HSPBAP1 is found extensively in the anterior temporal neocortex of patients with intractable epilepsy

Xi, Zhiqin; Sun, Jijun; Wang, Xuefeng; Li, Mingwei; Liu, Xianzeng; Wang, Linyuan; Zhu, Xiongwei; Xiao, Fei; Gong, Yun; Guan, Li-feng

doi:10.1002/syn.20417

Cited by 18 publications

(21 citation statements)

References 33 publications

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“…Interestingly, in this context, HSPBAP1 inhibits the ability of Hsp27 to protect cells against heat shock (Liu et al 2000) and it is abnormally expressed in the anterior temporal neocortex of patients with intractable epilepsy (IE) (Xi et al 2007). These results indicate that deregulation of HSPBAP1 may play a role in the development IE.…”

Section: Hspbap1mentioning

confidence: 99%

Erasing the methyl mark: histone demethylases at the center of cellular differentiation and disease

Cloos

Christensen²,

Agger³

et al. 2008

Genes Dev.

588

559

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The enzymes catalyzing lysine and arginine methylation of histones are essential for maintaining transcriptional programs and determining cell fate and identity. Until recently, histone methylation was regarded irreversible. However, within the last few years, several families of histone demethylases erasing methyl marks associated with gene repression or activation have been identified, underscoring the plasticity and dynamic nature of histone methylation. Recent discoveries have revealed that histone demethylases take part in large multiprotein complexes synergizing with histone deacetylases, histone methyltransferases, and nuclear receptors to control developmental and transcriptional programs. Here we review the emerging biochemical and biological functions of the histone demethylases and discuss their potential involvement in human diseases, including cancer.Histones constitute the basic scaffold proteins around which DNA is wound to form the highly ordered structure of chromatin. Histones, and in particular their tails, are subjected to a plethora of post-translational modifications that have been implicated in chromatin remodeling and closely linked to transcriptional regulation, DNA replication, and DNA repair (for recent reviews, see Berger 2007; Kouzarides 2007). Histone acetylation and methylation represent the most common modifications of the histone tails. These modifications differ in two ways: Histone acetylation results in a negative charge of the modified lysine residue, causing a decreased interaction between the histone and DNA that is generally associated with active transcription. In contrast, methylation of histones occurs at both arginine and lysine residues, and does not influence the net charge of the affected residues, and hence, has no effect on DNA-histone interactions. Rather, the effect of histone methylation impacts on the transcriptional activity of the underlying DNA by acting as a recognition template for effector proteins modifying the chromatin environment and leading to either repression or activation. Thus, histone methylation can be associated with either activation or repression of transcription depending on which effector protein is being recruited. It should be noted that the unmodified residues can also serve as a binding template for effector proteins leading to specific chromatin states (Lan et al. 2007b).Arginine residues can be modified by one or two methyl groups; the latter form in either a symmetric or asymmetric conformation (Rme1, Rme2s, and Rme2a), permitting a total of four states: one unmethylated and three methylated forms.Similarly, lysine residues can be unmethylated, mono-, di-, or trimethylated (Kme1, Kme2, and Kme3), and the extent of methylation at a specific residue is important for the recognition of effector proteins and has therefore impact on chromatin and the transcriptional outcome.Histone methylation is involved in the regulation of a variety of nuclear processes essential for cellular regulation, homeostasis, and fate. Previously, methylation...

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Section: Hspbap1mentioning

confidence: 99%

Erasing the methyl mark: histone demethylases at the center of cellular differentiation and disease

Cloos

Christensen²,

Agger³

et al. 2008

Genes Dev.

