geneimprint : Hot off the Press

'; ?> 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 Wed, 15 Apr 2026 09:55:35 EDT Wed, 15 Apr 2026 09:55:35 EDT jirtle@radonc.duke.edu james001@jirtle.com PCdb: A comprehensive plant genome-editing database integrating sgRNA efficiency, off-target predictions, and epigenomic landscapes. Wang F, Lu S, Zhu C, Yang L
Plant Commun (Apr 2026)

CRISPR-Cas-based genome editing has transformed plant biotechnology by enabling precise genomic modifications for crop improvement and functional genomics. The success of these applications hinges on the design of single guide RNAs (sgRNAs) that maximize on-target efficiency while minimizing off-target effects. However, existing resources for sgRNA design and performance evaluation in plants remain fragmented and lack integration with genomic and epigenomic contexts that influence both editing efficacy and specificity. Here, we present PCdb (Plant CRISPR Database; https://gmo.sjtu.edu.cn/pcdb), a comprehensive plant-focused database that integrates experimentally validated sgRNAs, annotated genomic contexts, genome-wide off-target predictions, and multilayer epigenomic annotations. PCdb encompasses 6172 manually curated editing records from 2132 publications, covering 4320 unique sgRNAs and 6 117 424 predicted off-target sites across nine major plant species. Notably, PCdb contextualizes potential editing outcomes-both on target and off target-within the chromatin landscape by incorporating DNA methylation profiles, chromatin accessibility data, and histone modification patterns. The database features an intuitive web interface that supports flexible queries, interactive visualization tools, and comprehensive analytical modules for sgRNA efficiency assessment and off-target analysis. A case study reanalysis of Oryza sativa yield-related genes demonstrates PCdb's ability to generate a detailed performance profile by evaluating both on-target characteristics and off-target risks within their native epigenomic context. Systematic analysis of the database further identifies key sequence and chromatin features that influence editing outcomes, providing novel insights to improve gene-editing efficacy and specificity.]]> Wed, 31 Dec 1969 19:00:00 EST Epigenetic analyses suggest different pathways during pregnancy for development of type 1 diabetes in children with high versus low-neutral human leukocyte antigen-risk. Alipoor SD, Ahrens A, Ãkesson J, Hillerton T, Gustafsson M, Lerm M, Ludvigsson J
J Intern Med (May 2026)

The development of Type 1 diabetes (T1D) is shaped by genetic predisposition and epigenetic regulation. Human leukocyte antigen (HLA) risk alleles are major genetic determinants, but the epigenetic landscape in relation to disease onset remains unclear. Early-life epigenetic modifications may reveal how environmental and epigenetic factors interact in T1D pathogenesis.]]> Wed, 31 Dec 1969 19:00:00 EST Interactions between nutrition and the epigenome: how can it be harnessed for public health? Anastasopoulou M, Dereki I, Sgourou A, Lagoumintzis G
Future Sci OA (Dec 2026)

A substantial body of evidence shows that dietary habits influence gene expression and epigenetic processes, holding significant implications for public health policies. Epigenetic modifications are increasingly associated with metabolic state, disease risk, and biological aging. Translating mechanistic results into scalable, efficient nutritional epigenetics treatments is difficult.]]> Wed, 31 Dec 1969 19:00:00 EST Multi-omics Approaches for Biomarker Discovery of Uterine Fibroids: A Systematic Review. Hussein F, Elamin O, Al-Hendy A, Mousa M
Adv Ther (Apr 2026)

Uterine fibroids are the most common benign gynecological tumors, affecting up to 70-80% of women, yet still lack clinically validated biomarkers for disease stratification, monitoring, or therapeutic targeting. Advances in multi-omics technologies offer unprecedented opportunities for biomarker discovery; however, their application in fibroid research remains fragmented across platforms, biological samples, and study designs, limiting translational progress.]]> Wed, 31 Dec 1969 19:00:00 EST Melatonin-enabled omics: understanding plant responses to single and combined abiotic stresses for climate-smart agriculture. Raza A, Li Y, Charagh S, Guo C, Zhao M, Hu Z
GM Crops Food (Dec 2026)

