Nerve Tissue Proteins

Publication Title: 
Biochimica Et Biophysica Acta

The hippocampus is one of the most essential components of the human brain and plays an important role in learning and memory. The hippocampus has drawn great attention from scientists and clinicians due to its clinical importance in diseases such as Alzheimer's disease (AD), non-AD dementia, and epilepsy. Understanding the function of the hippocampus and related disease mechanisms requires comprehensive knowledge of the orchestration of the genome, epigenome, transcriptome, proteome, and post-translational modifications (PTMs) of proteins.

Author(s): 
Kang, Myoung-Goo
Byun, Kyunghee
Kim, Jae Ho
Park, Nam Hyun
Heinsen, Helmut
Ravid, Rivka
Steinbusch, Harry W.
Lee, Bonghee
Park, Young Mok
Publication Title: 
Neuron

One of the exceptional properties of the brain is its ability to acquire new knowledge through learning and to store that information through memory. The epigenetic mechanisms linking changes in neuronal transcriptional programs to behavioral plasticity remain largely unknown. Here, we identify the epigenetic signature of the neuronal enhancers required for transcriptional regulation of synaptic plasticity genes during memory formation, linking this to Reelin signaling.

Author(s): 
Telese, Francesca
Ma, Qi
Perez, Patricia Montilla
Notani, Dimple
Oh, Soohwan
Li, Wenbo
Comoletti, Davide
Ohgi, Kenneth A.
Taylor, Havilah
Rosenfeld, Michael G.
Publication Title: 
Cell Cycle (Georgetown, Tex.)

Abnormal protein interactions of mutant huntingtin (Htt) triggered by polyglutamine expansion are thought to mediate Huntington's disease (HD) pathogenesis. Here, we explored a functional interaction of Htt with protein arginine methyltransferase 5 (PRMT5), an enzyme mediating symmetrical dimethylation of arginine (sDMA) of key cellular proteins, including histones, and spliceosomal Sm proteins. Gene transcription and RNA splicing are impaired in HD. We demonstrated PRMT5 and Htt interaction and their co-localization in transfected neurons and in HD brain.

Author(s): 
Ratovitski, Tamara
Arbez, Nicolas
Stewart, Jacqueline C.
Chighladze, Ekaterine
Ross, Christopher A.
Publication Title: 
Journal of Child Psychology and Psychiatry, and Allied Disciplines

BACKGROUND: Peripheral epigenetic marks hold promise for understanding psychiatric illness and may represent fingerprints of gene-environment interactions. We conducted an initial examination of CpG methylation variation in children with or without attention-deficit/hyperactivity disorder (ADHD). METHODS: Children age 7-12 were recruited, screened, evaluated and assigned to ADHD or non-ADHD groups by defined research criteria. Two independent age-matched samples were examined, a discovery set (n = 92, all boys, half control, half ADHD) and a confirmation set (n = 20, half ADHD, all boys).

Author(s): 
Wilmot, Beth
Fry, Rebecca
Smeester, Lisa
Musser, Erica D.
Mill, Jonathan
Nigg, Joel T.
Publication Title: 
PloS One

Huntington's disease (HD) is an autosomal-dominant neurodegenerative disorder resulting from expansion of CAG repeats in the Huntingtin (HTT) gene. Previous studies have shown mutant HTT can alter expression of genes associated with dysregulated epigenetic modifications. One of the most widely studied chromatin modifications is trimethylated lysine 4 of histone 3 (H3K4me3).

Author(s): 
Dong, Xianjun
Tsuji, Junko
Labadorf, Adam
Roussos, Panos
Chen, Jiang-Fan
Myers, Richard H.
Akbarian, Schahram
Weng, Zhiping
Publication Title: 
International Journal of Molecular Sciences

Borderline personality disorder (BPD) is a serious psychic disease with a high risk for suicide. DNA methylation is a hallmark for aberrant epigenetic regulation and could be involved in the etiology of BPD. Previously, it has been reported that increased DNA methylation of neuropsychiatric genes is found in the blood of patients with BPD compared to healthy controls.

Author(s): 
Teschler, Stefanie
Gotthardt, Julia
Dammann, Gerhard
Dammann, Reinhard H.
Publication Title: 
Biological Research

Schizophrenia is a severe psychiatric disorder that results in a significant disability for the patient. The disorder is characterized by impairment of the adaptive orchestration of actions, a cognitive function that is mainly dependent on the prefrontal cortex. This behavioral deficit, together with cellular and neurophysiological alterations in the prefrontal cortex, as well as reduced density of GABAergic cells and aberrant oscillatory activity, all indicate structural and functional deficits of the prefrontal cortex in schizophrenia.

Author(s): 
NegrÛn-Oyarzo, Ignacio
Lara-V·squez, Ariel
Palacios-GarcÌa, Ismael
Fuentealba, Pablo
Aboitiz, Francisco
Publication Title: 
Biology Letters

We test the hypothesis that polymorphisms of the brain regulator genes MCPH1 and ASPM contribute to variations in human brain size and its correlates. We measured general mental ability, head circumference and social intelligence in 644 Canadian adults (496 Caucasians, 36 Orientals, 84 Mixed Race/Other and 28 Blacks; 257 men and 387 women). The gene polymorphisms were assessed from buccal DNA; mental ability by Wonderlic Personnel Test and Multidimensional Aptitude Battery; head circumference by stretchless tape; and social intelligence by prosocial attitude questionnaires.

Author(s): 
Rushton, J. Philippe
Vernon, Philip A.
Bons, Trudy Ann
Publication Title: 
The Journal of Pharmacology and Experimental Therapeutics

The relationship between circadian rhythms in the pharmacological actions of meperidine and hexobarbital and similar rhythms in the hepatic metabolism of these drugs was examined in mice under a variety of environmental alterations to determine whether such rhythms may be causally related. The rate of metabolism of p-nitroanisole and hexobarbital by hepatic 9000 X g supernatant fractions was found to be higher at 2400 hours (middark phase) compared to 1200 hours (midlight phase).

Author(s): 
Holcslaw, T. L.
Miya, T. S.
Bousquet, W. S.
Publication Title: 
The Journal of Neuroscience: The Official Journal of the Society for Neuroscience

General anesthetics cause sedation, hypnosis, and immobilization via CNS mechanisms that remain incompletely understood; contributions of particular anesthetic targets in specific neural pathways remain largely unexplored. Among potential molecular targets for mediating anesthetic actions, members of the TASK subgroup [TASK-1 (K2P3.1) and TASK-3 (K2P9.1)] of background K(+) channels are appealing candidates since they are expressed in CNS sites relevant to anesthetic actions and activated by clinically relevant concentrations of inhaled anesthetics.

Author(s): 
Lazarenko, Roman M.
Willcox, Sarah C.
Shu, Shaofang
Berg, Allison P.
Jevtovic-Todorovic, Vesna
Talley, Edmund M.
Chen, Xiangdong
Bayliss, Douglas A.

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