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https://www.readbyqxmd.com/read/27913677/phlpping-through-history-a-decade-in-the-life-of-phlpp-phosphatases
#1
REVIEW
Agnieszka T Grzechnik, Alexandra C Newton
In the decade since their discovery, the PH domain leucine-rich repeat protein phosphatases (PHLPP) have emerged as critical regulators of cellular homeostasis, and their dysregulation is associated with various pathophysiologies, ranging from cancer to degenerative diseases, such as diabetes and heart disease. The two PHLPP isozymes, PHLPP1 and PHLPP2, were identified in a search for phosphatases that dephosphorylate Akt, and thus suppress growth factor signaling. However, given that there are over 200 000 phosphorylated residues in a single cell, and fewer than 50 Ser/Thr protein phosphatases, it is not surprising that PHLPP has many other cellular functions yet to be discovered, including a recently identified role in regulating the epigenome...
December 15, 2016: Biochemical Society Transactions
https://www.readbyqxmd.com/read/27913608/the-clinical-utility-of-circulating-neuroendocrine-gene-transcript-analysis-in-well-differentiated-paragangliomas-and-pheochromocytomas
#2
M Pęczkowska, J Cwikla, M Kidd, A Lewczuk, A Kolasinska-Ćwikła, D Niec, I Michałowska, A Prejbisz, A Januszewicz, J Chiarelli, L Bodei, I Modlin
CONTEXT: Paragangliomas and pheochromocytomas (PPGLs) exhibit variable malignancy, which is difficult to determine by histopathology, amine measurements or tissue genetic analyses. OBJECTIVE: To evaluate whether a 51-neuroendocrine gene blood analysis has clinical utility as a diagnostic and prognostic marker. DESIGN: Prospective cohort study. Well-differentiated PPGLs (n = 32), metastatic (n = 4); SDHx mutation (n = 25); 12 biochemically active, Lanreotide treated (n = 4)...
February 2017: European Journal of Endocrinology
https://www.readbyqxmd.com/read/27912061/tumor-interferon-signaling-regulates-a-multigenic-resistance-program-to-immune-checkpoint-blockade
#3
Joseph L Benci, Bihui Xu, Yu Qiu, Tony J Wu, Hannah Dada, Christina Twyman-Saint Victor, Lisa Cucolo, David S M Lee, Kristen E Pauken, Alexander C Huang, Tara C Gangadhar, Ravi K Amaravadi, Lynn M Schuchter, Michael D Feldman, Hemant Ishwaran, Robert H Vonderheide, Amit Maity, E John Wherry, Andy J Minn
Therapeutic blocking of the PD1 pathway results in significant tumor responses, but resistance is common. We demonstrate that prolonged interferon signaling orchestrates PDL1-dependent and PDL1-independent resistance to immune checkpoint blockade (ICB) and to combinations such as radiation plus anti-CTLA4. Persistent type II interferon signaling allows tumors to acquire STAT1-related epigenomic changes and augments expression of interferon-stimulated genes and ligands for multiple T cell inhibitory receptors...
December 1, 2016: Cell
https://www.readbyqxmd.com/read/27911260/population-scale-mapping-of-transposable-element-diversity-reveals-links-to-gene-regulation-and-epigenomic-variation
#4
Tim Stuart, Steven Eichten, Jonathan Cahn, Yuliya Karpievitch, Justin Borevitz, Ryan Lister
Variation in the presence or absence of transposable elements (TEs) is a major source of genetic variation between individuals. Here, we identified 23,095 TE presence/absence variants between 216 Arabidopsis accessions. Most TE variants were rare, and we find these rare variants associated with local extremes of gene expression and DNA methylation levels within the population. Of the common alleles identified, two thirds were not in linkage disequilibrium with nearby SNPs, implicating these variants as a source of novel genetic diversity...
December 2, 2016: ELife
https://www.readbyqxmd.com/read/27909437/differentially-methylated-dna-regions-in-monozygotic-twin-pairs-discordant-for-rheumatoid-arthritis-an-epigenome-wide-study
#5
Anders J Svendsen, Kristina Gervin, Robert Lyle, Lene Christiansen, Kirsten Kyvik, Peter Junker, Christian Nielsen, Gunnar Houen, Qihua Tan
OBJECTIVES: In an explorative epigenome-wide association study (EWAS) to search for gene independent, differentially methylated DNA positions and regions (DMRs) associated with rheumatoid arthritis (RA) by studying monozygotic (MZ) twin pairs discordant for RA. METHODS: Genomic DNA was isolated from whole blood samples from 28 MZ twin pairs discordant for RA. DNA methylation was measured using the HumanMethylation450 BeadChips. Smoking, anti-cyclic citrullinated peptide antibodies, and immunosuppressive treatment were included as covariates...
