'; ?> geneimprint : Hot off the Press http://www.geneimprint.com/site/hot-off-the-press Daily listing of the most recent articles in epigenetics and imprinting, collected from the PubMed database. en-us Sun, 31 Aug 2014 11:26:55 PDT Sun, 31 Aug 2014 11:26:55 PDT jirtle@radonc.duke.edu james001@jirtle.com Genetic differentiation of hypothalamus parentally biased transcripts in populations of the house mouse implicate the Prader-Willi syndrome imprinted region as a possible source of behavioral divergence. Lorenc A, Linnenbrink M, Montero I, Schilhabel MB, Tautz D
Mol Biol Evol (Aug 2014)

Parentally biased expression of transcripts (genomic imprinting) in adult tissues, including the brain, can influence and possibly drive the evolution of behavioral traits. We have previously found that paternally determined cues are involved in population-specific mate choice decisions between two populations of the Western house mouse (M. m. domesticus). Here we ask whether this could be mediated by genomically imprinted transcripts that are subject to fast differentiation between these populations. We focus on three organs that are of special relevance for mate choice and behavior: the vomeronasal organ (VNO), the hypothalamus, and the liver. To first identify candidate transcripts at a genome-wide scale, we used reciprocal crosses between M. m. domesticus and M. m. musculus inbred strains and RNA sequencing of the respective tissues. Using a false discovery cutoff derived from mock reciprocal cross comparisons, we find a total of 66 imprinted transcripts, 13 of which have previously not been described as imprinted. The largest number of imprinted transcripts were found in the hypothalamus; fewer were found in the VNO, and the least were found in the liver. To assess molecular differentiation and imprinting in the wild-derived M. m. domesticus populations, we sequenced the RNA of the hypothalamus from individuals of these populations. This confirmed the presence of the above identified transcripts also in wild populations and allowed us to search for those that show a high genetic differentiation between these populations. Our results identify the Ube3a - Snrpn imprinted region on chromosome 7 as a region that encompasses the largest number of previously not described transcripts with paternal expression bias, several of which are at the same time highly differentiated. For four of these, we confirmed their imprinting status via SNP-specific pyro-sequencing assays with RNA from reciprocal crosses. In addition, we find the paternally expressed Peg13 transcript within the Trappc9 gene region on chromosome 15 to be highly differentiated. Interestingly, both regions have been implicated in Prader-Willi nervous system disorders in humans. We suggest that these genomically imprinted regions are candidates for influencing the population-specific mate-choice in mice.]]>
Sat, 30 Aug 2014 00:00:00 PDT
Long Noncoding RNAs: Emerging Stars in Gene Regulation, Epigenetics and Human Disease. Bhan A, Mandal SS
ChemMedChem (Sep 2014)

Noncoding RNAs (ncRNAs) are classes of transcripts that are encoded by the genome and transcribed but never get translated into proteins. Though not translated into proteins, ncRNAs play pivotal roles in a variety of cellular functions. Here, we review the functions of long noncoding RNAs (lncRNAs) and their implications in various human diseases. Increasing numbers of studies demonstrate that lncRNAs play critical roles in regulation of protein-coding genes, maintenance of genomic integrity, dosage compensation, genomic imprinting, mRNA processing, cell differentiation, and development. Misregulation of lncRNAs is associated with a variety of human diseases, including cancer, immune and neurological disorders. Different classes of lncRNAs, their functions, mechanisms of action, and associations with different human diseases are summarized in detail, highlighting their as yet untapped potential in therapy.]]>
Fri, 29 Aug 2014 00:00:00 PDT
Genome-wide DNA methylation patterns in LSH mutant reveals de-repression of repeat elements and redundant epigenetic silencing pathways. Yu W, McIntosh C, Lister R, Zhu I, Han Y, Ren J, Landsman D, Lee E, Briones V, Terashima M, Leighty R, Ecker JR, Muegge K
Genome Res (Aug 2014)