Climate change-driven single and combined abiotic stresses pose escalating threats to sustainable, climate-smart agriculture and global food security. Melatonin (MLT, a powerful plant biostimulant) has established noteworthy potential in improving stress tolerance by regulating diverse physiological, biochemical, and molecular responses. Therefore, this review delivers a comprehensive synopsis of MLT-enabled omics responses across genomics, transcriptomics, proteomics, metabolomics, miRNAomics, epigenomics, phenomics, ionomics, and microbiomics levels that collectively regulate plant adaptation to multiple abiotic stresses. We also highlight the crosstalk between these omics layers and the power of integrated multi-omics (panomics) approaches to harness the complex regulatory networks underlying MLT-enabled stress tolerance. Lastly, we argue for translating these omics insights into actionable strategies through advanced genetic engineering and synthetic biology platforms to develop MLT-enabled, stress-smart crop plants.]]> Wed, 31 Dec 1969 19:00:00 EST Cholangiocyte Biology in Primary Sclerosing Cholangitis and Other Cholangiopathies: . Jalan-Sakrikar N, Anwar AA, Ali A, Nasser-Ghodsi N, Felzen A, Huebert RC, LaRusso NF, O'Hara SP
Physiol Rev (Apr 2026)

Cholangiocytes are specialized epithelial cells that line the intrahepatic and extrahepatic biliary tree and play a critical role in bile modification, liver homeostasis, and response to injury. Cholangiocytes exhibit notable heterogeneity and plasticity, and their dysfunction is central to a spectrum of diseases targeting the bile ducts, collectively called cholangiopathies. These disorders include genetic, infectious, immune-mediated, and malignant diseases, with Primary Sclerosing Cholangitis (PSC) representing one of the most complex and enigmatic of these disorders. PSC is a progressive, fibro-inflammatory disease of the bile ducts that is closely linked to inflammatory bowel disease, carries a heightened risk of cancer, and lacks any approved therapies. This review explores the biology of cholangiocytes, including their development, functional plasticity, and roles in secretion, absorption, and cellular signaling. We provide a detailed examination of cholangiopathies, particularly PSC, a complex cholangiopathy characterized by a paradoxical state of cholangiocyte senescence and hyperproliferation. We describe how immune cell dysfunction, the gut microbiome, genetic predispositions, and environmental factors converge to mediate PSC pathogenesis. We revisit the foundational technologies that empowered early discoveries and shaped the field as we know it today. We also explore how newer techniques such as organoid cultures, single-cell transcriptomics, epigenomics, and spatialomics have transformed our modern understanding of biliary pathophysiology. Lastly, we provide an overview of existing rodent models of cholangiopathies and discuss their relevance to human disease. PSC remains therapeutically unaddressed, and thus ongoing multidisciplinary efforts are essential to developing targeted interventions. This review serves as a comprehensive resource for researchers and clinicians navigating the rapidly evolving landscape of cholangiocyte-centered liver disease research.]]> Wed, 31 Dec 1969 19:00:00 EST A cell type enrichment analysis tool for brain DNA methylation data (CEAM). MÃ¼ller J, Laroche VT, Imm J, Weymouth L, Harvey J, Reijnders RA, Smith AR, van den Hove D, Lunnon K, Cavill R, Pishva E
Epigenetics (Dec 2026)

DNA methylation (DNAm) signatures are highly cell type-specific, yet most epigenome-wide association studies (EWAS) are performed on bulk tissue, potentially obscuring critical cell type-specific patterns. Existing computational tools for detecting cell type-specific DNAm changes are often limited by the accuracy of cell type deconvolution algorithms. Here, we introduce CEAM (Cell-type Enrichment Analysis for Methylation), a robust and interpretable framework for cell type enrichment analysis in DNA methylation data. CEAM applies over-representation analysis with cell type-specific CpG panels from Illumina EPIC arrays derived from nuclei-sorted cortical post-mortem brains from neurologically healthy aged individuals. The constructed CpG panels were systematically evaluated using both simulated datasets and published EWAS results from Alzheimer's disease, Lewy body disease, and multiple sclerosis. CEAM demonstrated resilience to shifts in cell type composition, a common confounder in EWAS, and remained robust across a wide range of differentially methylated positions, when upstream modeling of cell type composition was modeled with sufficient accuracy. Application to existing EWAS findings generated in neurodegenerative diseases revealed enrichment patterns concordant with established disease biology, confirming CEAM's biological relevance. The workflow is publicly available as an interactive Shiny app (https://um-dementia-systems-biology.shinyapps.io/CEAM/) enabling rapid, interpretable analysis of cell type-specific DNAm changes from bulk EWAS.]]> Wed, 31 Dec 1969 19:00:00 EST Childhood immune imprinting shapes cohort and period influenza mortality. Hoffman KA, Saad-Roy CM, Mahmud AS
Sci Adv (Apr 2026)

