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Thematische Bibliographien / Epigenomic regulators / Zeitschriftenartikel

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Zeitschriftenartikel zum Thema „Epigenomic regulators“

Autor: Grafiati

Veröffentlicht am 25. Mai 2024

Zuletzt aktualisiert am 31. Juli 2025

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1

Al-Janabi, Ismail. "Therapeutic Targeting of the Regulators of Cancer Epigenomes." Al-Rafidain Journal of Medical Sciences ( ISSN 2789-3219 ) 5 (July 1, 2023): 1–13. http://dx.doi.org/10.54133/ajms.v5i.128.

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Aim: To assess the value of targeting the various molecules that regulate the epigenome in the management of cancer. Method: Peer-reviewed articles were examined in PubMed, Google Scholar, and ResearchGate search tools using keywords given in the manuscript. Main points: Three major epigenomic modifications, namely DNA methylation, histone methylation, and histone acetylation, attracted the most research interest and led to a few globally approved drugs for the treatment of various malignancies. The DNA methylation profiles of cancer have been successfully employed in many aspects of the manag

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Paul, Aswathy Mary, Madhavan Radhakrishna Pillai, and Rakesh Kumar. "Prognostic Significance of Dysregulated Epigenomic and Chromatin Modifiers in Cervical Cancer." Cells 10, no. 10 (2021): 2665. http://dx.doi.org/10.3390/cells10102665.

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To broaden the understanding of the epigenomic and chromatin regulation of cervical cancer, we examined the status and significance of a set of epigenomic and chromatin modifiers in cervical cancer using computational biology. We observed that 61 of 917 epigenomic and/or chromatin regulators are differentially upregulated in human cancer, including 25 upregulated in invasive squamous cell carcinomas and 29 in cervical intraepithelial neoplasia 3 (CIN3), of which 14 are upregulated in cervical intraepithelial neoplasia 2 (CIN2). Interestingly, 57 of such regulators are uniquely upregulated in c

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Schmitz, Ulf, Jaynish S. Shah, Bijay P. Dhungel, et al. "Widespread Aberrant Alternative Splicing despite Molecular Remission in Chronic Myeloid Leukaemia Patients." Cancers 12, no. 12 (2020): 3738. http://dx.doi.org/10.3390/cancers12123738.

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Vast transcriptomics and epigenomics changes are characteristic of human cancers, including leukaemia. At remission, we assume that these changes normalise so that omics-profiles resemble those of healthy individuals. However, an in-depth transcriptomic and epigenomic analysis of cancer remission has not been undertaken. A striking exemplar of targeted remission induction occurs in chronic myeloid leukaemia (CML) following tyrosine kinase inhibitor (TKI) therapy. Using RNA sequencing and whole-genome bisulfite sequencing, we profiled samples from chronic-phase CML patients at diagnosis and rem

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Tseng, Yen-Tzu, Hung-Fu Liao, Chih-Yun Yu, Chu-Fan Mo, and Shau-Ping Lin. "Epigenetic factors in the regulation of prospermatogonia and spermatogonial stem cells." REPRODUCTION 150, no. 3 (2015): R77—R91. http://dx.doi.org/10.1530/rep-14-0679.

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Appropriate regulation of epigenome within cells is crucial for the determination of cell fate and contributes to the lifelong maintenance of tissue homeostasis. Epigenomic re-establishment during embryonic prospermatogonia development and fine-tune of the epigenetic landscape in postnatal spermatogonial stem cells (SSCs) are two key processes required for functional male germ cell formation. Repression of re-activated transposons and male germline-specific epigenome establishment occur in prospermatogonia, whereas modulations of the epigenetic landscape is important for SSC self-renewal and d

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Zhou, Huaijun. "97 Dissection of Evolution of Cis-Regulatory Elements and Its Application on Genetic Control of Complex Traits in Farm Animals." Journal of Animal Science 101, Supplement_3 (2023): 51–52. http://dx.doi.org/10.1093/jas/skad281.063.

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Abstract Functional Annotation of Animal Genomes (FAANG) has made significant progress on the improvement of the annotation of the functional elements, particularly non-coding regions in farm animal genomes. Different epigenomes including ChIP-seq for 4 histone marks, ATAC-seq, CTCF-seq, RNA-seq, and Hi-C across different tissues in different animal species were generated. Thousands of cis-regulatory elements including promoters and enhancers across different tissues in different species were identified and annotated. A comprehensive characterization and comparison of cis-regulatory elements a

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Deng, Xian, Xianwei Song, Liya Wei, Chunyan Liu, and Xiaofeng Cao. "Epigenetic regulation and epigenomic landscape in rice." National Science Review 3, no. 3 (2016): 309–27. http://dx.doi.org/10.1093/nsr/nww042.