Cytosine methylation is critical in mammalian development and plays a role in diverse biologic processes such as genomic imprinting, X chromosome inactivation, and silencing of repeat elements. Several factors regulate DNA methylation in early embryogenesis, but their precise role in the establishment of DNA methylation at a given site remains unclear. We have generated a comprehensive methylation map in fibroblasts derived from the murine DNA methylation mutant Hells(-/-) (helicase, lymphoid specific, also known as LSH). It has been previously shown that HELLS can influence de novo methylation of retroviral sequences and endogenous genes. Here, we describe that HELLS controls cytosine methylation in a nuclear compartment that is in part defined by lamin B1 attachment regions. Despite widespread loss of cytosine methylation at regulatory sequences, including promoter regions of protein-coding genes and noncoding RNA genes, overall relative transcript abundance levels in the absence of HELLS are similar to those in wild-type cells. A subset of promoter regions shows increases of the histone modification H3K27me3, suggesting redundancy of epigenetic silencing mechanisms. Furthermore, HELLS modulates CG methylation at all classes of repeat elements and is critical for repression of a subset of repeat elements. Overall, we provide a detailed analysis of gene expression changes in relation to DNA methylation alterations, which contributes to our understanding of the biological role of cytosine methylation.]]>
Fri, 29 Aug 2014 00:00:00 PDT
The miR-379/miR-410 cluster at the imprinted Dlk1-Dio3 domain controls neonatal metabolic adaptation. Labialle S, Marty V, Bortolin-Cavaillé ML, Hoareau-Osman M, Pradère JP, Valet P, Martin PG, Cavaillé J
EMBO J (Aug 2014)

In mammals, birth entails complex metabolic adjustments essential for neonatal survival. Using a mouse knockout model, we identify crucial biological roles for the miR-379/miR-410 cluster within the imprinted Dlk1-Dio3 region during this metabolic transition. The miR-379/miR-410 locus, also named C14MC in humans, is the largest known placental mammal-specific miRNA cluster, whose 39 miRNA genes are expressed only from the maternal allele. We found that heterozygote pups with a maternal-but not paternal-deletion of the miRNA cluster display partially penetrant neonatal lethality with defects in the maintenance of energy homeostasis. This maladaptive metabolic response is caused, at least in part, by profound changes in the activation of the neonatal hepatic gene expression program, pointing to as yet unidentified regulatory pathways that govern this crucial metabolic transition in the newborn's liver. Not only does our study highlight the physiological importance of miRNA genes that recently evolved in placental mammal lineages but it also unveils additional layers of RNA-mediated gene regulation at the Dlk1-Dio3 domain that impose parent-of-origin effects on metabolic control at birth and have likely contributed to mammal evolution.]]>
Thu, 21 Aug 2014 00:00:00 PDT
Histone deacetylase 9 represses cholesterol efflux and alternatively activated macrophages in atherosclerosis development. Cao Q, Rong S, Repa JJ, Clair RS, Parks JS, Mishra N
Arterioscler Thromb Vasc Biol (Sep 2014)

Recent genome-wide association studies revealed that a genetic variant in the loci corresponding to histone deacetylase 9 (HDAC9) is associated with large vessel stroke. HDAC9 expression was upregulated in human atherosclerotic plaques in different arteries. The molecular mechanisms how HDAC9 might increase atherosclerosis is not clear.]]>
Thu, 21 Aug 2014 00:00:00 PDT
DNA modifications in the mammalian brain. Shin J, Ming GL, Song H
Philos Trans R Soc Lond B Biol Sci (Sep 2014)

DNA methylation is a crucial epigenetic mark in mammalian development, genomic imprinting, X-inactivation, chromosomal stability and suppressing parasitic DNA elements. DNA methylation in neurons has also been suggested to play important roles for mammalian neuronal functions, and learning and memory. In this review, we first summarize recent discoveries and fundamental principles of DNA modifications in the general epigenetics field. We then describe the profiles of different DNA modifications in the mammalian brain genome. Finally, we discuss roles of DNA modifications in mammalian brain development and function.]]>
Tue, 19 Aug 2014 00:00:00 PDT
DNA methyltransferase haplotype is associated with Alzheimer's disease. Pezzi JC, Ens CM, Borba EM, Schumacher-Schuh AF, de Andrade FM, Chaves ML, Fiegenbaum M, Camozzato AL
Neurosci Lett (Sep 2014)