2016: Frontiers in Immunology
https://www.readbyqxmd.com/read/27906046/chromatin-landscapes-and-genetic-risk-in-systemic-lupus
#6
Joyce S Hui-Yuen, Lisha Zhu, Lai Ping Wong, Kaiyu Jiang, Yanmin Chen, Tao Liu, James N Jarvis
BACKGROUND: Systemic lupus erythematosus (SLE) is a multi-system, complex disease in which the environment interacts with inherited genes to produce broad phenotypes with inter-individual variability. Of 46 single nucleotide polymorphisms (SNPs) shown to confer genetic risk for SLE in recent genome-wide association studies, 30 lie within noncoding regions of the human genome. We therefore sought to identify and describe the functional elements (aside from genes) located within these regions of interest...
December 1, 2016: Arthritis Research & Therapy
https://www.readbyqxmd.com/read/27903908/ing1-regulates-rrna-levels-by-altering-nucleolar-chromatin-structure-and-mtor-localization
#7
Uma Karthika Rajarajacholan, Subhash Thalappilly, Karl Riabowol
Epigenetic, transcriptional and signaling processes in the nucleolus regulate rRNA transcription and cell growth. We report here that the tumor suppressor ING1b binds rDNA, regulates rDNA chromatin modifications and affects nucleolar localization of mTOR to modulate rRNA levels. ING1 represses rDNA transcription by recruiting HDAC1 to rDNA loci, increasing its association with the NoRC complex and deacetylating the histone H3K9 and H3K27 marks of active transcription. Loss of ING1 enhances nucleolar localization of phospho-mTOR and its association with Raptor and GβL, even during rapamycin treatment...
November 29, 2016: Nucleic Acids Research
https://www.readbyqxmd.com/read/27899935/editorial-advances-in-genomics-and-epigenomics-of-social-insects
#8
EDITORIAL
Greg J Hunt, Juergen R Gadau
No abstract text is available yet for this article.
2016: Frontiers in Genetics
https://www.readbyqxmd.com/read/27899645/efficient-targeted-dna-methylation-with-chimeric-dcas9-dnmt3a-dnmt3l-methyltransferase
#9
Peter Stepper, Goran Kungulovski, Renata Z Jurkowska, Tamir Chandra, Felix Krueger, Richard Reinhardt, Wolf Reik, Albert Jeltsch, Tomasz P Jurkowski
DNA methylation plays a critical role in the regulation and maintenance of cell-type specific transcriptional programs. Targeted epigenome editing is an emerging technology to specifically regulate cellular gene expression in order to modulate cell phenotypes or dissect the epigenetic mechanisms involved in their control. In this work, we employed a DNA methyltransferase Dnmt3a-Dnmt3L construct fused to the nuclease-inactivated dCas9 programmable targeting domain to introduce DNA methylation into the human genome specifically at the EpCAM, CXCR4 and TFRC gene promoters...
November 29, 2016: Nucleic Acids Research
https://www.readbyqxmd.com/read/27898587/maternal-epigenetics-and-fetal-and-neonatal-growth
#10
Sofia Kitsiou-Tzeli, Maria Tzetis
PURPOSE OF REVIEW: The article provides an update on new insights of factors altering inherited maternal epigenome that ultimately affect fetal and neonatal growth. RECENT FINDINGS: A number of new publications have identified mechanisms through which maternal nutrition, environmental exposures such as stress and toxic substances altering expression of imprinted genes during pregnancy can influence fetal and neonatal phenotype and susceptibility to disease development later in life...