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Abstract Epigenetic regulation has been implicated in the control of complex agronomic traits in rice (Oryza sativa), a staple food crop and model monocot plant. Recent advances in high-throughput sequencing and the moderately complex genome of rice have made it possible to study epigenetic regulation in rice on a genome-wide scale. This review discusses recent advances in our understanding of epigenetic regulation in rice, with an emphasis on the roles of key epigenetic regulators, the epigenomic landscape, epigenetic variation, transposon repression, and plant development.

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Rada-Iglesias, Alvaro, Ruchi Bajpai, Sara Prescott, Samantha A. Brugmann, Tomek Swigut, and Joanna Wysocka. "Epigenomic Annotation of Enhancers Predicts Transcriptional Regulators of Human Neural Crest." Cell Stem Cell 11, no. 5 (2012): 633–48. http://dx.doi.org/10.1016/j.stem.2012.07.006.

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Smetanina, Mariya A., Valeria A. Korolenya, Alexander E. Kel, et al. "Epigenome-Wide Changes in the Cell Layers of the Vein Wall When Exposing the Venous Endothelium to Oscillatory Shear Stress." Epigenomes 7, no. 1 (2023): 8. http://dx.doi.org/10.3390/epigenomes7010008.

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Epigenomic changes in the venous cells exerted by oscillatory shear stress towards the endothelium may result in consolidation of gene expression alterations upon vein wall remodeling during varicose transformation. We aimed to reveal such epigenome-wide methylation changes. Primary culture cells were obtained from non-varicose vein segments left after surgery of 3 patients by growing the cells in selective media after magnetic immunosorting. Endothelial cells were either exposed to oscillatory shear stress or left at the static condition. Then, other cell types were treated with preconditione

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Boix, Carles A., Benjamin T. James, Yongjin P. Park, Wouter Meuleman, and Manolis Kellis. "Regulatory genomic circuitry of human disease loci by integrative epigenomics." Nature 590, no. 7845 (2021): 300–307. http://dx.doi.org/10.1038/s41586-020-03145-z.

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AbstractAnnotating the molecular basis of human disease remains an unsolved challenge, as 93% of disease loci are non-coding and gene-regulatory annotations are highly incomplete1–3. Here we present EpiMap, a compendium comprising 10,000 epigenomic maps across 800 samples, which we used to define chromatin states, high-resolution enhancers, enhancer modules, upstream regulators and downstream target genes. We used this resource to annotate 30,000 genetic loci that were associated with 540 traits4, predicting trait-relevant tissues, putative causal nucleotide variants in enriched tissue enhance

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Williams, Ruth M., Guneş Taylor, Irving T. C. Ling, et al. "Chromatin remodeller Chd7 is developmentally regulated in the neural crest by tissue-specific transcription factors." PLOS Biology 22, no. 10 (2024): e3002786. http://dx.doi.org/10.1371/journal.pbio.3002786.

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Neurocristopathies such as CHARGE syndrome result from aberrant neural crest development. A large proportion of CHARGE cases are attributed to pathogenic variants in the gene encoding CHD7, chromodomain helicase DNA binding protein 7, which remodels chromatin. While the role for CHD7 in neural crest development is well documented, how this factor is specifically up-regulated in neural crest cells is not understood. Here, we use epigenomic profiling of chick and human neural crest to identify a cohort of enhancers regulating Chd7 expression in neural crest cells and other tissues. We functional

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Kumar, Suresh, Pallavi ., Ashok K. Singh, and Trilochan Mohapatra. "Recent advances in epigenomic techniques: Analysis of DNA base modifications." Indian Journal of Genetics and Plant Breeding (The) 84, no. 02 (2024): 143–55. http://dx.doi.org/10.31742/isgpb.84.2.1.

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Epigenetics refers to the study of modifications in DNA bases, histone proteins and/or alterations in non-coding-RNA biogenesis that cause changes in gene expression without affecting the underlying nucleotide sequence. Epigenetic variation is emerging as one of the regulators of developmental processes and stress responses in animals and plants. Identification and interrogation of epigenetic changes provide unprecedented opportunities for resolving some of the enigmas that could not be solved based on genetic principles. Moreover, epigenome editing might become a preferred technique for the m

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kong, ranran, Ayushi S. Patel, Takashi Sato, et al. "Abstract 5709: Transcriptional circuitry of NKX2-1 and SOX1 defines a previously unrecognized lineage subtype of small cell lung cancer." Cancer Research 82, no. 12_Supplement (2022): 5709. http://dx.doi.org/10.1158/1538-7445.am2022-5709.

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Abstract Introduction: The current molecular classification of small cell lung cancer (SCLC) based on expression of four lineage transcription factors, SCLC-A (ASCL1), SCLC-N (NEUROD1), SCLC-P (POU2F3), and SCLC-Y (YAP1) still leaves its major subtype SCLC-A as a large heterogeneous group, necessitating more precise characterization of lineage subclasses. Experimental procedure: To refine the current SCLC classification and to identify specific lineage features of the SCLC subtypes, we performed unsupervised hierarchical clustering of H3K27ac profiles on transcriptional regulators from 25 SCLC

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Lu, Jia, Xiaoyi Cao, and Sheng Zhong. "EpiAlignment: alignment with both DNA sequence and epigenomic data." Nucleic Acids Research 47, W1 (2019): W11—W19. http://dx.doi.org/10.1093/nar/gkz426.