Epigenetic mechanisms have been implicated in syndromes associated with neuropsychiatric disorders, but little is known about the role of epigenetics in Alzheimer's disease (AD). DNA methylation, one of the main epigenetic mechanisms, is a complex process carried out by specific enzymes, such as DNMT1 and DNMT3B. This study aimed to investigate the association between DNMT1 and DNMT3B polymorphisms and AD. Two hundred and ten elderly subjects (108 healthy controls and 102 with AD-NINCDS/ARDA, DSM-IV-TR criteria) were assessed. DNA was obtained from whole blood, and genotypes were detected by an allelic discrimination assay using TaqMan(®) MGB probes on a real-time PCR system. The polymorphisms studied were rs2162560, rs759920 (DNMT1) and rs998382, rs2424913, rs2424932 (DNMT3B). For both genes, the polymorphisms were in strong linkage disequilibrium. Carriers of the DNMT3B TGG haplotype were associated with AD (OR=3.03, 95% CI 1.63 to 5.63, P<0.001). No significant difference between AD and the control group were observed for DNMT1 polymorphisms. This study is one of the first describing a significant association between DNMT3B polymorphisms and AD. This enzyme, which is responsible for methylation in a general way, may be involved in AD.]]>
Mon, 18 Aug 2014 00:00:00 PDT
Comparative epigenomics: defining and utilizing epigenomic variations across species, time-course, and individuals. Xiao S, Cao X, Zhong S
Wiley Interdiscip Rev Syst Biol Med (Sep 2014)

Epigenomic profiling, by revealing genome-wide distributions of epigenetic modifications, generated a large amount of structural information about the chromosomes. Epigenomic analysis has quickly become a big data science, posing tremendous challenges on its translation into knowledge. To meet this challenge, comparative analysis of epigenomes, dubbed comparative epigenomics, has emerged as an active research area. Here, we summarize the recent developments in comparative epigenomic analyses into three major directions, namely the comparisons across species, the time-course of a biological process, and individuals. We review the main ideas, methods, and findings in each direction, and discuss the implications to understanding the regulatory functions of the genomes. WIREs Syst Biol Med 2014, 6:345-352. doi: 10.1002/wsbm.1274 For further resources related to this article, please visit the WIREs website.]]>
Mon, 18 Aug 2014 00:00:00 PDT
Genome-wide association identifies regulatory Loci associated with distinct local histogram emphysema patterns. Castaldi PJ, Cho MH, San José Estépar R, McDonald ML, Laird N, Beaty TH, Washko G, Crapo JD, Silverman EK,  
Am J Respir Crit Care Med (Aug 2014)

Emphysema is a heritable trait that occurs in smokers with and without chronic obstructive pulmonary disease. Emphysema occurs in distinct pathologic patterns, but the genetic determinants of these patterns are unknown.]]>
Sat, 16 Aug 2014 00:00:00 PDT
Human in vitro oocyte maturation is not associated with increased imprinting error rates at LIT1, SNRPN, PEG3 and GTL2. Kuhtz J, Romero S, De Vos M, Smitz J, Haaf T, Anckaert E
Hum Reprod (Sep 2014)

Does in vitro maturation (IVM) of cumulus-enclosed germinal vesicle (GV) stage oocytes retrieved from small antral follicles in minimally stimulated cycles without an ovulatory hCG dose induce imprinting errors at LIT1, SNRPN, PEG3 and GTL2 in human oocytes?]]>
Fri, 15 Aug 2014 00:00:00 PDT
Epigenetic upregulation of large-conductance Ca2+-activated k+ channel expression in uterine vascular adaptation to pregnancy. Chen M, Dasgupta C, Xiong F, Zhang L
Hypertension (Sep 2014)

Our previous study demonstrated that pregnancy increased large-conductance Ca(2+)-activated potassium channel β1 subunit (BKβ1) expression and large-conductance Ca(2+)-activated potassium channel activity in uterine arteries, which were abrogated by chronic hypoxia. The present study tested the hypothesis that promoter methylation/demethylation is a key mechanism in epigenetic reprogramming of BKβ1 expression patterns in uterine arteries. Ovine BKβ1 promoter of 2315 bp spanning from -2211 to +104 of the transcription start site was cloned, and an Sp1-380 binding site that contains CpG dinucleotide in its core binding sequences was identified. Site-directed deletion of the Sp1 site significantly decreased the BKβ1 promoter activity. Estrogen receptor-α bound to the Sp1 site through tethering to Sp1 and upregulated the expression of BKβ1. The Sp1 binding site at BKβ1 promoter was highly methylated in uterine arteries of nonpregnant sheep, and methylation inhibited transcription factor binding and BKβ1 promoter activity. Pregnancy caused a significant decrease in CpG methylation at the Sp1 binding site and increased Sp1 binding to the BKβ1 promoter and BKβ1 mRNA abundance. Chronic hypoxia during gestation abrogated this pregnancy-induced demethylation and upregulation of BKβ1 expression. The results provide evidence of a novel mechanism of promoter demethylation in pregnancy-induced reprogramming of large-conductance Ca(2+)-activated potassium channel expression and function in uterine arteries and suggest new insights of epigenetic mechanisms linking gestational hypoxia to aberrant uteroplacental circulation and increased risk of preeclampsia.]]>
Fri, 15 Aug 2014 00:00:00 PDT
[Influence of assisted reproduction technologies on genomic imprinting of embryos and offspring]. Hu C, Wang L, Le F, Jin F
Zhonghua Yi Xue Yi Chuan Xue Za Zhi (Aug 2014)