588

559

View full text Add to dashboard Cite

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“…Inactivating mutations in KDM5C impairs REST-dependent silencing of neuronal genes such as BDNF and SCN2A, thereby intensifying seizures and contributing to X-linked mental retardation. In addition, heat-shock 27-kDa-associated protein 1 (HSPBAP1), a member of the histone demethylase family JmjC, is expressed in the anterior temporal neocortex of patients with intractable epilepsy, but not in normal controls (Xi et al, 2007;Cloos, 2011). Although it is not yet known by which mechanism upregulation of HSPBAP1 contributes to epilepsy or neuronal death, an attractive scenario is that HSPBAP1 represses expression of the protective protein HSP27, thereby exacerbating neuronal death.…”

Section: Histone Modification and Transcriptional Regulation In Epilepsymentioning

confidence: 99%

Epigenetic Mechanisms in Stroke and Epilepsy

Hwang

Aromolaran

Zukin

2012

Neuropsychopharmacol

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Epigenetic remodeling and modifications of chromatin structure by DNA methylation and histone modifications represent central mechanisms for the regulation of neuronal gene expression during brain development, higher-order processing, and memory formation. Emerging evidence implicates epigenetic modifications not only in normal brain function, but also in neuropsychiatric disorders. This review focuses on recent findings that disruption of chromatin modifications have a major role in the neurodegeneration associated with ischemic stroke and epilepsy. Although these disorders differ in their underlying causes and pathophysiology, they share a common feature, in that each disorder activates the gene silencing transcription factor REST (repressor element 1 silencing transcription factor), which orchestrates epigenetic remodeling of a subset of 'transcriptionally responsive targets' implicated in neuronal death. Although ischemic insults activate REST in selectively vulnerable neurons in the hippocampal CA1, seizures activate REST in CA3 neurons destined to die. Profiling the array of genes that are epigenetically dysregulated in response to neuronal insults is likely to advance our understanding of the mechanisms underlying the pathophysiology of these disorders and may lead to the identification of novel therapeutic strategies for the amelioration of these serious human conditions.

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“…GPS1 is known to suppress survival-associated mitogen-activated protein kinase-mediated signal transduction [34]–[38]. Hspbap1 is believed to inhibit the neuroprotective effects of heat shock protein 27, and is found extensively in the anterior temporal neocortex of patients with intractable epilepsy [39]. MRVI1 and SMCHD1 are respectively linked to blood coagulation and chromosome organization.…”

Section: Discussionmentioning

confidence: 99%

Mining Gene Expression Data of Multiple Sclerosis

et al. 2014

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ObjectivesMicroarray produces a large amount of gene expression data, containing various biological implications. The challenge is to detect a panel of discriminative genes associated with disease. This study proposed a robust classification model for gene selection using gene expression data, and performed an analysis to identify disease-related genes using multiple sclerosis as an example.Materials and methodsGene expression profiles based on the transcriptome of peripheral blood mononuclear cells from a total of 44 samples from 26 multiple sclerosis patients and 18 individuals with other neurological diseases (control) were analyzed. Feature selection algorithms including Support Vector Machine based on Recursive Feature Elimination, Receiver Operating Characteristic Curve, and Boruta algorithms were jointly performed to select candidate genes associating with multiple sclerosis. Multiple classification models categorized samples into two different groups based on the identified genes. Models’ performance was evaluated using cross-validation methods, and an optimal classifier for gene selection was determined.ResultsAn overlapping feature set was identified consisting of 8 genes that were differentially expressed between the two phenotype groups. The genes were significantly associated with the pathways of apoptosis and cytokine-cytokine receptor interaction. TNFSF10 was significantly associated with multiple sclerosis. A Support Vector Machine model was established based on the featured genes and gave a practical accuracy of ∼86%. This binary classification model also outperformed the other models in terms of Sensitivity, Specificity and F1 score.ConclusionsThe combined analytical framework integrating feature ranking algorithms and Support Vector Machine model could be used for selecting genes for other diseases.

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HSPBAP1 is found extensively in the anterior temporal neocortex of patients with intractable epilepsy

Cited by 18 publications

References 33 publications

Erasing the methyl mark: histone demethylases at the center of cellular differentiation and disease

Erasing the methyl mark: histone demethylases at the center of cellular differentiation and disease

Epigenetic Mechanisms in Stroke and Epilepsy

Mining Gene Expression Data of Multiple Sclerosis

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