Genome-Wide Epigenetics

Capell, Brian C.; Berger, Shelley L.

doi:10.1038/jid.2013.173

Cited by 19 publications

(11 citation statements)

References 10 publications

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“…Researchers in dermatology use a wide variety of HTS techniques, many of which have been discussed previously in the Research Techniques Made Simple series. These include transcriptome analysis with RNA sequencing (RNA-seq) (Antonini et al, 2017;Whitley et al, 2016), immunosequencing (Matos et al, 2017), genome-wide epigenetics (Capell and Berger, 2013), proteomics, metabolomics, metagenomics, and assessment of the microbiome (Jo et al, 2016). Additionally, the Molecular Revolution in Cutaneous Biology series provided an overview of HTS techniques (Anbunathan and Bowcock, 2017;Botchkareva, 2017;Johnston et al, 2017;Kong and Segre, 2017;Sarig et al, 2017), as did Grada and Weinbrecht (2013) in an earlier Research Techniques Made Simple publication.…”

Section: Considerations Before Data Collection Experimental Designmentioning

confidence: 99%

Research Techniques Made Simple: Bioinformatics for Genome-Scale Biology

Foulkes

Watson

Griffiths

et al. 2017

Journal of Investigative Dermatology

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High-throughput biology presents unique opportunities and challenges for dermatological research. Drawing on a small handful of exemplary studies, we review some of the major lessons of these new technologies. We caution against several common errors and introduce helpful statistical concepts that may be unfamiliar to researchers without experience in bioinformatics. We recommend specific software tools that can aid dermatologists at varying levels of computational literacy, including platforms with command line and graphical user interfaces. The future of dermatology lies in integrative research, in which clinicians, laboratory scientists, and data analysts come together to plan, execute, and publish their work in open forums that promote critical discussion and reproducibility. In this article, we offer guidelines that we hope will steer researchers toward best practices for this new and dynamic era of data intensive dermatology.

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Section: Considerations Before Data Collection Experimental Designmentioning

confidence: 99%

Research Techniques Made Simple: Bioinformatics for Genome-Scale Biology

Foulkes

Watson

Griffiths

et al. 2017

Journal of Investigative Dermatology

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“…Nearly every DNA-based array platform has been mirrored to sequencing-based technological procedures. With the enormous high-throughput capabilities of NGS technology, whole-genome approaches if affordable can be performed, including transcription analysis [RNAseq, reviewed in (Mutz et al 2013)], targeted genomic or even whole-genome re-sequencing (Ng et al 2009Tsuji 2010), comparison of genomes, mapping of DNA-binding proteins and chromatin analysis, epigenetics [reviewed in (Capell and Berger 2013;Mensaert et al 2014)], methylation analysis [reviewed in (Olkhov-Mitsel and Bapat 2012)], or meta-genomics [reviewed in (Cox et al 2013;Miller et al 2013)]. …”

Section: Lab-on-a-chip Devices: Applicable For Multiparametricmentioning

confidence: 99%

RNA and DNA Diagnostics

Erdmann¹,

Jurga²,

Barciszewski³

2015

RNA Technologies

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“…The term epigenetics was coined by Conrad Waddington to describe "the branch of biology which studies the casual interactions between genes and their products, which bring the phenotype into being" [54]. Today the term broadly applies to changes in gene regulation and cellular phenotype without changes to the DNA sequence itself, as the phenotype of a cell is determined by its expression profile [55].…”

Section: Overview Of Epigeneticsmentioning

confidence: 99%

The Potential Role of Epigenetics in Alzheimer?s Disease Etiology

Shewale¹,

Huebinger²,

Allen³

et al. 2012

Biol Syst Open Access

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Alzheimer's disease (AD) is an etiologically heterogeneous disorder. While many genes have been found to be associated with Early and Late onset AD, a large portion of the predicted heritability remains unidentified. Here we review AD pathology, with an overview of AD genetics. In addition, we review epigenetic mechanisms and the current literature that suggests a relationship between epigenetic mechanisms and AD pathology. The genome wide association studies conducted to date can explain a percentage of AD cases. The remainder may be best explained by complex interactions between epigenetic and environmental factors that differ between individuals.hypothesis postulates that the disease is the result of an imbalance between the production and degradation of β-Amyloid [9]. Normally, β-Amyloidis degraded by peptidases such as neprilysin, insulindegrading enzyme, and endothelin-converting enzyme [2]. This central theory has strong support, from work beginning with Alois Alzheimer [1]and continuing through the deduction of the sequence of the amyloid beta protein [10] and cloning of mutations in APP [11,12], PSEN1 and PSEN2genes [13,14]. A recent development that significantly strengthened the amyloid hypothesis was the discovery by Jonssonet al.[15] of an APP mutation that reduces production of β-Amyloid and is protective against Alzheimer's disease as well as age-related cognitive decline.It has been hypothesized that β-Amyloid protein deposition precedes neurofibrillary tangles [16], cell loss, and vascular damage [17]. In transgenic murinemodels, β-Amyloid deposition developed prior to tangles [18]. Working witha transgenic mouse model, Xu et al. [16] described an accumulation of β-Amyloid precipitateda loss of solubility of intracellular cytosolic proteins such as glycolytic enzymes and members of the chaperone family. β-Amyloidplaques have also been thought to induce neuronal oxidative stress, resulting in phospholipid peroxidation and protein oxidation in AD brain [19].The second hallmark of AD is the presence of hyperphosphorylated microtubule associated protein tau (MAPT). The tau protein is primarily expressed in neurons [20] and has been shown to be involved with tubulin polymerization as well as acting to stabilize microtubules against depolymerization [21], stabilize microtubules responsible for axonal transport [20], increase neuritic stability, impact the rate of neurite elongation, and increase net microtubule stability [2,22]. Different iso forms of the tau protein are expressed due to alternative RNA splicing, and all iso forms are capable of forming the fibrillary tangles that are a hallmark of AD [23] , [23,24]. A balance between kinases (ex. GSK-3Beta, CDK5) and phosphatases (ex. PP-1,PP2) plays a role in regulating tau phosphorylation [2]. Tau A widely held theory of AD pathogenesis is the amyloid cascade hypothesis, which states that the deposition of the β-Amyloidpeptide in the brain is the initiating event in disease pathology [8]. The amyloid

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Genome-Wide Epigenetics

Cited by 19 publications

References 10 publications

Research Techniques Made Simple: Bioinformatics for Genome-Scale Biology

Research Techniques Made Simple: Bioinformatics for Genome-Scale Biology

RNA and DNA Diagnostics

The Potential Role of Epigenetics in Alzheimer?s Disease Etiology

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