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Abstract Comparative epigenomics, which subjects both epigenome and genome to interspecies comparison, has become a powerful approach to reveal regulatory features of the genome. Thus elucidated regulatory features surpass the information derived from comparison of genomic sequences alone. Here, we present EpiAlignment, a web-based tool to align genomic regions with both DNA sequence and epigenomic data. EpiAlignment takes DNA sequence and epigenomic profiles derived by ChIP-seq from two species as input data, and outputs the best semi-global alignments. These alignments are based on EpiAlignm

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Bond, Danielle R., Kumar Uddipto, Anoop K. Enjeti, and Heather J. Lee. "Single-cell epigenomics in cancer: charting a course to clinical impact." Epigenomics 12, no. 13 (2020): 1139–51. http://dx.doi.org/10.2217/epi-2020-0046.

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Cancer is a disease of global epigenetic dysregulation. Mutations in epigenetic regulators are common events in multiple cancer types and epigenetic therapies are emerging as a treatment option in several malignancies. A major challenge for the clinical management of cancer is the heterogeneous nature of this disease. Cancers are composed of numerous cell types and evolve over time. This heterogeneity confounds decisions regarding treatment and promotes disease relapse. The emergence of single-cell epigenomic technologies has introduced the exciting possibility of linking genetic and transcrip

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Golimbet, V. E., A. K. Golov, and N. V. Kondratyev. "Post-GWAS era in genetics of schizophrenia." V.M. BEKHTEREV REVIEW OF PSYCHIATRY AND MEDICAL PSYCHOLOGY, no. 4-1 (December 9, 2019): 6–7. http://dx.doi.org/10.31363/2313-7053-2019-4-1-6-7.

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Genome-wide association studies (GWASs) discovered multiple genetic variants associated with schizophrenia. Te next step (post-GWAS analysis) is aimed at identifying the causal genetic variants and biological mechanisms underlying the associations with disease risk. Te following strategies are considered: the study of transcriptional regulation in neuronal human cells and the use of epigenomic information for searching for regulatory elements involved in the pathogenesis of schizophrenia. Te frst strategy includes identifcation of neuronal enhancers, mapping of potential target genes and funct

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Brunmeir, Reinhard, Jingyi Wu, Xu Peng, et al. "Comparative Transcriptomic and Epigenomic Analyses Reveal New Regulators of Murine Brown Adipogenesis." PLOS Genetics 12, no. 12 (2016): e1006474. http://dx.doi.org/10.1371/journal.pgen.1006474.

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Binder, Moritz, Alexandre Gaspar Maia, Ryan M. Carr, et al. "Epigenomic Determinants of Transcriptional Activity in ASXL1-Mutant Chronic Myelomonocytic Leukemia." Blood 134, Supplement_1 (2019): 2987. http://dx.doi.org/10.1182/blood-2019-123191.

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Introduction: Truncating mutations in the Additional Sex Combs-Like 1 (ASXL1) gene are associated with a proliferative disease phenotype and poor survival outcomes across the spectrum of myeloid malignancies including chronic myelomonocytic leukemia (CMML). ASXL1 is thought to act as a chromatin modifier regulating transcriptional activity, however the exact mechanisms and resulting chromatin states remain controversial. We interrogated the epigenome of 16 patients with ASXL1-mutant and -wildtype CMML using a multiomics approach. Methods: Bone marrow mononuclear cells from patients with CMML (

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Cescon, DW. "Abstract ES13-3: Novel epigenomic targets in TNBC." Cancer Research 82, no. 4_Supplement (2022): ES13–3—ES13–3. http://dx.doi.org/10.1158/1538-7445.sabcs21-es13-3.

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Abstract Triple negative breast cancer is a heterogenous disease, characterized by a dearth of recurrent actionable genetic alterations. Epigenetic alterations have been implicated in the pathogenesis of triple negative breast cancer, as well as in the acquisition of drug resistance, which is a commonly observed phenomenon and persisting clinical challenge. An expanding array of tools for epigenomic characterization, together with novel selective inhibitors of epigenetic regulators are enabling new opportunities to identify and target these processes in triple negative breast cancer. Examples

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Blank-Giwojna, Alena, Anna Postepska-Igielska, and Ingrid Grummt. "lncRNA KHPS1 Activates a Poised Enhancer by Triplex-Dependent Recruitment of Epigenomic Regulators." Cell Reports 26, no. 11 (2019): 2904–15. http://dx.doi.org/10.1016/j.celrep.2019.02.059.

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Yildirim, Ferah, Christopher W. Ng, Vincent Kappes, et al. "Early epigenomic and transcriptional changes reveal Elk-1 transcription factor as a therapeutic target in Huntington’s disease." Proceedings of the National Academy of Sciences 116, no. 49 (2019): 24840–51. http://dx.doi.org/10.1073/pnas.1908113116.