Assisted reproduction technologies (ART) include controlled ovarian hyperstimulation, in vitro fertilization-embryo transfer, intracytoplasmic sperm injection, in vitro maturation of oocytes, pre-implantation genetic diagnosis, etc. They have been used for the treatment of impaired fertility but may damage the health of offspring. The ART procedures may alter the epigenetic status of these offspring and DNA methylation may be a crucial mechanism. This paper summarizes epigenetic alterations in ART embryos and offspring, and discusses the risks.]]>
Thu, 14 Aug 2014 00:00:00 PDT
Personalized nutrition and obesity. Qi L
Ann Med (Aug 2014)

Abstract The past few decades have witnessed a rapid rise in nutrition-related disorders such as obesity in the United States and over the world. Traditional nutrition research has associated various foods and nutrients with obesity. Recent advances in genomics have led to identification of the genetic variants determining body weight and related dietary factors such as intakes of energy and macronutrients. In addition, compelling evidence has lent support to interactions between genetic variations and dietary factors in relation to obesity and weight change. Moreover, recently emerging data from other 'omics' studies such as epigenomics and metabolomics suggest that more complex interplays between the global features of human body and dietary factors may exist at multiple tiers in affecting individuals' susceptibility to obesity; and a concept of 'personalized nutrition' has been proposed to integrate this novel knowledge with traditional nutrition research, with the hope ultimately to endorse person-centric diet intervention to mitigate obesity and related disorders.]]>
Mon, 04 Aug 2014 00:00:00 PDT
Reactivation of maternal SNORD116 cluster via SETDB1 knockdown in Prader-Willi syndrome iPSCs. Cruvinel E, Budinetz T, Germain N, Chamberlain S, Lalande M, Martins-Taylor K
Hum Mol Genet (Sep 2014)

Prader-Willi syndrome (PWS), a disorder of genomic imprinting, is characterized by neonatal hypotonia, hypogonadism, small hands and feet, hyperphagia and obesity in adulthood. PWS results from the loss of paternal copies of the cluster of SNORD116 C/D box snoRNAs and their host transcript, 116HG, on human chromosome 15q11-q13. We have investigated the mechanism of repression of the maternal SNORD116 cluster and 116HG. Here, we report that the zinc-finger protein ZNF274, in association with the histone H3 lysine 9 (H3K9) methyltransferase SETDB1, is part of a complex that binds to the silent maternal but not the active paternal alleles. Knockdown of SETDB1 in PWS-specific induced pluripotent cells (iPSCs) causes a decrease in the accumulation of H3K9 trimethylation (H3K9me3) at 116HG and corresponding accumulation of the active chromatin mark histone H3 lysine 4 dimethylation (H3K4me2). We also show that upon knockdown of SETDB1 in PWS-specific iPSCs, expression of maternally silenced 116HG RNA is partially restored. SETDB1 knockdown in PWS iPSCs also disrupts DNA methylation at the PWS-IC where a decrease in 5-methylcytosine is observed in association with a concomitant increase in 5-hydroxymethylcytosine. This observation suggests that the ZNF274/SETDB1 complex bound to the SNORD116 cluster may protect the PWS-IC from DNA demethylation during early development. Our findings reveal novel epigenetic mechanisms that function to repress the maternal 15q11-q13 region.]]>
Mon, 04 Aug 2014 00:00:00 PDT
Multi-ethnic fine-mapping of 14 central adiposity loci. Liu CT, Buchkovich ML, Winkler TW, Heid IM,  ,  , Borecki IB, Fox CS, Mohlke KL, North KE, Adrienne Cupples L
Hum Mol Genet (Sep 2014)

