Identification of a negative regulatory DNA element for neuronal BC1 RNA expression by RNA polymerase III

Kobayashi, Shunsuke; Kamo, Sakurako; Ohmae, Akiko; Agui, Keisuke; Li, Yanmei; Anzai, Kentaro

doi:10.1016/s0167-4781(00)00175-5

Cited by 11 publications

(5 citation statements)

References 37 publications

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“…Further, the absence of BC1 leads to neuronal hyperexcitability with significantly elevated group I mGluR-mediated gamma frequency oscillations on cortical electroencephalogram (EEG) recordings and a propensity for convulsive seizures (Zhong et al, 2009). Moreover, the administration of kainic acid transiently increases the level of BC1 through effects on factors that bind to regulatory motifs in the BC1 gene promoter (Kobayashi et al, 2000). Intriguingly, the BC1 gene promoter contains both positive and negative regulatory elements, including a motif similar to but distinct from the neuron-restrictive silencer element (NRSE) that is bound by REST, and BC1 is a binding partner of FMRP.…”

Section: Epigenetic Mechanisms In Epileptic Disorders and The Processmentioning

confidence: 99%

Epigenetic mechanisms underlying human epileptic disorders and the process of epileptogenesis

Qureshi

Mehler

2010

Neurobiology of Disease

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The rapidly emerging science of epigenetics and epigenomic medicine promises to reveal novel insights into the susceptibility to and the onset and progression of epileptic disorders. Epigenetic regulatory mechanisms are now implicated in orchestrating aspects of neural development (e.g., cell fate specification and maturation), homeostasis and stress responses (e.g., immediate early gene transcription), and neural network function (e.g., excitation-inhibition coupling and activitydependent plasticity). These same neurobiological processes are responsible for determining the heterogeneous features of complex epileptic disease states. Thus, we highlight recent evidence that is beginning to elucidate the specific roles played by epigenetic mechanisms, including DNA methylation, histone code modifications and chromatin remodeling, non-coding RNAs and RNA editing, in human epilepsy syndromes and in the process of epileptogenesis. The highly integrated layers of the epigenome are responsible for the cell type specific and exquisitely environmentally responsive deployment of genes and functional gene networks that underlie the molecular pathophysiology of epilepsy and its associated co-morbidities, including but not limited to neurotransmitter receptors (e.g, GluR2, GLRA2, and GLRA3), growth factors (e.g, BDNF), extracellular matrix proteins (e.g., RELN) and diverse transcriptional regulators (e.g., CREB, c-fos, and c-jun). These important observations suggest that future epigenetic studies are necessary to better understand, classify, prevent and treat epileptic disorders.

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Section: Epigenetic Mechanisms In Epileptic Disorders and The Processmentioning

confidence: 99%

Epigenetic mechanisms underlying human epileptic disorders and the process of epileptogenesis

Qureshi

Mehler

2010

Neurobiology of Disease

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“…It is a redox sensitive leucine zipper transcription factor which interacts with the inhibitory binding domain, Kelch‐like ECH associated protein 1 (Keap 1). Keap1 acts as an adaptor for an E3 ubiquitin ligase, thereby targeting Nrf2 to the proteasome for degradation . Free oxygen radicals and electrophiles can modify the binding association between Keap1 and Nrf2, hence permitting Nrf2 to detach and translocate to the nucleus where it binds to a sequence known as the antioxidant or electrophilic response element (ARE/EpRE) in DNA.…”

Section: Introductionmentioning

confidence: 99%

“…Keap1 acts as an adaptor for an E3 ubiquitin ligase, thereby targeting Nrf2 to the proteasome for degradation. [8] Free oxygen radicals and electrophiles can modify the binding association between Keap1 and Nrf2, hence permitting Nrf2 to detach and translocate to the nucleus where it binds to a sequence known as the antioxidant or electrophilic response element (ARE/EpRE) in DNA. The Nrf2 is essential for the induction of a sequence of phase II detoxification genes through ARE that lies in the promoter region.…”

Section: Introductionmentioning

confidence: 99%

Study of nuclear factor-2 erythroid related factor-2 activator, berberine, in paclitaxel induced peripheral neuropathy pain model in rats

Singh

Saha

Singh

et al. 2018

Journal of Pharmacy and Pharmacology

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Objectives The role of nuclear factor‐2 erythroid related factor‐2 (Nrf2) activator, berberine (BBR), has been established in rat model of streptozotocin induced diabetic neuropathy. Around 30–40% of cancer patients, on paclitaxel (PTX) chemotherapy develop peripheral neuropathy. The present study was contemplated with the aim of establishing the neuropathy preventive role of BBR, in paclitaxel induced peripheral neuropathy model in rats. Methods A total of 30 Wistar rats were divided into five groups as follows: Group I: dimethyl sulfoxide; Group II: PTX+ 0.9% NaCl; Group III: Amitriptyline (ATL) + PTX; Group IV: BBR (10 mg/kg) + PTX and Group V: BBR (20 mg/kg) + PTX. Animals were assessed for tail flick latency, tail cold allodynia latency, histopathological scores, oxidative stress parameters, and mRNA expression of the Nrf2 gene in the sciatic nerve. Key findings Berberine significantly increased the tail flick and tail cold allodynia latencies and significantly decreased the histopathological score. BBR reduced oxidative stress by significantly decreasing the lipid peroxidation, increasing the superoxide dismutase and reduced glutathione levels in the sciatic nerve. BBR also increased the mRNA expression of Nrf2 gene in rat sciatic nerve. Conclusions All of these results showed the neuropathy preventing role of BBR in PTX induced neuropathy pain model in rats.

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“…BC1 RNA gene represents unique Pol III-transcribed gene that is expressed preferentially in the brain in a developmentally-regulated and neuronal activitydependent manner (5,16,39). BC1 RNA expression is dependent upon internal Pol III promoters and external TATA-like sequences and PSE (14,40).…”

Section: Discussionmentioning

confidence: 99%

“…BC1 RNA expression is dependent upon internal Pol III promoters and external TATA-like sequences and PSE (14,40). An E-box sequence (E2 site) within the 5Ј-flanking sequence acts as a transcriptional activator (15) and a repressor/ silencer element BCRE (BC1 RNA repressing element) within the further upstream region downregulates BC1 RNA transcription (16). These findings suggest that the balance of positive and negative regulatory elements and their binding proteins may control activity-dependent BC1 RNA expression.…”

Section: Discussionmentioning

confidence: 99%

Neural BC1 RNA Associates with Pur α, a Single-Stranded DNA and RNA Binding Protein, Which Is Involved in the Transcription of the BC1 RNA Gene

Kobayashi

Agui

Kamo

et al. 2000

Biochemical and Biophysical Research Communications

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Identification of a negative regulatory DNA element for neuronal BC1 RNA expression by RNA polymerase III

Cited by 11 publications

References 37 publications

Epigenetic mechanisms underlying human epileptic disorders and the process of epileptogenesis

Epigenetic mechanisms underlying human epileptic disorders and the process of epileptogenesis

Study of nuclear factor-2 erythroid related factor-2 activator, berberine, in paclitaxel induced peripheral neuropathy pain model in rats

Neural BC1 RNA Associates with Pur α, a Single-Stranded DNA and RNA Binding Protein, Which Is Involved in the Transcription of the BC1 RNA Gene

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