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Huntington’s disease (HD) is a chronic neurodegenerative disorder characterized by a late clinical onset despite ubiquitous expression of the mutant Huntingtin gene (HTT) from birth. Transcriptional dysregulation is a pivotal feature of HD. Yet, the genes that are altered in the prodromal period and their regulators, which present opportunities for therapeutic intervention, remain to be elucidated. Using transcriptional and chromatin profiling, we found aberrant transcription and changes in histone H3K27acetylation in the striatum of R6/1 mice during the presymptomatic disease stages. Integrat

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Wattacheril, Julia J., Srilakshmi Raj, David A. Knowles, and John M. Greally. "Using epigenomics to understand cellular responses to environmental influences in diseases." PLOS Genetics 19, no. 1 (2023): e1010567. http://dx.doi.org/10.1371/journal.pgen.1010567.

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It is a generally accepted model that environmental influences can exert their effects, at least in part, by changing the molecular regulators of transcription that are described as epigenetic. As there is biochemical evidence that some epigenetic regulators of transcription can maintain their states long term and through cell division, an epigenetic model encompasses the idea of maintenance of the effect of an exposure long after it is no longer present. The evidence supporting this model is mostly from the observation of alterations of molecular regulators of transcription following exposure

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Rovira, Meritxell, Goutham Atla, Miguel Angel Maestro, et al. "REST is a major negative regulator of endocrine differentiation during pancreas organogenesis." Genes & Development 35, no. 17-18 (2021): 1229–42. http://dx.doi.org/10.1101/gad.348501.121.

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Multiple transcription factors have been shown to promote pancreatic β-cell differentiation, yet much less is known about negative regulators. Earlier epigenomic studies suggested that the transcriptional repressor REST could be a suppressor of endocrinogenesis in the embryonic pancreas. However, pancreatic Rest knockout mice failed to show abnormal numbers of endocrine cells, suggesting that REST is not a major regulator of endocrine differentiation. Using a different conditional allele that enables profound REST inactivation, we observed a marked increase in pancreatic endocrine cell formati

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Zibetti, Cristina. "Deciphering the Retinal Epigenome during Development, Disease and Reprogramming: Advancements, Challenges and Perspectives." Cells 11, no. 5 (2022): 806. http://dx.doi.org/10.3390/cells11050806.

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Retinal neurogenesis is driven by concerted actions of transcription factors, some of which are expressed in a continuum and across several cell subtypes throughout development. While seemingly redundant, many factors diversify their regulatory outcome on gene expression, by coordinating variations in chromatin landscapes to drive divergent retinal specification programs. Recent studies have furthered the understanding of the epigenetic contribution to the progression of age-related macular degeneration, a leading cause of blindness in the elderly. The knowledge of the epigenomic mechanisms th

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Torres-Campana, Daniela, Béatrice Horard, Sandrine Denaud, Gérard Benoit, Benjamin Loppin, and Guillermo A. Orsi. "Three classes of epigenomic regulators converge to hyperactivate the essential maternal gene deadhead within a heterochromatin mini-domain." PLOS Genetics 18, no. 1 (2022): e1009615. http://dx.doi.org/10.1371/journal.pgen.1009615.

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The formation of a diploid zygote is a highly complex cellular process that is entirely controlled by maternal gene products stored in the egg cytoplasm. This highly specialized transcriptional program is tightly controlled at the chromatin level in the female germline. As an extreme case in point, the massive and specific ovarian expression of the essential thioredoxin Deadhead (DHD) is critically regulated in Drosophila by the histone demethylase Lid and its partner, the histone deacetylase complex Sin3A/Rpd3, via yet unknown mechanisms. Here, we identified Snr1 and Mod(mdg4) as essential fo

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Malta, Tathiane, Thais Sabedot, Indrani Datta, et al. "OTEH-10. Evolutionary trajectory of epigenomic of gliomas." Neuro-Oncology Advances 3, Supplement_2 (2021): ii12. http://dx.doi.org/10.1093/noajnl/vdab070.049.

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Abstract Gliomas are the most common malignant brain tumor, have an aggressive behavior, and invariably relapse and progress. Despite the recent advancements, little is known about the role of the epigenome in glioma disease progression and recurrence. To investigate the molecular dynamics over time and in response to therapeutic pressures, the Glioma Longitudinal AnalySiS (GLASS) Consortium, a multinational collaboration, is investigating epigenome-wide molecular data from primary and recurrent matched pairs, including IDH mutant (IDHmut) and IDH wildtype (IDHwt) gliomas. We have compiled a t

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Duraisingh, Manoj T., and Kristen M. Skillman. "Epigenetic Variation and Regulation in Malaria Parasites." Annual Review of Microbiology 72, no. 1 (2018): 355–75. http://dx.doi.org/10.1146/annurev-micro-090817-062722.