The Genetic Investigation of Anthropometric Traits (GIANT) consortium identified 14 loci in European Ancestry (EA) individuals associated with waist-to-hip ratio (WHR) adjusted for body mass index. These loci are wide and narrowing the signals remains necessary. Twelve of 14 loci identified in GIANT EA samples retained strong associations with WHR in our joint EA/individuals of African Ancestry (AA) analysis (log-Bayes factor >6.1). Trans-ethnic analyses at five loci (TBX15-WARS2, LYPLAL1, ADAMTS9, LY86 and ITPR2-SSPN) substantially narrowed the signals to smaller sets of variants, some of which are in regions that have evidence of regulatory activity. By leveraging varying linkage disequilibrium structures across different populations, single-nucleotide polymorphisms (SNPs) with strong signals and narrower credible sets from trans-ethnic meta-analysis of central obesity provide more precise localizations of potential functional variants and suggest a possible regulatory role. Meta-analysis results for WHR were obtained from 77 167 EA participants from GIANT and 23 564 AA participants from the African Ancestry Anthropometry Genetics Consortium. For fine mapping we interrogated SNPs within ±250 kb flanking regions of 14 previously reported index SNPs from loci discovered in EA populations by performing trans-ethnic meta-analysis of results from the EA and AA meta-analyses. We applied a Bayesian approach that leverages allelic heterogeneity across populations to combine meta-analysis results and aids in fine-mapping shared variants at these locations. We annotated variants using information from the ENCODE Consortium and Roadmap Epigenomics Project to prioritize variants for possible functionality.]]>
Mon, 04 Aug 2014 00:00:00 PDT
Imprinted loci in domestic livestock species as epigenomic targets for artificial selection of complex traits. Magee DA, Spillane C, Berkowicz EW, Sikora KM, MacHugh DE
Anim Genet (Aug 2014)

The phenomenon of genomic imprinting, whereby a subset of mammalian genes display parent-of-origin-specific monoallelic expression, is one of the most active areas of epigenetics research. Over the past two decades, more than 100 imprinted mammalian genes have been identified, while considerable advances have been made in elucidating the molecular mechanisms governing imprinting. These studies have helped to unravel the epigenome - a separate layer of regulatory information contained in eukaryotic chromosomes that influences gene expression and phenotypes without involving changes to the underlying DNA sequence. Although most studies of genomic imprinting in mammals have focussed on mouse models or human biomedical disorders, there is burgeoning interest in the phenotypic effects of imprinted genes in domestic livestock species. In particular, research has focused on imprinted genes influencing foetal growth and development, which are associated with economically important production traits in cattle, sheep and pigs. These findings, when coupled with the data emerging from the various different livestock genome projects, have major implications for the future of animal breeding, health and management. Here, we review current scientific knowledge regarding genomic imprinting in livestock species and evaluate how this information can be used in modern livestock improvement programmes.]]>
Mon, 28 Jul 2014 00:00:00 PDT
A high-resolution whole-genome map of the distinctive epigenomic landscape induced by butyrate in bovine cells. Shin JH, Xu L, Li RW, Gao Y, Bickhart D, Liu GE, Baldwin R, Li CJ
Anim Genet (Aug 2014)

This report presents a study utilizing next-generation sequencing technology, combined with chromatin immunoprecipitation (ChIP-seq) technology to analyze histone modification induced by butyrate and to construct a high-definition map of the epigenomic landscape with normal histone H3 and H4 and their variants in bovine cells at the whole-genome scale. A total of 10 variants of histone H3 and H4 modifications were mapped at the whole-genome scale (acetyl-H3K18-ChIP-seq, trimethy-H3K9, histone H4 ChIP-seq, acetyl-H4K5 ChIP-seq, acetyl-H4K12 ChIP-seq, acetyl-H4K16 ChIP-seq, histone H3 ChIP-seq, acetyl H3H9 ChIP-seq, acetyl H3K27 ChIP-seq and tetra-acetyl H4 ChIP-seq). Integrated experiential data and an analysis of histone and histone modification at a single base resolution across the entire genome are presented. We analyzed the enriched binding regions in the proximal promoter (within 5 kb upstream or at the 5'-untranslated region from the transcriptional start site (TSS)), and the exon, intron and intergenic regions (defined by regions 25 kb upstream and 10 kb downstream from the TSS). A de novo search for the binding motif of the 10 ChIP-seq datasets discovered numerous motifs from each of the ChIP-seq datasets. These consensus sequences indicated that histone modification at different locations changes the histone H3 and H4 binding preferences. Nevertheless, a high degree of conservation in histone binding also was presented in these motifs. This first extensive epigenomic landscape mapping in bovine cells offers a new framework and a great resource for testing the role of epigenomes in cell function and transcriptomic regulation.]]>
Mon, 28 Jul 2014 00:00:00 PDT
Two deletions overlapping a distant FOXF1 enhancer unravel the role of lncRNA LINC01081 in etiology of alveolar capillary dysplasia with misalignment of pulmonary veins. Szafranski P, Dharmadhikari AV, Wambach JA, Towe CT, White FV, Grady RM, Eghtesady P, Cole FS, Deutsch G, Sen P, Stankiewicz P
Am J Med Genet A (Aug 2014)

