and biochemical assays as well as computational simulations, we analyzed how the shifts of the conformational equilibrium influence binding affinity, target search kinetics, and efficiency in displacing other proteins from the target sites. A shift toward the recognition mode caused an increase in affinity for DNA and a decrease in search efficiency. In contrast, a shift toward the search mode caused a decrease in affinity and an increase in search efficiency. This accelerated site-specific DNA cleavage by the zinc-finger nuclease, without enhancing off-target cleavage. Our study shows that appropriate modulation of the dynamic conformational ensemble can greatly improve zinc-finger technology, which has used Egr-1 (Zif268) as a major scaffold for engineering.
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44

Nakamura, Tomoya, Kohei Kurosaki, Munenori Kanemoto, Masakiyo Sasahara, and Hiroyuki Ichijo. "Early-life experiences altered the maturation of the lateral habenula in mouse models, resulting in behavioural disorders in adulthood." Journal of Psychiatry & Neuroscience 46, no. 4 (July 1, 2021): E480—E489. http://dx.doi.org/10.1503/jpn.200226.

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Background: Abnormally high activity in the lateral habenula causes anxiety- or depression-like behaviours in animal experimental models. It has also been reported in humans that excessive stress in early life is correlated with the onset of psychiatric disorders in adults. These findings raise the question of whether maturation of the lateral habenula is affected under the influence of early-life experiences, which could govern behaviours throughout life. Methods: We examined the maturation of the lateral habenula in mice based on neuronal activity markers and plastic components: Zif268/Egr1, parvalbumin and perineuronal nets. We examined the effect of early-life stress using repeated maternal deprivation. Results: First, we found a transient highly sensitive period of the lateral habenula under stress. The lateral habenula matured through 4 stages: postnatal days 1–9 (P1–9), P10–20, around P35 and after P35. At P10–20, the lateral habenula was highly sensitive to stress. We also observed experience-dependent maturation of the lateral habenula. Only mice exposed to chronic stress from P10–20 exhibited changes specific to the lateral habenula at P60: abnormally high stress reactivity shown by Zif268/Egr1 and fewer parvalbumin neurons. These mice showed anxiety- or depression-like behaviours in the light–dark box test and forced swim test. Limitations: The effect of parvalbumin neurons in the lateral habenula on behavioural alterations remains unknown. It will be important to understand the “sensitive period” of the neuronal circuits in the lateral habenula and how the period P10–20 is different from P9 or earlier, or P35 or later. Conclusion: In mice, early-life stress in the period P10–20 led to late effects in adulthood: hyperactivity in the lateral habenula and anxiety or depression, indicating differences in neuronal plasticity between stages of lateral habenula maturation.
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45

Shirayama, Yukihiko, Kenji Hashimoto, Hideyuki Matsuki, Ko-ichi Tsunashima, Masaomi Iyo, Teruhiko Higuchi, and Yoshio Minabe. "Increased expression of zif268 mRNA in rat retrosplenial cortex following administration of phencyclidine." Brain Research 839, no. 1 (August 1999): 180–85. http://dx.doi.org/10.1016/s0006-8993(99)01738-2.

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46

Lowe, S. T., I. Irrcher, L. Nunes, and D. A. Hood. "INTEGRIN SIGNALING DOES NOT MEDIATE THE INCREASE IN ZIF268 MRNA DURING CONTRACTILE ACTIVITY." Medicine & Science in Sports & Exercise 33, no. 5 (May 2001): S65. http://dx.doi.org/10.1097/00005768-200105001-00370.

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47

Takayama, Yuki, Debashish Sahu, and Junji Iwahara. "NMR Studies of Translocation of the Zif268 Protein between Its Target DNA Sites." Biochemistry 49, no. 37 (September 21, 2010): 7998–8005. http://dx.doi.org/10.1021/bi100962h.

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48

Conway, Ann-Marie, Allan B. James, Jie Zang, and Brian J. Morris. "Regulation of neuronal cdc20 (p55cdc) expression by the plasticity-related transcription factor zif268." Synapse 61, no. 6 (2007): 463–68. http://dx.doi.org/10.1002/syn.20387.

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49

Lambert, P. D., T. D. Ely, R. E. Gross, and C. D. Kilts. "Neurotensin induces Fos and Zif268 expression in limbic nuclei of the rat brain." Neuroscience 75, no. 4 (November 1996): 1141–51. http://dx.doi.org/10.1016/0306-4522(96)00210-2.

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50

Malkani, S. "An egr-1 (zif268) Antisense Oligodeoxynucleotide Infused Into the Amygdala Disrupts Fear Conditioning." Learning & Memory 11, no. 5 (September 1, 2004): 617–24. http://dx.doi.org/10.1101/lm.73104.

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