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Eukaryotic pathogens must survive in different hosts, respond to changing environments, and exploit specialized niches to propagate. Plasmodium parasites cause human malaria during bloodstream infections, where they must persist long enough to be transmitted. Parasites have evolved diverse strategies of variant gene expression that control critical biological processes of blood-stage infections, including antigenic variation, erythrocyte invasion, innate immune evasion, and nutrient acquisition, as well as life-cycle transitions. Epigenetic mechanisms within the parasite are being elucidated,

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Wu, Tuoqi, Ziang Zhu, Safuwra Wizzard, and Chen Yao. "Joint single-cell transcriptomic and epigenomic analysis reveals key regulators of CAR T cell stemness and antitumor immunity." Journal of Immunology 212, no. 1_Supplement (2024): 1425_4772. http://dx.doi.org/10.4049/jimmunol.212.supp.1425.4772.

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Abstract The differentiation of antitumor T cells is tightly controlled by transcriptional and epigenetic pathways. Understanding the programs governing the differentiation of therapeutic T cells such as chimeric antigen receptor (CAR) T cells is crucial for improving their efficacy. Using a single-cell multi-omics approach, we simultaneously profiled chromatin accessibility and transcription within the same single CAR T cell in mice with B-cell leukemia or melanoma. One of the CAR T-cell subsets displayed stem cell-like properties and greater proliferative potential upon tumor challenge. In a

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Tan, Jiaxing, Yali Ding, Bing He, et al. "Abstract 2727: Histone deacetylase (HDAC1) and IKAROS are critical regulators of histone methylation and epigenomic landscape in T-cell acute lymphoblastic leukemia." Cancer Research 85, no. 8_Supplement_1 (2025): 2727. https://doi.org/10.1158/1538-7445.am2025-2727.

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Abstract Objective: To dissect the role of IKAROS-HDAC1 complexes in global regulation of gene expression and chromatin landscape in T-ALL. Methods: We studied IKAROS and HDAC1 role in epigenomic regulation of gene expression in primary human T-ALL, IKZF1-null human T-ALL, Ikzf1-null mouse T-ALL cells and following IKZF1-re-introduction into IKZF1-null human and mouse T-ALL cells. We used ATAC-seq and ChIP-seq of IKAROS, HDAC1, Enhancer of zeste homolog 2 (EZH2), along with CUT&Tag of histone modification markers, coupled with RNA-seq to study dynamic effect of IKAROS in IKZF1- null T-ALL

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Li, Cong-Jun, and Robert W. Li. "Bioinformatic Dissecting of TP53 Regulation Pathway Underlying Butyrate-induced Histone Modification in Epigenetic Regulation." Genetics & Epigenetics 6 (January 2014): GEG.S14176. http://dx.doi.org/10.4137/geg.s14176.

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Butyrate affects cell proliferation, differentiation, and motility. Butyrate inhibits histone deacetylase (HDAC) activities and induces cell-cycle arrest and apoptosis. TP53 is one of the most active upstream regulators discovered by ingenuity pathways analysis (IPA) in our RNA-sequencing data set. TP53 signaling pathway plays key role in many cellular processes. TP53 pathway and their involvement in cellular functions modified by butyrate treatment were scrutinized in this report by data mining the RNA-sequencing data using IPA (Ingenuity System®). The TP53 mechanistic pathway targets more th

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Wan, Chunhua, Sylvia Mahara, Claire Sun та ін. "Genome-scale CRISPR-Cas9 screen of Wnt/β-catenin signaling identifies therapeutic targets for colorectal cancer". Science Advances 7, № 21 (2021): eabf2567. http://dx.doi.org/10.1126/sciadv.abf2567.

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Aberrant activation of Wnt/β-catenin pathway is a key driver of colorectal cancer (CRC) growth and of great therapeutic importance. In this study, we performed comprehensive CRISPR screens to interrogate the regulatory network of Wnt/β-catenin signaling in CRC cells. We found marked discrepancies between the artificial TOP reporter activity and β-catenin–mediated endogenous transcription and redundant roles of T cell factor/lymphoid enhancer factor transcription factors in transducing β-catenin signaling. Compiled functional genomic screens and network analysis revealed unique epigenetic regul

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Zhang, Kai, Mengchi Wang, Ying Zhao, and Wei Wang. "Taiji: System-level identification of key transcription factors reveals transcriptional waves in mouse embryonic development." Science Advances 5, no. 3 (2019): eaav3262. http://dx.doi.org/10.1126/sciadv.aav3262.

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Transcriptional regulation is pivotal to the specification of distinct cell types during embryonic development. However, it still lacks a systematic way to identify key transcription factors (TFs) orchestrating the temporal and tissue specificity of gene expression. Here, we integrated epigenomic and transcriptomic data to reveal key regulators from two cells to postnatal day 0 in mouse embryogenesis. We predicted three-dimensional chromatin interactions in 12 tissues across eight developmental stages, which facilitates linking TFs to their target genes for constructing transcriptional regulat

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Sun, Qian-Hui, Zi-Yu Kuang, Guang-Hui Zhu, Bao-Yi Ni, and Jie Li. "Multifaceted role of microRNAs in gastric cancer stem cells: Mechanisms and potential biomarkers." World Journal of Gastrointestinal Oncology 16, no. 2 (2024): 300–313. http://dx.doi.org/10.4251/wjgo.v16.i2.300.