November 24, 2016: Current Opinion in Endocrinology, Diabetes, and Obesity
https://www.readbyqxmd.com/read/27898055/increased-dna-methylation-variability-in-type-1-diabetes-across-three-immune-effector-cell-types
#11
Dirk S Paul, Andrew E Teschendorff, Mary A N Dang, Robert Lowe, Mohammed I Hawa, Simone Ecker, Huriya Beyan, Stephanie Cunningham, Alexandra R Fouts, Anita Ramelius, Frances Burden, Samantha Farrow, Sophia Rowlston, Karola Rehnstrom, Mattia Frontini, Kate Downes, Stephan Busche, Warren A Cheung, Bing Ge, Marie-Michelle Simon, David Bujold, Tony Kwan, Guillaume Bourque, Avik Datta, Ernesto Lowy, Laura Clarke, Paul Flicek, Emanuele Libertini, Simon Heath, Marta Gut, Ivo G Gut, Willem H Ouwehand, Tomi Pastinen, Nicole Soranzo, Sabine E Hofer, Beate Karges, Thomas Meissner, Bernhard O Boehm, Corrado Cilio, Helena Elding Larsson, Åke Lernmark, Andrea K Steck, Vardhman K Rakyan, Stephan Beck, R David Leslie
The incidence of type 1 diabetes (T1D) has substantially increased over the past decade, suggesting a role for non-genetic factors such as epigenetic mechanisms in disease development. Here we present an epigenome-wide association study across 406,365 CpGs in 52 monozygotic twin pairs discordant for T1D in three immune effector cell types. We observe a substantial enrichment of differentially variable CpG positions (DVPs) in T1D twins when compared with their healthy co-twins and when compared with healthy, unrelated individuals...
November 29, 2016: Nature Communications
https://www.readbyqxmd.com/read/27897002/a-methylation-to-expression-feature-model-for-generating-accurate-prognostic-risk-scores-and-identifying-disease-targets-in-clear-cell-kidney-cancer
#12
Jeffrey A Thompson, Carmen J Marsit
Many researchers now have available multiple high-dimensional molecular and clinical datasets when studying a disease. As we enter this multi-omic era of data analysis, new approaches that combine different levels of data (e.g. at the genomic and epigenomic levels) are required to fully capitalize on this opportunity. In this work, we outline a new approach to multi-omic data integration, which combines molecular and clinical predictors as part of a single analysis to create a prognostic risk score for clear cell renal cell carcinoma...
2016: Pacific Symposium on Biocomputing
https://www.readbyqxmd.com/read/27895806/genome-wide-epigenomic-profiling-for-biomarker-discovery
#13
REVIEW
René A M Dirks, Hendrik G Stunnenberg, Hendrik Marks
A myriad of diseases is caused or characterized by alteration of epigenetic patterns, including changes in DNA methylation, post-translational histone modifications, or chromatin structure. These changes of the epigenome represent a highly interesting layer of information for disease stratification and for personalized medicine. Traditionally, epigenomic profiling required large amounts of cells, which are rarely available with clinical samples. Also, the cellular heterogeneity complicates analysis when profiling clinical samples for unbiased genome-wide biomarker discovery...
2016: Clinical Epigenetics
https://www.readbyqxmd.com/read/27895805/blood-based-dna-methylation-as-biomarker-for-breast-cancer-a-systematic-review
#14
REVIEW
Qiuqiong Tang, Jie Cheng, Xue Cao, Harald Surowy, Barbara Burwinkel
Multiple studies have investigated global DNA methylation profiles and gene-specific DNA methylation in blood-based DNA to develop powerful screening markers for cancer. This systematic review summarizes the current evidence on methylation studies that investigated methylation level of blood-derived DNA of breast cancer (BC) patients in comparison to healthy controls by conducting a systematic literature review in PubMed and Web of Science. Essential results, such as methylation levels of BC cases and healthy controls, p values, and odds ratios, were extracted from these studies by two investigators independently...
2016: Clinical Epigenetics
https://www.readbyqxmd.com/read/27893464/the-h3k9-dimethyltransferases-ehmt1-2-protect-against-pathological-cardiac-hypertrophy
#15
Bernard Thienpont, Jan Magnus Aronsen, Emma Louise Robinson, Hanneke Okkenhaug, Elena Loche, Arianna Ferrini, Patrick Brien, Kanar Alkass, Antonio Tomasso, Asmita Agrawal, Olaf Bergmann, Ivar Sjaastad, Wolf Reik, Hywel Llewelyn Roderick
Cardiac hypertrophic growth in response to pathological cues is associated with reexpression of fetal genes and decreased cardiac function and is often a precursor to heart failure. In contrast, physiologically induced hypertrophy is adaptive, resulting in improved cardiac function. The processes that selectively induce these hypertrophic states are poorly understood. Here, we have profiled 2 repressive epigenetic marks, H3K9me2 and H3K27me3, which are involved in stable cellular differentiation, specifically in cardiomyocytes from physiologically and pathologically hypertrophied rat hearts, and correlated these marks with their associated transcriptomes...