Influenza viruses encountered in childhood can leave a lasting immunological imprint. To disentangle the mortality effects of age, the circulating seasonal strain, and immune history, we fit statistical mortality models to 54 years of influenza mortality data from the United States. We find strong signatures of subtype-level imprinting in H1N1-dominated seasons following the 2009 pandemic-cohorts imprinted with more similar H1N1 strains experience greater protection. Furthermore, we find large differences in age-specific mortality risk across cohorts based on their imprinted strain and the seasonal strains that were dominant throughout their lifetime. In contrast to older H1N1- and H2N2-imprinted cohorts, our results show that more recent cohorts imprinted with H3N2 have experienced substantially higher mortality through most of their lifetime. Our results highlight the long-term consequences of immune imprinting and its impact on period and cohort influenza mortality. Overall, our findings have important implications for vaccination efforts and future influenza mortality burden.]]> Wed, 31 Dec 1969 19:00:00 EST TiSMeD: A tissue-specific methylation and expression database for biomarker and translational applications. Cheng J, Lin Z, Wu L, Li Q, Yin H, Wang H, Chen H, Chen X, Ji ZL
Mol Ther Nucleic Acids (Jun 2026)

Tissue-specific methylation sites (TSMs) are important epigenetic features associated with gene regulation, tissue development, and disease pathogenesis. However, the lack of comprehensive and reliable resources for TSMs restricts advancements in epigenetic and translational research. We present TiSMeD (http://www.bio-add.org/TiSMeD/), a multi-omics database integrating 6,782 DNA methylation, 16,894 transcriptome, and 241 proteome profiles across 48 normal human tissues. Using a scoring framework based on SPM and Tscore, we identified 67,427 high-confidence TSMs, 4,607 tissue-specific genes, and 2,833 tissue-specific proteins, along with over 11 million housekeeping methylation sites. TiSMeD enables interactive exploration and data retrieval, supporting biomarker discovery and disease research. We demonstrate its utility in tracing the tissue-of-origin of cell-free DNA (cfDNA), prioritizing 1,849 cancer biomarkers from The Cancer Genome Atlas (TCGA), and constructing a multi-cancer tracing and diagnostic model achieving 95.7% accuracy. TiSMeD serves as a robust, user-friendly platform integrating multi-omics data to advance epigenetic research and biomarker translation.]]> Wed, 31 Dec 1969 19:00:00 EST Global analyses of genomic and epigenomic influences on gene expression reveal as a major regulator of cardiac gene expression in response to catecholamine challenge during heart failure. Lahue C, Ravindran S, Dalal A, Avetisyan R, Rau CD
Epigenetics (Dec 2026)

Heart failure arises from maladaptive remodelling driven by genetic and epigenetic networks. Using a systems genetics framework, we mapped how DNA variants and CpG methylation shape cardiac transcriptomes during beta adrenergic stress in the Hybrid Mouse Diversity Panel, a cohort of over 100 fully inbred mouse strains. Expression QTLs (eQTLs), methylation QTLs (mQTLs) and methylation-driven eQTLs (emQTLs) were generated from over 13k expressed genes and 200k hypervariable CpGs in left ventricles. We discovered hundreds of regulatory 'hotspots' that control large portions of the genome, including several that regulate over 10% of the transcriptome and/or methylome. Approximately 16% of these hotspots overlapped with prior GWAS or EWAS signals. We focus on a hotspot on chromosome 12 and identify the serpine peptidase inhibitor , as the most likely driver gene in this hotspot. Experimental knockdown of in neonatal rat ventricular cardiomyocytes blunted hypertrophy induced by a variety of hypertrophic signals, while altering predicted target expression and modulating the activity of and . Together, these findings position as a major regulator of stress-responsive cardiac gene programs, highlighting how integration of genetic and epigenetic signals can pinpoint key drivers of heart failure.]]> Wed, 31 Dec 1969 19:00:00 EST T-ChroNet: Time-aware chromatin network reconstruction to detect dynamic regulatory programs in longitudinal epigenetic dataset. Di Giovenale S, Lischio O, Cortile C, Corleone G, Fanciulli M, Bonchi F, Barozzi I
NAR Genom Bioinform (Jun 2026)