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MicroRNAs (miRNAs) have received much attention in the past decade as potential key epigenomic regulators of tumors and cancer stem cells (CSCs). The abnormal expression of miRNAs is responsible for different phenotypes of gastric cancer stem cells (GCSCs). Some specific miRNAs could be used as promising biomarkers and therapeutic targets for the identification of GCSCs. This review summarizes the coding process and biological functions of miRNAs and demonstrates their role and efficacy in gastric cancer (GC) metastasis, drug resistance, and apoptosis, especially in the regulatory mechanism of

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Ayyamperumal, Parichitran, Hemant Chandru Naik, Amlan Jyoti Naskar, Lakshmi Sowjanya Bammidi, and Srimonta Gayen. "Epigenomic states contribute to coordinated allelic transcriptional bursting in iPSC reprogramming." Life Science Alliance 7, no. 4 (2024): e202302337. http://dx.doi.org/10.26508/lsa.202302337.

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Two alleles of a gene can be transcribed independently or coordinatedly, which can lead to temporal expression heterogeneity with potentially distinct impacts on cell fate. Here, we profiled genome-wide allelic transcriptional burst kinetics during the reprogramming of MEF to induced pluripotent stem cells. We show that the degree of coordination of allelic bursting differs among genes, and alleles of many reprogramming-related genes burst in a highly coordinated fashion. Notably, we show that the chromatin accessibility of the two alleles of highly coordinated genes is similar, unlike the sem

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Nam, Chehyun. "Abstract 4461: Unveiling the links between methionine metabolism and epigenomic reprogramming in upper aerodigestive squamous cell carcinoma." Cancer Research 84, no. 6_Supplement (2024): 4461. http://dx.doi.org/10.1158/1538-7445.am2024-4461.

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Abstract Upper aerodigestive squamous cell carcinoma (UASCC) presents as a prevalent and aggressive malignancy, posing challenges in terms of effective therapeutic interventions. In this study, we explored the intricacies of amino acid metabolism within UASCC, revealing an unexpected observation that distinguishes UASCC among all human cancers, having the highest methionine levels, driven by the overexpression of its transporter LAT1. Notably, LAT1 exhibits peak expression levels in UASCC, regulated at the transcriptional level by UASCC-specific promoters and enhancers, co-regulated by SCC mas

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Bolitho, Annabelle, and Hongbing Liu. "Epigenetic Regulation in Wilms Tumor." Biomedicines 13, no. 7 (2025): 1678. https://doi.org/10.3390/biomedicines13071678.

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Wilms tumor (nephroblastoma), the most common pediatric renal malignancy, has a complex genetic and epigenetic landscape. While mutations in genes like WT1, CTNNB1, and WTX have been well characterized, accumulating evidence suggests that epigenetic dysregulation plays a pivotal role in WT pathogenesis. This review examines the various epigenetic mechanisms implicated in WT, including DNA methylation, histone modifications, chromatin remodeling, and non-coding RNA-mediated regulation. We discuss how epigenetic mechanisms contribute to tumor initiation, progression, and heterogeneity and their

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Kurowska, Aleksandra, Azari Bantan, Raghad Shuwaikan, et al. "Mapping Disease Transitions from Premalignant, Asymptomatic to Advanced Myeloma through Integrative Epigenomic and Transcriptional Analyses." Blood 144, Supplement 1 (2024): 1889. https://doi.org/10.1182/blood-2024-209833.

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Multiple myeloma (MM) is a complex malignancy marked by the abnormal proliferation of plasma cells (PCs) in the bone marrow (BM). This disease progresses from asymptomatic stages, including monoclonal gammopathy of undetermined significance (MGUS) and smouldering multiple myeloma (SMM), to active MM. The transition through these different states requires the acquisition of genetic aberrations and changes in gene expression patterns, which have been well characterized. Beyond genetics, the role of epigenetic modifications has transformed our understanding of malignant cellular transformation, i

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McKinsey, Timothy A., Thomas M. Vondriska, and Yibin Wang. "Epigenomic regulation of heart failure: integrating histone marks, long noncoding RNAs, and chromatin architecture." F1000Research 7 (October 29, 2018): 1713. http://dx.doi.org/10.12688/f1000research.15797.1.

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Epigenetic processes are known to have powerful roles in organ development across biology. It has recently been found that some of the chromatin modulatory machinery essential for proper development plays a previously unappreciated role in the pathogenesis of cardiac disease in adults. Investigations using genetic and pharmacologic gain- and loss-of-function approaches have interrogated the function of distinct epigenetic regulators, while the increased deployment of the suite of next-generation sequencing technologies have fundamentally altered our understanding of the genomic targets of thes

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Siu, Celia, Sam Wiseman, Sitanshu Gakkhar, et al. "Characterization of the human thyroid epigenome." Journal of Endocrinology 235, no. 2 (2017): 153–65. http://dx.doi.org/10.1530/joe-17-0145.