Position effects due to disruption of distant cis-regulatory regions have been reported for over 40 human gene loci; however, the underlying mechanisms of long-range gene regulation remain largely unknown. We report on two patients with alveolar capillary dysplasia with misalignment of pulmonary veins (ACDMPV) caused by overlapping genomic deletions that included a distant FOXF1 transcriptional enhancer mapping 0.3 Mb upstream to FOXF1 on 16q24.1. In one patient with atypical late-onset ACDMPV, a ∼1.5 Mb deletion removed the proximal 43% of this enhancer, leaving the lung-specific long non-coding RNA (lncRNA) gene LINC01081 intact. In the second patient with severe neonatal-onset ACDMPV, an overlapping ∼194 kb deletion disrupted LINC01081. Both deletions arose de novo on maternal copy of the chromosome 16, supporting the notion that FOXF1 is paternally imprinted in the human lungs. RNAi-mediated knock-down of LINC01081 in normal fetal lung fibroblasts showed that this lncRNA positively regulates FOXF1 transcript level, further indicating that decrease in LINC01081 expression can contribute to development of ACDMPV. © 2014 Wiley Periodicals, Inc.]]>
Mon, 21 Jul 2014 00:00:00 PDT
Oxidized low-density lipoprotein induces long-term proinflammatory cytokine production and foam cell formation via epigenetic reprogramming of monocytes. Bekkering S, Quintin J, Joosten LA, van der Meer JW, Netea MG, Riksen NP
Arterioscler Thromb Vasc Biol (Aug 2014)

Although the role of monocytes in the pathogenesis of atherosclerosis is well established, the persistent vascular inflammation remains largely unexplained. Recently, our group reported that stimulation of monocytes with various microbial products can induce a long-lasting proinflammatory phenotype via epigenetic reprogramming, a process termed trained immunity. We now hypothesize that oxidized low-density lipoprotein (oxLDL) also induces a long-lasting proinflammatory phenotype in monocytes, which accelerates atherosclerosis by proinflammatory cytokine production and foam cell formation.]]>
Thu, 17 Jul 2014 00:00:00 PDT
The ways of action of long non-coding RNAs in cytoplasm and nucleus. Zhang K, Shi ZM, Chang YN, Hu ZM, Qi HX, Hong W
Gene (Aug 2014)

Over the past fifteen years, small regulatory RNAs, such as siRNA and miRNA, have been extensively investigated and the underlying molecular mechanisms have been well documented, suggesting that ncRNAs play a major function in many cellular processes. An expanding body of evidence reveals that long non-coding RNAs (lncRNAs), once described as dark matter, are involved in diverse cellular progresses, including regulation of gene expression, dosage compensation, genomic imprinting, nuclear organization and nuclear-cytoplasm trafficking via a number of complex mechanisms. The emerging links between lncRNAs and diseases as well as their tissue-specific expression patterns also indicate that lncRNAs comprise a core transcriptional regulatory circuitry. The function of lncRNAs is based on their sequence and structure; and they can combine with DNA, RNA, and proteins both in the nucleus and the cytoplasm. However, detailed insights into their biological and mechanistic functions are only beginning to emerge. In this review, we will mainly talk about diverse ways of action of lncRNAs in different sub-cellular locations and provide clues for following studies.]]>
Tue, 08 Jul 2014 00:00:00 PDT