Networks are widely applied to investigate relationships among individual components of complex biological systems. Recent application of biological networks, such as gene co-expression networks and gene regulatory networks, has been instrumental to define principles of transcriptional modulation in development and disease. However, computational methods that can embed the activity of -regulatory elements (CRE) into a network are still limited. Capturing temporal CRE activity within a network could help reveal regulatory programs involved in cell fate commitment and disease development. To address this, we present T-ChroNet (Time-aware Chromatin Network), a network-based method that models CRE as nodes and their temporal co-accessibility as edges. Through the detection of CRE sharing similar accessibility patterns over time, T-ChroNet allows the inference of putative upstream regulators and downstream biological pathways. We applied T-ChroNet to temporally-resolved CRE datasets, from both human and mouse, including chromatin accessibility (ATAC-seq) and histone post-translational modifications (H3K27ac ChIP-seq). T-ChroNet successfully recovered known regulators and enriched pathways for both modalities and species, while also uncovering novel putative factors and mechanisms regulating cell identity, organ development and disease progression.]]> Wed, 31 Dec 1969 19:00:00 EST H2AK119ub1-MLL2 counteraction underlies heritable H3K27me3 formation in oocytes. Mei H, Kozuka C, Kumon M, Koseki H, Inoue A
Mol Cell (Apr 2026)

Polycomb group (PcG) and Trithorax group (TrxG) proteins establish bivalent chromatin marked by H3K27me3, H2AK119ub1, and H3K4me3. However, how bivalent chromatin is formed in vivo in mammals is poorly understood. In mouse oocytes, it arises at thousands of promoters, including noncanonical imprinted loci whose H3K27me3 is intergenerationally inherited by early embryos. Here, we show that H3K27me3 is deposited at H3K4me3-premarked promoters in an H2AK119ub1-dependent manner during oogenesis. We find that H2AK119ub1 deficiency causes transcriptional derepression and loss of H3K27me3 proportional to preexisting H3K4me3 levels in oocytes. Importantly, concomitant deficiency of H2AK119ub1 and MLL2-mediated H3K4me3 substantially restores transcriptional silencing and H3K27me3 deposition, leading to partial restoration of noncanonical imprinting in offspring. Taken together, we propose that H2AK119ub1 antagonizes MLL2 function to repress bivalent genes during oogenesis, thereby conferring heritable H3K27me3. This study reveals how PcG and TrxG counteraction shapes the maternal epigenome for the next generation's development.]]> Wed, 31 Dec 1969 19:00:00 EST H19 lncRNA in programming prenatal development and DOHaD due to maternal obesity. Islam S, Du M
Life Sci (Jun 2026)

Maternal obesity is a major global health challenge worldwide, significantly increasing the risk of pregnancy complications and long-term metabolic disorders in offspring. Maternal obesity, including associated gestational diabetes, induces epigenetic modifications that can reprogram fetal development and predispose children to lifelong health issues. Long non-coding RNA (lncRNA) H19, one of the first and most extensively studied lncRNAs, plays a pivotal role in developmental programming by regulating gene imprinting, microRNA processing, protein stabilization, and signaling pathways critical for growth and metabolism. Dysregulation of H19 expression under maternal obesity alters the H19/Igf2 (insulin-like growth factor 2) imprinting axis, disrupts skeletal muscle development, and modifies osteogenic and neurogenic pathways, thereby contributing to systemic insulin resistance, metabolic dysfunction, and neuro-disorder in offspring. This review highlights how maternal obesity reprograms offspring health through H19-mediated epigenetic and post-transcriptional regulation, emphasizing its role in the developmental origins of health and disease framework. Understanding the role of H19 offers valuable opportunities to develop targeted interventions that may reduce the transgenerational effects of obesity.]]> Wed, 31 Dec 1969 19:00:00 EST Geranium: Multimodal Retrieval of Genomics Data Visualizations. Nguyen HN, L'Yi S, Smits TC, Gao S, Zitnik M, Gehlenborg N
IEEE Trans Vis Comput Graph (Apr 2026)