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The thyroid gland, necessary for normal human growth and development, functions as an essential regulator of metabolism by the production and secretion of appropriate levels of thyroid hormone. However, assessment of abnormal thyroid function may be challenging suggesting a more fundamental understanding of normal function is needed. One way to characterize normal gland function is to study the epigenome and resulting transcriptome within its constituent cells. This study generates the first published reference epigenomes for human thyroid from four individuals using ChIP-seq and RNA-seq. We p

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Sobocińska, Joanna, Sara Molenda, Marta Machnik, and Urszula Oleksiewicz. "KRAB-ZFP Transcriptional Regulators Acting as Oncogenes and Tumor Suppressors: An Overview." International Journal of Molecular Sciences 22, no. 4 (2021): 2212. http://dx.doi.org/10.3390/ijms22042212.

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Krüppel-associated box zinc finger proteins (KRAB-ZFPs) constitute the largest family of transcriptional factors exerting co-repressor functions in mammalian cells. In general, KRAB-ZFPs have a dual structure. They may bind to specific DNA sequences via zinc finger motifs and recruit a repressive complex through the KRAB domain. Such a complex mediates histone deacetylation, trimethylation of histone 3 at lysine 9 (H3K9me3), and subsequent heterochromatization. Nevertheless, apart from their repressive role, KRAB-ZFPs may also co-activate gene transcription, likely through interaction with oth

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Yi, Mei, Yixin Tan, Li Wang, et al. "TP63 links chromatin remodeling and enhancer reprogramming to epidermal differentiation and squamous cell carcinoma development." Cellular and Molecular Life Sciences 77, no. 21 (2020): 4325–46. http://dx.doi.org/10.1007/s00018-020-03539-2.

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Abstract Squamous cell carcinoma (SCC) is an aggressive malignancy that can originate from various organs. TP63 is a master regulator that plays an essential role in epidermal differentiation. It is also a lineage-dependent oncogene in SCC. ΔNp63α is the prominent isoform of TP63 expressed in epidermal cells and SCC, and overexpression promotes SCC development through a variety of mechanisms. Recently, ΔNp63α was highlighted to act as an epidermal-specific pioneer factor that binds closed chromatin and enhances chromatin accessibility at epidermal enhancers. ΔNp63α coordinates chromatin-remode

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El Zarif, Talal, Karl Semaan, Marc Eid, et al. "Epigenomic profiling nominates master transcription factors (TFs) driving sarcomatoid differentiation (SD) of renal cell carcinoma (RCC)." Oncologist 28, Supplement_1 (2023): S8. http://dx.doi.org/10.1093/oncolo/oyad216.012.

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Abstract Background Sarcomatoid differentiation of RCC (sRCC) is associated with poor survival. Recent studies showed marked response of sRCC to immune checkpoint blockade (ICB). While distinctive patterns of gene expression in sRCC have been identified, the gene regulatory programs and TFs that drive SD remain unknown. The aim of this study is to nominate TFs responsible for SD and to investigate their association with the clinical outcomes of patients with RCC. Methods Chromatin immunoprecipitation and sequencing (ChIP-seq) for H3K27ac – a histone modification associated with active regulato

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Volpato, Viola. "Integration of functional genomics data to uncover cell type-specific pathways affected in Parkinson's disease." Biochemical Society Transactions 49, no. 5 (2021): 2091–100. http://dx.doi.org/10.1042/bst20210128.

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Parkinson's disease (PD) is the second most prevalent late-onset neurodegenerative disorder worldwide after Alzheimer's disease for which available drugs only deliver temporary symptomatic relief. Loss of dopaminergic neurons (DaNs) in the substantia nigra and intracellular alpha-synuclein inclusions are the main hallmarks of the disease but the events that cause this degeneration remain uncertain. Despite cell types other than DaNs such as astrocytes, microglia and oligodendrocytes have been recently associated with the pathogenesis of PD, we still lack an in-depth characterisation of PD-affe

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Yamagishi, Makoto. "The role of epigenetics in T-cell lymphoma." International Journal of Hematology, October 14, 2022. http://dx.doi.org/10.1007/s12185-022-03470-1.

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AbstractMalignant lymphomas are a group of diseases with epigenomic abnormalities fundamental to pathogenesis and pathophysiology. They are characterized by a high frequency of abnormalities related to DNA methylation regulators (DNMT3A, TET2, IDH2, etc.) and histone modifiers (EZH2, HDAC, KMT2D/MLL2, CREBBP, EP300, etc.). These epigenomic abnormalities directly amplify malignant clones. They also originate from a hematopoietic stem cell-derived cell lineage triggered by epigenomic changes. These characteristics are linked to their high affinity for epigenomic therapies. Hematology has led dis

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Bell, Christopher G. "Epigenomic insights into common human disease pathology." Cellular and Molecular Life Sciences 81, no. 1 (2024). http://dx.doi.org/10.1007/s00018-024-05206-2.

