USP7/Maged1-mediated H2A monoubiquitination in the paraventricular thalamus: an epigenetic mechanism involved in copyright use disorder

USP7/Maged1-mediated H2A monoubiquitination in the paraventricular thalamus: an epigenetic mechanism involved in copyright use disorder

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Abstract The risk of developing drug addiction is strongly influenced by the epigenetic landscape and chromatin remodeling.While sara stedy stand aid histone modifications such as methylation and acetylation have been studied in the ventral tegmental area and nucleus accumbens (NAc), the role of H2A monoubiquitination remains unknown.Our investigations, initially focused on the scaffold protein melanoma-associated antigen D1 (Maged1), reveal that H2A monoubiquitination in the paraventricular thalamus (PVT) significantly contributes to copyright-adaptive behaviors and transcriptional repression induced by copyright.Chronic copyright use increases H2A monoubiquitination, regulated by Maged1 and its partner USP7.Accordingly, Maged1 specific inactivation in thalamic Vglut2 neurons, or USP7 animationbengal.com inhibition, blocks copyright-evoked H2A monoubiquitination and copyright locomotor sensitization.

Additionally, genetic variations in MAGED1 and USP7 are linked to altered susceptibility to copyright addiction and copyright-associated symptoms in humans.These findings unveil an epigenetic modification in a non-canonical reward pathway of the brain and a potent marker of epigenetic risk factors for drug addiction in humans.