Effective visualization is essential for interpreting genomics data, yet researchers often face challenges in finding relevant, reusable examples. Existing tools offer limited support for searching the vast landscape of genomics visualizations, making the process of authoring new visualizations time-consuming and inefficient. To address this gap, we introduce Geranium, a data visualization retrieval system for searching and authoring genomics visualizations. Geranium supports multimodal retrieval, enabling users to query with images, text, or grammar based specifications. Retrieved examples serve as scaffolds for authoring, providing templates that researchers can adapt with their own data, thereby streamlining the mechanics of visualization construction. Geranium integrates three embedding methods to combine specialized and general knowledge: grammar-based embeddings tailored to genomics visualizations, multimodalem beddings from a biomedical vision-language foundation model, and text embeddings from a fine-tuned large language model. For each visualization, we construct a multimodal representation that includes a Gosling specification, a pixel-based rendering, and natural language descriptions. We evaluate embedding strategies to maximize top-k retrieval accuracy and conduct user studies with domain collaborators to gather feedback on usability. Our collection comprises 3,200 visualizations across 50 categories, ranging from single-view to coordinated multi-view designs and supporting applications from single-cell epigenomics to structural variation analysis.]]> Wed, 31 Dec 1969 19:00:00 EST Long noncoding RNA H19 in liver development and disease. Montoya-Durango DE, Gobejishvili L
Cell Signal (Jun 2026)

Liver disease is a global health problem responsible for more than two million deaths annually. Metabolic dysfunction-associated steatotic liver disease (MASLD) and alcohol-associated liver disease (ALD) are major contributors to chronic liver disease-related morbidity and mortality. Factors like diet and alcohol consumption have become key drivers of liver pathologies including steatosis, fibrosis/cirrhosis, and hepatocellular carcinoma. To date very few treatments are available, hence there is a critical need for the development of novel therapies to slow down the development/progression of liver damage. The long non-coding RNA H19 gene, H19, is an imprinted gene normally expressed from the maternally inherited chromosome and epigenetically silenced in the paternal chromosome. At the embryo stage H19 controls genome-wide methylation, directs the methylation of the imprinted gene network, and regulates organ size. In the livers of neonates, H19 is important for organ maturation but remains silent in the mature organ. H19 re-expression in the adult liver drives de novo lipogenesis and fibrosis and maintains a proliferative state in tumor cells. The complexity of H19 functions in the liver is reflected in its interaction and regulation of a growing number of proteins, and coding and non-coding RNAs involved in metabolism, pro-fibrotic gene networks, cell cycle progression, and chromatin regulation. This review summarizes the findings related to the role of H19 in liver development and in diseases such as fatty liver, fibrosis, and hepatocellular carcinoma.]]> Wed, 31 Dec 1969 19:00:00 EST CUT&Tag for High-Resolution Epigenomic Profiling From a Low Amount of Tissue. Fu Y, Schmid MW, Simonini S
Plant Direct (Apr 2026)

The genome-wide profiling of chromatin states that are defined by different histone posttranslational modifications, known as epigenomic profiling, is crucial for understanding the epigenetic regulations of gene expression, both in animal and plant systems. CUT&Tag (Cleavage Under Targets and Tagmentation) is a novel enzyme-tethering method for epigenomic profiling, initially developed for mammalian cells. CUT&Tag has several advantages compared to the most commonly used epigenomic profiling methods such as chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-seq). CUT&Tag allows epigenenomic profiling from a much smaller amount of starting material compared to ChIP-seq. Moreover, CUT&Tag relies on inÂ situ DNA cleavage mediated by a transposase tethered to antibodies, while ChIP-seq typically involves nearly random DNA fragmentation. This fundamental difference raises the important question of whether CUT&Tag provides distinct advantages in terms of resolution and the precision of epigenomic profiles compared to ChIP-seq.]]> Wed, 31 Dec 1969 19:00:00 EST Exposome-induced dysregulation of glycemic homeostasis: Emerging biomarkers for diabetes risk and progression. Amalraj S, Karthick V, Thamarai R, Suganya M
Environ Pollut (May 2026)

