GABAergic neuron deficit as an idiopathic generalized epilepsy mechanism: the role of BRD2 haploinsufficiency in juvenile myoclonic epilepsy. - Wikidata - awgldk - TriplyDB

GABAergic neuron deficit as an idiopathic generalized epilepsy mechanism: the role of BRD2 haploinsufficiency in juvenile myoclonic epilepsy.

GABAergic neuron deficit as an idiopathic generalized epilepsy mechanism: the role of BRD2 haploinsufficiency in juvenile myoclonic epilepsy.

http://www.wikidata.org/entity/Q34009474

about

The Bromodomain and Extra-Terminal Domain (BET) Family: Functional Anatomy of BET Paralogous Proteins Rac1 and rac3 GTPases control synergistically the development of cortical and hippocampal GABAergic interneurons Maternal separation with early weaning: a rodent model providing novel insights into neglect associated developmental deficits The C-terminal domain of Brd2 is important for chromatin interaction and regulation of transcription and alternative splicing.Pleiotrophin antagonizes Brd2 during neuronal differentiation.Genetic susceptibility in Juvenile Myoclonic Epilepsy: Systematic review of genetic association studies.Sex-specific behavioral traits in the Brd2 mouse model of juvenile myoclonic epilepsy Double-bromo and extraterminal (BET) domain proteins regulate dendrite morphology and mechanosensory function Sex, epilepsy, and epigenetics.The bromodomain-containing gene BRD2 is regulated at transcription, splicing, and translation levels.A Review of the Differences in Developmental, Psychiatric, and Medical Endophenotypes Between Males and Females with Autism Spectrum Disorder.Estradiol does not affect spasms in the betamethasone-NMDA rat model of infantile spasms.Bromodomains and their pharmacological inhibitors.Roles of Rac1 and Rac3 GTPases during the development of cortical and hippocampal GABAergic interneurons Bromodomain and extra-terminal (BET) family proteins: New therapeutic targets in major diseases.Genetic and epigenetic mechanisms of epilepsy: a review.Thalamic volume reduction in drug-naive patients with new-onset genetic generalized epilepsy.Frontal and thalamic changes of GABA concentration indicate dysfunction of thalamofrontal networks in juvenile myoclonic epilepsy.Identifying gene expression profile of spinal cord injury in rat by bioinformatics strategy.

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P2860

GABAergic neuron deficit as an idiopathic generalized epilepsy mechanism: the role of BRD2 haploinsufficiency in juvenile myoclonic epilepsy.

http://www.wikidata.org/entity/Q34009474

description

2011 nî lūn-bûn

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2011 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

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2011 թվականի օգոստոսին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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GABAergic neuron deficit as an ...... n juvenile myoclonic epilepsy.

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GABAergic neuron deficit as an ...... n juvenile myoclonic epilepsy.

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GABAergic neuron deficit as an ...... in juvenile myoclonic epilepsy

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David A Greenberg

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Debra J Wolgemuth

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Enyuan Shang

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Giorgi Maglakelidze

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Jana Velíšková

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Stephania Macchiarulo

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Tamar Chachua

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P2860

BRD2 (RING3) is a probable major susceptibility gene for common juvenile myoclonic epilepsy

Synaptic organisation of the basal ganglia

RING3 kinase transactivates promoters of cell cycle regulatory genes through E2F

Centrotemporal sharp wave EEG trait in rolandic epilepsy maps to Elongator Protein Complex 4 (ELP4).

KCNQ2 and KCNQ3 potassium channel genes in benign familial neonatal convulsions: expansion of the functional and mutation spectrum

Identification of a variant associated with adult-type hypolactasia

Selective recognition of acetylated histones by bromodomain proteins visualized in living cells

The double bromodomain protein Brd4 binds to acetylated chromatin during interphase and mitosis

Focal structural changes and cognitive dysfunction in juvenile myoclonic epilepsy.

The control of seizures by the basal ganglia? A review of experimental data.

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e23656

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10.1371/JOURNAL.PONE.0023656

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haploinsufficiency

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