November 28, 2016: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/27892767/epigenetic-modifications-in-multiple-myeloma-recent-advances-on-the-role-of-dna-and-histone-methylation
#16
Nicola Amodio, Patrizia D'Aquila, Giuseppe Passarino, Pierfrancesco Tassone, Dina Bellizzi
Multiple Myeloma (MM) is a clonal late B-cell disorder accounting for about 13% of hematological cancers and 1% of all neoplastic diseases. Recent studies on the molecular pathogenesis and biology of MM have highlighted a complex epigenomic landscape contributing to MM onset, prognosis and high individual variability. Areas covered: We describe here the current knowledge on epigenetic events characterizing MM initiation and progression, focusing on the role of DNA and histone methylation and on the most promising epi-therapeutic approaches targeting the methylation pathway...
November 28, 2016: Expert Opinion on Therapeutic Targets
https://www.readbyqxmd.com/read/27892496/ewas-epigenome-wide-association-studies-software-1-0-identifying-the-association-between-combinations-of-methylation-levels-and-diseases
#17
Jing Xu, Di Liu, Linna Zhao, Ying Li, Zhaoyang Wang, Yang Chen, Changgui Lei, Lin Gao, Fanwu Kong, Lijun Yuan, Yongshuai Jiang
Similar to the SNP (single nucleotide polymorphism) data, there is non-random association of the DNA methylation level (we call it methylation disequilibrium, MD) between neighboring methylation loci. For the case-control study of complex diseases, it is important to identify the association between methylation levels combination types (we call it methylecomtype) and diseases/phenotypes. We extended the classical framework of SNP haplotype-based association study in population genetics to DNA methylation level data, and developed a software EWAS to identify the disease-related methylecomtypes...
November 28, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27891192/the-quest-for-an-effective-and-safe-personalized-cell-therapy-using-epigenetic-tools
#18
REVIEW
T A L Brevini, G Pennarossa, E F M Manzoni, C E Gandolfi, A Zenobi, F Gandolfi
In the presence of different environmental cues that are able to trigger specific responses, a given genotype has the ability to originate a variety of different phenotypes. This property is defined as plasticity and allows cell fate definition and tissue specialization. Fundamental epigenetic mechanisms drive these modifications in gene expression and include DNA methylation, histone modifications, chromatin remodeling, and microRNAs. Understanding these mechanisms can provide powerful tools to switch cell phenotype and implement cell therapy...
2016: Clinical Epigenetics
https://www.readbyqxmd.com/read/27891191/birth-weight-for-gestational-age-is-associated-with-dna-methylation-at-birth-and-in-childhood
#19
Golareh Agha, Hanine Hajj, Sheryl L Rifas-Shiman, Allan C Just, Marie-France Hivert, Heather H Burris, Xihong Lin, Augusto A Litonjua, Emily Oken, Dawn L DeMeo, Matthew W Gillman, Andrea A Baccarelli
BACKGROUND: Both higher and lower fetal growth are associated with cardio-metabolic health later in life, suggesting that prenatal developmental programming determines long-term cardiovascular disease risk. Epigenetic mechanisms, which orchestrate fetal growth and development, may offer insight on the early programming of health and disease. We investigated whether birth weight-for-gestational is associated with DNA methylation at birth and mid-childhood, measured via the Infinium 450K array...
2016: Clinical Epigenetics
https://www.readbyqxmd.com/read/27890672/epigenetics-of-cell-fate-reprogramming-and-its-implications-for-neurological-disorders-modelling
#20
REVIEW
Maciej Grzybek, Aleksandra Golonko, Marta Walczak, Pawel Lisowski
The reprogramming of human induced pluripotent stem cells (hiPSCs) proceeds in a stepwise manner with reprogramming factors binding and epigenetic composition changes during transition to maintain the epigenetic landscape, important for pluripotency. There arises a question as to whether the aberrant epigenetic state after reprogramming leads to epigenetic defects in induced stem cells causing unpredictable long term effects in differentiated cells. In this review, we present a comprehensive view of epigenetic alterations accompanying reprogramming, cell maintenance and differentiation as factors that influence applications of hiPSCs in stem cell based technologies...
November 23, 2016: Neurobiology of Disease
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