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AbstractThe epigenome—the chemical modifications and chromatin-related packaging of the genome—enables the same genetic template to be activated or repressed in different cellular settings. This multi-layered mechanism facilitates cell-type specific function by setting the local sequence and 3D interactive activity level. Gene transcription is further modulated through the interplay with transcription factors and co-regulators. The human body requires this epigenomic apparatus to be precisely installed throughout development and then adequately maintained during the lifespan. The causal role o

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Henaff, Carole Le, Nicola Partridge, Frederic Jehan, and Valerie Geoffroy. "Identification of epigenomic regulators of osteoblast function." Bone Abstracts, April 21, 2016. http://dx.doi.org/10.1530/boneabs.5.p249.

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Sikora, Matthew Joseph, and Joseph Sottnik. "Estrogen Receptor co-opts Mediator of DNA Damage Checkpoint 1 (MDC1) to Drive Epigenomic Remodeling and Transcriptional Regulation in ILC Cells." Endocrinology 166, Supplement_1 (2025). https://doi.org/10.1210/endocr/bqaf043.007.

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Abstract Text Estrogen receptor-α (ER) has unique regulatory activities in invasive lobular carcinoma (ILC) of the breast associated with endocrine response and anti-estrogen resistance. 95 percent of ILC tumors are ER+ yet respond poorly to endocrine therapies. We previously linked these observations to an ILC-specific interaction between ER and Mediator of DNA Damage Checkpoint 1 (MDC1). MDC1 is a keystone of DNA damage repair, yet in ILC it has a novel and critical role in ER-mediated gene regulation. We sought to define the putative ILC-specific co-regulatory function of MDC1 to identify t

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Lee, Ji-Eun, Hannah Schmidt, Binbin Lai, and Kai Ge. "Transcriptional and Epigenomic Regulation of Adipogenesis." Molecular and Cellular Biology 39, no. 11 (2019). http://dx.doi.org/10.1128/mcb.00601-18.

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ABSTRACT Understanding adipogenesis, the process of adipocyte development, may provide new ways to treat obesity and related metabolic diseases. Adipogenesis is controlled by coordinated actions of lineage-determining transcription factors and epigenomic regulators. Peroxisome proliferator-activated receptor gamma (PPARγ) and C/EBPα are master “adipogenic” transcription factors. In recent years, a growing number of studies have reported the identification of novel transcriptional and epigenomic regulators of adipogenesis. However, many of these novel regulators have not been validated in adipo

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Pandey, Saurabh Prakash, Ruben M. Benstein, Yanwei Wang, and Markus Schmid. "Epigenetic Regulation of Temperature Responses – Past Successes and Future Challenges." Journal of Experimental Botany, May 29, 2021. http://dx.doi.org/10.1093/jxb/erab248.

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Abstract In contrast to animals, plants cannot avoid unfavorable temperature conditions. Instead, plants have evolved intricate signaling pathways that enable them to perceive and respond to temperature. General acclimation processes that prepare the plant to respond to stressful heat and cold, usually occur throughout the whole plant. More specific temperature responses, however, are limited to certain tissues or cell types. While global responses are amenable to epigenomic analyses, responses which are highly localized are more problematic as the chromatin in question is not easily accessibl

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Abdulla, Amith Z., Cédric Vaillant, and Daniel Jost. "Painters in chromatin: a unified quantitative framework to systematically characterize epigenome regulation and memory." Nucleic Acids Research, August 26, 2022. http://dx.doi.org/10.1093/nar/gkac702.

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Abstract In eukaryotes, many stable and heritable phenotypes arise from the same DNA sequence, owing to epigenetic regulatory mechanisms relying on the molecular cooperativity of ‘reader–writer’ enzymes. In this work, we focus on the fundamental, generic mechanisms behind the epigenome memory encoded by post-translational modifications of histone tails. Based on experimental knowledge, we introduce a unified modeling framework, the painter model, describing the mechanistic interplay between sequence-specific recruitment of chromatin regulators, chromatin-state-specific reader–writer processes

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Zhao, Yanding, Yadong Dong, Wei Hong, Chongming Jiang, Kevin Yao, and Chao Cheng. "Computational modeling of chromatin accessibility identified important epigenomic regulators." BMC Genomics 23, no. 1 (2022). http://dx.doi.org/10.1186/s12864-021-08234-5.

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AbstractChromatin accessibility is essential for transcriptional activation of genomic regions. It is well established that transcription factors (TFs) and histone modifications (HMs) play critical roles in chromatin accessibility regulation. However, there is a lack of studies that quantify these relationships. Here we constructed a two-layer model to predict chromatin accessibility by integrating DNA sequence, TF binding, and HM signals. By applying the model to two human cell lines (GM12878 and HepG2), we found that DNA sequences had limited power for accessibility prediction, while both TF

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