Publications by authors named "Wenpeng Liang"

Skeletal muscular atrophy is a complex disease involving a large number of gene expression regulatory networks and various biological processes. Despite extensive research on this topic, its underlying mechanisms remain elusive, and effective therapeutic approaches are yet to be established. Recent studies have shown that epigenetics play an important role in regulating skeletal muscle atrophy, influencing the expression of numerous genes associated with this condition through the addition or removal of certain chemical modifications at the molecular level.

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Objective: To explore the mechanism involved in variable phenotypes of epilepsy models induced by γ-aminobutyric acid type A γ2 subunit (GABRG2) mutations.

Methods: The zebrafish carrying wild-type (WT) GABRG2, mutant GABRG2(P282S), GABRG2(F343L) and GABRG2(I107T) were established by Tol2kit transgenesis system and Gateway method. Behavioral analysis of different transgenic zebrafish was performed with the DanioVision Video-Track framework and the brain activity was analyzed by field potential recording with MD3000 Bio-signal Acquisition and Processing System.

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Inflammation is considered to be involved in epileptogenesis. However, the relationship between fever and inflammation as well as the mechanisms of fever in the occurrence and development of childhood epilepsy need further investigation. Here, we described an in vivo model of hyperthermia-induced seizures in zebrafish larvae with pentylenetetrazole (PTZ) exposure.

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Epilepsy is a common and severe chronic neurological disorder. Recently, post-translational modification (PTM) mechanisms, especially protein acetylation modifications, have been widely studied in various epilepsy models or patients. Acetylation is regulated by two classes of enzymes, histone acetyltransferases (HATs) and histone deacetylases (HDACs).

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Mutations in the γ-aminobutyric acid type A (GABAA) receptor γ2 subunit gene, GABRG2, have been associated with a variety of epilepsy syndromes. A de novo mutation (c.T1027C, p.

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Background: Skeletal muscle atrophy, characterized by accelerated protein degradation, occurs in such conditions as unloading, immobilization, fasting, and denervation. Effective treatments for skeletal muscle atrophy are not yet available. Considering that microRNAs (miRs) may play an important role in the regulation of muscle atrophy, in the present study, we aimed to examine the effect of miR-125b-5p-based therapeutic strategies on skeletal muscle atrophy, and to explore the underlying mechanisms.

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