Environmental exposures throughout life profoundly influence the development and progression of diabetes mellitus. The exposome, representing the totality of environmental exposures from conception to adulthood, interacts with genetic and metabolic pathways, leaving measurable signatures termed biomarkers. These biomarkers encompass indicators of exposure, biological effect, and susceptibility, providing mechanistic insights into glycemic regulation and disease progression. This review synthesizes current evidence on exposome-linked biomarkers in both Type 1 and Type 2 diabetes, highlighting chemical pollutants, dietary patterns, lifestyle factors, psychosocial stressors, and microbiome-derived metabolites as critical contributors to glycemic dysregulation. Advanced omics technologies, including metabolomics, proteomics, transcriptomics, and epigenomics, have facilitated the identification of these biomarkers, enabling a holistic understanding of environmental impacts on diabetes. Integrating exposomics with biomarker research offers potential for early detection, risk stratification, personalized interventions, and improved management of glycemic control. Knowledge gaps remain, particularly in longitudinal exposure mapping, causal inference, and translation into clinical practice. This review provides a comprehensive framework for understanding how environmental imprints shape metabolic health and identifies future directions for research in precision diabetes medicine.]]> Wed, 31 Dec 1969 19:00:00 EST Unraveling the complexity of skin's biological aging utilizing epigenetic clocks. Bienkowska A, Qi M, Kanta K, Del Pilar Bonilla-Tobar M, VÃ¶lzke H, Gallinat S, Jaspers S, Clemann S, Winnefeld M, GrÃ¶nniger E, Kaderali L, Falckenhayn C
Clin Epigenetics (Apr 2026)

DNA methylation (DNAm) plays a pivotal role in regulating gene expression and tissue function in the skin, which exhibits a high degree of responsiveness to environmental and lifestyle factors. These factors are believed to contribute to epigenetic drift, a hallmark of aging marked by increased methylation variability and changes in regulatory regions. While epigenetic clocks have advanced our understanding of skin aging, the effects of many modifiable factors on the skin methylome remain largely unknown.]]> Wed, 31 Dec 1969 19:00:00 EST Multiâomics and their integration in psoriasis research (Review). Zhang H, Li D, Zhu L, Yan H, Yang L, Yang X, Zhou Y
Mol Med Rep (May 2026)

Psoriasis is a chronic, immuneâmediated skin disorder characterized by keratinocyte hyperproliferation, inflammatory infiltrates and systemic comorbidities. While genetic predisposition and immune dysregulation are established contributors, recent advancements in highâthroughput omics technologies have provided deeper insights into the molecular complexity of psoriasis. The present review synthesized findings from various omics layers, genomics, epigenomics, transcriptomics, proteomics, metabolomics and microbiomics, to elucidate their roles in psoriasis pathogenesis. Largeâscale genomeâwide association studies have identified both common and regionâspecific susceptibility loci. Epigenetic factors and transcription factors regulate psoriasisârelated genes by modulating chromatin accessibility, DNA methylation, nonâcoding RNAs and direct gene activation/inactivation, thereby reshaping the transcriptome. Genetic and epigenetic influences also drive significant alterations in the proteome and metabolome, both in the skin and plasma, shedding light on disease mechanisms and offering potential for biomarker discovery. While microbiome research in psoriasis remains in its early stages, shifts in skin and gut microbial communities have been observed, suggesting their involvement in disease pathogenesis. Together, the multiâlayered insights underscore the future potential of integrated systems approaches to unravel disease mechanisms and support the discovery of clinically actionable biomarkers and therapeutic targets, paving the way for more precise diagnosis and targeted therapeutic development in psoriasis.]]> Wed, 31 Dec 1969 19:00:00 EST Partitioning genetic pleiotropy within tissue-specific regulatory patterns. Panja P, Biswas D, Bhattacharjee S
Cell Genom (Apr 2026)

GWAS-associated variants of related complex traits indicate the presence of pleiotropic clusters often related to tissue-specific epigenomic profiles. The authors introduce J-PEP, a novel framework that enables tissue-aware interpretation of complex trait genetic architecture and PEPA, a cross-modal validation metric. J-PEP factorizes trait and tissue data matrices jointly to identify soft clusters of SNPs that capture both pleiotropic and shared epigenomic patterns in tissues, improving both clustering efficiency and mechanistic interpretation.]]> Wed, 31 Dec 1969 19:00:00 EST